Call for participation in the Fourteen Razi Researchthc.tums.ac.ir/UserFiles/File/The Journal of...

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Call for participation in the Fourteen Razi Research

Festival on Medical Sciences

The National Research Center for Medical Sciences of the Islamic Republic of Iran organizes the

annual Razi Research Festival on medical sciences to encourage and identify talents and contribute to

the improvement of research on medical sciences and encourage further development in medicine

The prize will be presented to the researcher, faculty member, talented students of medical sciences

whose works and researches have led to significant advances in medical and health sciences.

The 14th

Razi Medical Sciences Research Festival will be held in collaboration with the

researchers of member states of the Islamic Educational, Scientific and Cultural Organization (ISESCO)

in December 2008, the year with the theme of innovation and flourishing. The objective behind holding

the conference is to introduce the best practices on medical sciences researches with emphasis on

innovation in the field of research and technology.

Highlight of Razi Festival

Razi Festival was initiated at Tehran University of Medical Sciences in 1995. The Festival prize for

medical resean is designated to encourage and reward medical researchers. The prize is awarded

annually for an outstanding, ground-breaking medical research project and may be awarded to an

individual or a research team. Prize recipients are selected on the basis of two principal criteria, equally

scored: (1) nobility of the article; (2) mastery of the candidates. Other evaluation criteria would be:

1. Universities and student research centers will be evaluated on the basis of their quality and

quantity of knowledge production, resource mobilization and capacity building in research.

2. Evaluation of the research centers are based on the annual assessment carried out by the

Undersecretary for Research and Technology, MOHME

3. NGOs, institutes, companies and charities awarding research grants are nominated by the

recipients.

The eligible candidates will be mainly within two categories:

National:

1- Researchers

2- Junior researchers (non-student, 30 years old and less)

3- Student researchers in all fields of medical sciences (official document from university is needed)

4- Investigators on the subject of Health Sector Reform

5- Innovators, inventers and creators of confirmed medical hypothesis and ideas

6- Universities of Medical Sciences

7- Approved Medical Sciences Research Centers

8- Student Medical Sciences Research Committee

9- NGO companies, charities and scientific societies that support research on medical sciences

10- Approved scientific research journals of medical sciences.

2

International:

1-Iranian researchers who stay abroad

2- Researchers from member states of ISESCO

Peer Review processing

Prize recipients are selected on the basis of two principal criteria, equally scored:

(1) Nobility of the article; (2) Mastery of the candidates.

Applicants should specifically address how their work meets the following criteria:

Judging criteria for article:

1. Priority;

2. Innovation;

3. Applicability;

4. Scientific Methodology;

5. Nature of Outputs (e.g. scientific papers in quality journals);

6. The size of work;

7. Participatory work;

8. Potential Impact.

Research criteria:

Brief biography including major scientific/ technical accomplishments, published articles in

credited journals indexed by Medical Journals Databases

Significant publications (books)

Sustained leadership contributions in improving healthcare, technology customizing, and patient

care; or who have successfully pursued innovative improvement in public health with

demonstrated translational benefits applied to improve quality of life.

Curriculum vitae

Supporting Documents:

1- A printed copy of online entry form

2- Full text of the article entered in this Festival, the applicant should be the first or second author

3- Recent 5 year CV

4- Copies of 5 recent significant articles and a copy of published book

5- Complete list of recent 5 years publications that are indexed by Medical Journal Databases

The festival will include basic sciences, health sciences, surgical and non-surgical medical sciences,

pharmacology, nutrition, dentistry, rehabilitation, modern technology, health sector reform.

The article should be published in a credited medical journal after 2006

The candidate should be the main investigator of the research team or the first or second author

of the article.

Postal Address:

No 26-Yekom Alley, Kohenoor Avenue, Motaharie Street, Tehran-IRAN,

Postal Cod : 1587656811

or By email: [email protected]

Tel: (+9821) 88504057, 88504053

Fax: (+9821) 88730830

Email: www.razi.hbi.ir

THE

JOURNAL OF

TEHRAN UNIVERSITY

HEART CENTER

Editor-in-Chief

ABBASALI KARIMI, MD

ASSOCIATE PROFESSOR OF CARDIAC SURGERY

TEHRAN UNIVERSITY OF MEDICAL SCIENCES

Managing Editor

SEYED HESAMEDDIN ABBASI, MD

TEHRAN HEART CENTER

TEHRAN UNIVERSITY OF MEDICAL SCIENCES

International Editors

Jean Marco, MD, FESC

Centre Cardio- Thoracique de Monaco

France

Zohair Yousef Al-halees, MD , FRCSC, FACS

King Faisal Heart Institute

Saudi Arabia

Ali Massumi, MD

Texas Heart Institute

U. S. A

Hooshang Bolooki, MD, FRCS (C), FACS, FCCP

University of Miami, School of Medicine

U. S. A

Carlos-A. Mestres, MD

University of Barcelona

Spain

Yadolah Dodge, PhD

University of Neuchâtel

Switzerland

Mohammed T. Numan, MD

Hamad Medical Corporation

Qatar

Ali Dodge–Khatami, MD, PhD

University of Zürich

Switzerland

Ahmand S. Omran, MD, FACC, FASE

King Abdulaziz Cardiac Center

Saudi Arabia

Iradj Gandjbakhch, MD

Hopital Pitie

France

Mehrdad Rezaee, MD, PhD

Stanford University, School of Medicine

U. S. A

Omer Isik, MD

Yeditepe University, School of Medicine

Turkey

Lee Samuel Wann, MD

Wisconsin Heart Hospital

U. S. A

Sami S. Kabbani, MD

Damascus University Cardiovascular Surgical Center

Syria

Kayvan Kamalvand, MD, FRCP, FACC

William Harvey Hospital

United Kingdom

Editorial Board

Sina Moradmand Badie, MD

Amir Alam Hospital Tehran University of Medical Sciences

Hossien Ahmadi, MD

Tehran Heart Center Tehran University of Medical Sciences

Mohammad-Hasan Namazi

Shaheed Modarres Hospital

Shaheed beheshti University of Medical Sciences

Shahin Akhondzadeh, PhD

Roozbeh Psychiatric Hospital

Tehran University of Medical Sciences

Ebrahim Nematipour, MD

Tehran Heart Center


Mohammad Ali Boroumand, MD

Tehran Heart Center


Rezayat Parvizi, MD

Shaheed Madani Heart Hospital Tabriz University of Medical Sciences

Ahmad Reza Dehpour, PhD

Department of Pharmacology Tehran University of Medical Sciences

Masoud Pezeshkian

Shaheed Madani Heart Hospital

Tabriz University of Medical Sciences

Abbasali Karimi, MD

Tehran Heart Center


Hassan Radmehr, MD

Imam Khomeini HospitalDavood Kazemi Saleh, MD

Baghiatallah HospitalTehran University of Medical SciencesBaghiatallah University of Medical Sciences

Saeed Sadeghian, MD

Tehran Heart Center


Majid Maleki, MD

Shaheed Rajaie Cardiovascular Medical Center

Iran University of Medical Sciences

Mojtaba Salarifar, MD


Mehrab Marzban, MD


Nizal Sarraf –Zadegan, MD

Isfahan Cardiovascular Research Center

Isfahan University of Medical Sciences

Seyed Rasoul Mirsharifi, MD

Imam Khomeini Hospital


Ahmad Yaminisharif, MD

Tehran Heart Center


Ahmad Mohebi, MD

Shaheed Rajaie Cardiovascular Medical Center


Mohammad Reza Zafarghandi, MD

Sina Hospital Tehran University of Medical Sciences

Seyed Mahmood Mirhoseini, MD, DSc, FACC, FAES


Aliakbar Zeinaloo, MD

Children Medical Center's Hospital


Mansor Moghadam, MD

Imam Khomeini Hospital


Advisory Editors

Seyed Ebrahim Kassaian, MD Tehran Heart Center


Kiyomars Abbasi, MD Tehran Heart Center


Ali Kazemi Saeed, MD Tehran Heart Center


Seifollah Abdi, MD Shaheed Rajaie Cardiovascular Medical Center


Elise Langdon- NeunerThe editor of The Write Stuff (The Journal of The

European Medical Writers Association), Austria

Mohammad Alidoosti, MDTehran Heart Center


Jalil Majd Ardekani, MD Tehran Heart Center


Naser Aslanabadi, MD Shaheed Madani Heart Hospital

Tabriz University of Medical Sciences

Fardin Mirbolook, MD Dr. Heshmat Hospital

Gilan University of Medical Sciences

Alireza Amirzadegan, MD Tehran Heart Center


Mehdi Najafi, MDTehran Heart Center


Sirous Darabian, MD Tehran Heart Center


Younes Nozari, MD Imam Khomeini Hospital


Gholamreza Davoodi, MD Tehran Heart Center


Hamid Reza Pour Hosseini, MD Tehran Heart Center


Saeed Davoodi, MD Tehran Heart Center


Hakimeh Sadeghian, MDTehran Heart Center


Iraj Firoozi, MD Shaheed Rajaie Cardiovascular Medical Center


Mohammad Saheb Jam, MD & PT Tehran Heart Center


Seyed Khalil Foroozannia, MD Afshar Haspital

Shaheed Sadoghi University of Medical Sciences

Abbas Salehi Omran, MD Tehran Heart Center


Armen Gasparyan MD, PhD Yerevan State Medical University

Armenia

Abbas Soleimani, MD Tehran Heart Center


Ali Ghaemian, MD Mazandaran Heart Center

Mazandaran University of Medical Sciences

Mahmood Shabestari, MD Imam Reza Hospital

Mashhad University of Medical Sciences

Namvar Ghasemi Movahedi, MD Tehran Heart Center


Shapour Shirani, MDTehran Heart Center


Abbas Ghiasi, MD Tehran Heart Center


Seyed Abdolhosein Tabatabaei, MD Shariati Hospital


Seyed Kianoosh Hoseini Tehran Heart Center


Arezou Zoroufian, MD Tehran Heart Center


Mohammad Jafar Hashemi, MD Shaheed Rajaie Cardiovascular Medical Center


Statistical Consultant

Mahmood Sheikh Fathollahi,

Technical Editors

Pedram Amouzadeh Fatemeh Talebian

Office

Fatemeh Esmaeili Darabi

The Journal of Tehran University Heart Center is indexed in EMBASE, CAB Abstracts, Global Health, DOAJ, Geneva Index

Copernicus, Index Medicus for the WHO Eastern Mediterranean Region (IMEMR), SID, Iranmedex and Magiran

Address

North Kargar Street, Tehran Heart Center, Tehran, Iran 1411713138. Tel: +98-21-88029720. Fax: +98-21-88029702.

Web Site: http://jthc.tums.ac.ir. E-mail: [email protected].

The Journal of Tehran University Heart Center

Editorial

Pretty Pictures: Assessing the Value of Cardiac ImagingSamuel Wann ........................................................................................................................................................................................................................... 57

Review Article

Echocardiographic Evaluation of Intracardiac MassesMaryam Esmaeilzadeh .............................................................................................................................................................................................................59

Original Articles

Coronary Artery Bypass Combined with Total Occlusion of Internal Carotid ArteryKyomars Abbasi, Shapour Shirani, Mohsen Fadaei Araghi, Abbasali Karimi, Hossein Ahmadi, Seyed Hesameddin Abbasi, Naghmeh Moshtaghi .......................................................................................................................................77

Prevention of Atrioventricular Block During Radiofrequency Ablation by Pace Mapping of Koch’s TriangleMohammad Hasan Namazi, Hassan Kamalzadeh, Morteza Safi, Reza Karbasi Afshar, Mohammad Reza Motamedi, Habibollah Saadat, Hossein Vakili ............................................................................................................................................83

Repair Versus Replacement for Ischemic Mitral RegurgitationHakimeh Sadeghian, Abbasali Karimi, Mehran Mahmoodian, Hossein Ahmadi, Seyed Hesameddin Abbasi .......................................................................89

Intracardiac Shunts and Role of Tissue Doppler Imaging in Diagnosis and Discrimination Mohammad Asadpour Piranfar, Mersedeh Karvandi, Arash Mohammadi Tofigh ...................................................................................................................95

Quality of Life in Coronary Artery Disease: SF-36 Compared to WHOQOL-BREFMahdi Najafi, Mehrdad Sheikhvatan, Ali Montazeri, Seyed Hesameddin Abbasi, Mahmood Sheikhfatollahi ................................................................... 101

An Echocariographic Study of Heart in a Group of Male Adult Elite Athletes

Soheila Dabiran, Parichehr Tutunchi, Amir Sasan Tutunchi, Gholamhasan Khosravi, Ahmad Mohebi, Hamidreza Goodarzynejad ................................. 107

Case Report

Device-Induced Perforation of Right Atrium Following Interventional Closure of Atrial Septal Defect (ASD)Ramin Baghaei Tehrani, Alireza Rostami, Hosein Ali Basiri, Hojatollah Mortezaiian ..........................................................................................................113

ContentVolume: 3 Number: 2 Spring 2008



“The Journal of Tehran University Heart Center’’

The Journal of Tehran University Heart Center is indexed

in EMBASE, CAB Abstracts, Global Health, DOAJ, Geneva

Foundation for Medical Education and Research, Index

Copernicus, Index Medicus for the WHO Eastern Mediterranean

Region (IMEMR), SID, Iranmedex and Magiran

57The Journal of Tehran University Heart Center

Editorial

Pretty Pictures: Assessing the

Value of Cardiac Imaging

Samuel Wann MD, MACC*

Wisconsin Heart Hospital, Milwaukee, WI, USA.

This issue of the Journal includes three papers which employ the latest in high technology ultrasonic imaging to delineate various features of cardiovascular disease. Dabiran et al took advantage of the high resolution, noninvasive nature of echocardiography to detect subtle differences in cardiac adaptation to dynamic versus static exercise. Sadeghian et al employed color Doppler to document the degree of mitral regurgitation in patients undergoing CABG with and without mitral valve repair. Piranafar et al used recently developed technology for tissue Doppler imaging to detect intracardiac shunts in patients with congenital heart disease.

These papers all reflect our enthusiasm for new and increasingly sophisticated imaging technology. Surely, modern medical imaging is one of the most important scientific accomplishments of the last century, if not the last millennium. The potential for this new technology to provide enhanced and expanded understanding of fundamental disease processes such as atherosclerosis, myocardial infarction, and other acquired and congenital heart diseases is truly mind boggling.

However, unrestricted growth in imaging, particularly cardiac imaging, has become an increasing burden on our already over-burdened health care budgets. We are being now being called upon to validate the value added by new imaging tests and to measure the direct impact each imaging test performed has on the care of each individual patients. In developing new procedures and refining the application of existing modalities, we need to ask not just how a given test compares to another test, or how elegantly a test can delineate anatomic structures, but rather, how does performing a given test alter clinical decision making. Superior image quality and higher resolution must translate into clinically relevant information which ultimately improves patient care.

This paradigm shift in how we think about imaging is not really all that new. The fundamental goal of medical practice has always been to help our patients feel better and live longer. The production of highly detailed, anatomically

accurate and esthetically pleasing images may help achieve this goal, but producing “pretty pictures” is not good enough by itself. Wennberg and his colleagues1,2 have pointed out that recent rapidly expanding use of noninvasive imaging is not explained by increasing disease prevalence. This increased use of noninvasive imaging may confer benefit for some, but may not help others and certainly increases costs. We must identify those patients who benefit from imaging and avoid imaging those in whom imaging has little chance of influencing management or the ultimate patient outcome.

The value of cardiac imaging begins with technical excellence - highly trained and innovative people using well engineered equipment to image seminal aspects of a disease process. The technical quality of the imaging process and the accuracy of image interpretation must be assured and improved on a continuous basis, with iterative checks against other corroborating clinical data.

Technical quality and accuracy are essential first steps for value-based imaging, but this is not enough. The next step in diagnostic imaging is to exclusively employ imaging in appropriate patients, and to avoid wasteful or even potentially harmful imaging of patients who do not need the test. Only patients for whom the marginal health benefits of the imaging procedure exceed their marginal risk should be imaged.3 The cost of imaging must also be weighed against the benefit. Definition of appropriateness and assessment of the contribution of imaging to patient outcomes is especially difficult, but nonetheless essential. In some cases, we must pursue randomized controlled trials to prove the value of imaging. However, not all evidence is amenable to collection in such trials.4 Real world registries provide important data, and use of surrogate endpoints can supplement achievement of hard outcomes.5

Those of us involved in developing and applying new imaging technology share with all physicians the desire to deliver the best health care possible to each and every one

*Corresponding Author: Samuel Wann, Chairman, Department of Cardiovascular Medicine, Wisconsin Heart Hospital, 10000 Bluemound Road,

Milwaukee, Wisconsin 53226 USA. Tel: +1 414 2669700. E-mail: [email protected].


58

of our patients. Responsible stewardship of the resources available to us requires that we carefully examine the evidence supporting the use of imaging in any given circumstance, as we try to provide the right imaging procedure to the right patient at the right time.

References

1. Wennberg DE, Girkmeyer JD, Birkmeyer NJO, Lucas FL, Malenka DJ, McGrath PD, Lurie JD, O’Connor GE, Quinton HB, Shawyer TA, Siewers AE. The Dartmouth Atlas of Cardiovascular Health Care. In: Wennberg DE, Girkmeyer JD, Birkmeyer NJO, Lucas FL, Malenka DJ, McGrath PD, Lurie JD, O’Connor GE, Quinton HB, Shawyer TA, Siewers AE, eds. The Dartmouth Atlas of Cardiovascular Health Care. Chicago: AHA Press; 1999. p. 1-390.2. Lucas FL, DeLonerzo MA, Siewers AE, Wennberg DE. Temporal trends in the utilization of diagnostic testing and treatments for cardiovascular disease in the United States, 1993-2001. Circulation 2006;13:374-379.3. Committee on quality of health care in America. Crossing the Quality Chasm: A New Health Care System for the 21st Century. In: Committee on quality of health care in America, eds. Crossing the Quality Chasm: A New Health Care System for the 21st Century. Washington DC: Institute of Medicine/ National Academies Press; 2001. p. 1-298.4. Berwick DM. The science of improvement. JAMA 2008;299:1182-1183.5. Beller GA. Assessment of new technologies: surrogate endpoints versus outcomes, and the cost of health care. J Nucl Cardiol 2008;15:299-300.

Samuel Wann


*Corresponding Author: Maryam Esmaeilzadeh, Shaheed Rajaei Cardiovascular Medical and Research Center, Tehran, Iran. Tel: +98 21 23922524. Fax:

+98 21 22055594. E-mail: [email protected].

Review Article

Echocardiographic Evaluation of

Intracardiac Masses

Maryam Esmaeilzadeh, MD, FCAPSC*

Shaheed Rajaie Cardiovascular Medical and Research Center, Tehran, Iran.

Abstract

Echocardiography plays a fundamental role in the evaluation of patients with an intracardiac mass. The ability to distinguish

tissue characteristics, location, attachment, shape, size, and mobility non-invasively, quickly, and without the use of ionizing

radiation makes echocardiography the ideal diagnostic modality. With careful attention to mass location and morphology,

and appropriate application of clinical information, echocardiography can usually distinguish between the three principal

intracardiac masses: tumor, thrombus, and vegetation. Equivocal transthoracic findings typically indicate the need for a

transesophageal evaluation, during which the atria and great vessels might be better imaged. Surgical intervention is often

indicated based on possible echocardiographic findings, without the need for additional time-consuming procedures. This

review will focus on cardiac tumors.

J Teh Univ Heart Ctr 2 (2008) 59-76

Keywords: Echocardiography • Heart • Tumors • Diagnostic imaging

Introduction

Neoplasms of the heart divided into primary cardiac tumors arising in the heart and secondary cardiac tumors that have metastasized to the heart. Primary cardiac tumors stratified into benign and malignant tumors. Secondary involvement of the heart is relatively uncommon; 10% to 20% of patients dying of disseminated cancer have metastatic involvement of the heart or pericardium.1,2 Primary tumors of the heart are uncommon but not rare. The incidence of primary cardiac neoplasm ranges between 0.17% and 0.19% in unselected autopsy series.3-8

Approximately 75% of primary cardiac tumors are benign and 25% are malignant.2,9 Approximately 50% of the benign tumors are myxomas, and about 75% of the malignant tumors are sarcomas.2,9 Echocardiography is an invaluable technique for the evaluation of intracardiac masses,

and can reliably identify mass location, attachment, shape, size, and mobility, while defining the presence and extent of any consequent hemodynamic derangement. With careful attention to mass location and morphology, and appropriate application of clinical information, echocardiography can usually distinguish between the three principal intracardiac mass lesions: tumor, thrombus, and vegetation. Transesophageal imaging frequently adds additional important information to the assessment of masses and should always be considered when image quality is inadequate or pertinent clinical questions remain unanswered with surface imaging. It can be performed at the bedside, operating theater and in critically ill patients. However, echocardiographic image quality can be suboptimal, and ultrasound artifacts


60

Maryam Esmaeilzadeh

can occasionally be mistaken for an anatomic mass. Careful identification of a mass lesion throughout the cardiac cycle in more than one imaging plane is an important first step in evaluating a suggested mass, and will decrease the likelihood of misinterpreting artifact as pathology.

A thorough understanding of normal anatomy, normal variants, embryologic remnants, and the structural changes seen with certain operative and interventional procedures is crucial and will further avoid misdiagnosis. Finally, it is important that clinical and historic information be available and thoughtfully applied to the final echocardiographic interpretation.

Normal variants

Numerous normal anatomic variants exist that can easily be confused with primary mass lesions. In the left ventricle, webs and chords, prominent or calcified papillary muscles, prominent apical trabeculations, and dense mitral annular calcification (Figure 1) can mimic abnormal pathology. Ventricular noncompaction (Figure 2) and the apical form of hypertrophic cardiomyopathy can also be confused with tumors.10-13

ow)

Figure 1. Mitral annular calcification (MAC); apical four-chamber view showing significant calcification of posterior mitral annulus (arrow)

Figure 2. Non-compaction left ventricle; transgastric view showing markedly thickened two-layered myocardial wall with multiple trabeculations and deep intertrabecular recesses (arrow)

In the left atrium, beam-width artifacts can cause interpretive confusion, as can the suture lines associated with cardiac transplantation. Left atrium cords are rare but well-recognized findings. These cords typically originate at the atrial septum and insert into the atrial surface of the mitral leaflets; no clinical significance has ever been described. These cords should not be confused with true obstructive cor triatriatum. An interatrial septal aneurysm may appear as a cystic mass bulging into either atrium. A dilated coronary sinus can mimic an LA mass in the parasternal long axis view, as can a prominent descending aorta from the apical view. A left arm injection of agitated saline will define a persistent left superior vena cava draining into the coronary sinus, which is the most common structural anomaly associated with the dilatation of the coronary sinus. When a large accumulation of pericardial fluid is present, the transverse sinus can become prominent.

Pectinate muscles in the appendage can mimic a thrombus. An inverted left atrium appendage (a postoperative finding) can also be confused with a tumor.14,15 A hiatal hernia can impinge on both atria and can be confirmed after ingestion of carbonated beverage.

A prominent moderator band or tricuspid papillary muscles can create diagnostic confusion in the right ventricle. A fatty tricuspid annulus can be quite prominent. A substantial number of congenital remnants are seen in the right atrium, all of which can create diagnostic confusion.

The crista terminalis is a dense muscle ridge that extends between the right sides of the superior and inferior caval orifices and continues cephalad to open into the right atrium appendage (Figure 3).


Echocardiographic Evaluation of Intracardiac Masses

A

BFigure 3. Prominent crista terminalis (arrows); transthoracic (A) and transesophageal (B) views

It can be quite prominent but is commonly seen in the same image plane as the superior vena cava, which should be a clue to its identity.16 The Eustachian valve is an incompetent valve flap of variable thickness and mobility at the orifice of the inferior vena cava.

The Chiari network is a network of both coarse and fine fibers with attachments extending from the region of the crista terminalis to the Eustachian valve or floor of the right atrium (Figure 4).

Figure 4. The Chiari network (arrow); transesophageal view

These fibers may become the site of thrombus formation or a catheter entrapment, requiring thoracotomy for retrieval; several recent reports describe entanglement of an atrial septal defect closure device and septal ablation guide wire in the Chiari network.17-19

Pectinate muscles can be seen on the right atrium appendage and the right atrium free wall and, when prominent, can mimic a thrombus. Venous varicose (clumps of veins) of the heart, rare lesions of unknown incidence and with no distinct or specific echocardiographic characteristics, are surprisingly well described in the pathology literature.20 They almost always occur in the right atrium at the posteroinferior border of the fossa ovalis. They are clumpy, dilated venous channels with irregular borders.21

Monitoring lines and pacer wires will also be evident in the right atrium and can occasionally become coiled, simulating a mass.

Fatty infiltrates of the atrial septum, termed as lipomatous hypertrophy, are preferential to the right atrium. Although they can occasionally be quite prominent (>6 cm), they should be distinguishable from a tumor by their typical location and shape.

Certain valvular structures can be confused with mass lesions as well. The nodules of Arantius and Lunula and the threadlike Lambl’s excrescences (Figure 5), which are commonly found on the aortic valve in patients older than 60 years, can be confused with vegetations. Redundant supporting apparatus and redundant leaflet tissue of the mitral valve may mimic vegetations as well. Thoughtful application of clinical information is necessary to distinguish


62

degenerative from infectious processes. Excess epicardial fat may be confused with a tumor contained in the pericardium, as can fibrinous debris in the free pericardial fluid. Atelectatic segments of the lung can be misinterpreted as primary masses in the pleura.

Figure 5. Lambl’s excrescence of the aortic valve; mid esophageal long-axis view of the Aorta (arrow)

Primary tumors

A primary cardiac neoplasm was first described by Realdo Colombo in 1559.22,23 Primary tumors of the heart and pericardium are difficult to diagnose because they are so uncommon and because their clinical presentation is so variable. The incidence of primary tumors at autopsy ranges from 0.002% to 0.3%.24,25 Approximately, 75% of primary cardiac tumors are benign. In adults, the most common cardiac tumor is the myxoma; in children younger than 15 years, the most common tumor is the rhabdomyoma.25 Of the primary malignant tumors, sarcomas are by far the most common, including angiosarcoma, rhabdomyosarcoma, and fibrosarcoma. Mesothelioma and primary intracardiac lymphoma comprise approximately 6% of the malignant tumors of the heart.26 Primary malignant cardiac tumors are rare in children.

Myxoma

Myxomas comprise 25% of all cardiac neoplasms and 50% of benign cardiac tumors in adults but only 15% of such tumors in children. Myxomas usually occur sporadically and

are more common in women than men.4,27

The peak incidence is between the third and sixth decades of life, and 94% of tumors are solitary.28 Tumors are unlikely to be associated with other abnormal conditions and have a low recurrence rate.4,28 However, they can be familial or complex (syndrome myxoma). Less than 10% of myxoma patients show a familial pattern based on autosomal dominance inheritance.29-30 These patients and 20% of those with sporadic myxomas have an abnormal DNA genotype chromosomal pattern.31 In contrast to “typical” sporadic myxomas, familial myxoma patients are more likely to be younger, equally likely to be male and female, and more often (22%) have multicentric tumors originating from either the atrium or the ventricle.32-37

Familial myxomas have a higher recurrence rate after surgical resection (21%- 67%).33,38,39 The familial variety may be part of a syndrome (Carney’s complex, NAME, LAMB), frequently includes multiple tumors in several chambers, and has a high rate of tumor recurrence.24 If the patient is young with multiple tumors, the screening of first-degree relatives is indicated. The complex variety, also known as Carney’s complex, may include a combination of the following: (1) multiple pigmented skin lesions (lentigines), (2) breast adenomas, (3) skin myxomas, (4) endocrine overactivity (e.g. pituitary adenomas), and (5) cardiac myxomas, often multiple.40,41 Syndrome myxomas are also occasionally referred to as the NAME syndrome (nevi, atrial myxoma, myxoid neurofibroma, and ephelides) or the LAMB syndrome (lentigines, atrial myxoma, and blue nevi).41

Myxomas occur in any chamber of the heart but have a special predilection for the left atrium, from which approximately 75% originate (Figure 6).42

Figure 6. Large left atrial myxoma; transesophageal long-axis view showing the attachment of the tumor to the fossa region (arrow)

Maryam Esmaeilzadeh


The next most frequent site is the right atrium, where 15-20% are found. The remaining 6% to 8% are equally distributed between the left and right ventricles.2 Both biatrial and multicentric tumors are more common in familial disease. Biatrial tumors probably arise from the bidirectional growth of a tumor originating within the atrial septum.43 Atrial myxomas generally arise from the interatrial septum at the border of the fossa ovalis but can originate anywhere within the atrium including the appendage.4 In addition, isolated reports confirm that myxomas arise from the cardiac valves, pulmonary artery and vein, and vena cava.44,45 Right atrial myxomas are more likely to have broad-based attachments than left atrial tumors; they also are more likely to be calcified and thus visible on chest radiographs.34,35 Ventricular myxomas occur more often in women and children and may be multicentric.2,46

Right ventricular tumors typically arise from the free wall, and left ventricular tumors tend to originate in the proximity of the posterior papillary muscle.

Grossly, about two thirds of myxomas are round or oval tumors with a smooth or slightly lobulated surface.27 Most are polypoid, relatively compact, pedunculated, and mobile.2,4 Mobility depends on the length of the stalk and the extent of attachment to the heart.4 Sessile forms are unusual (approximately 10%).2,47

Less common villous or papillary myxomas are gelatinous and fragile and prone to fragmentation and embolization, occurring about in one third.27,48 Focal areas of hemorrhage, cyst formation, or necrosis may be seen. The average size is about 5 cm in diameter but growth to 15 cm in diameter and larger has been reported. Most myxoma tumors appear to grow rapidly, but growth rates vary and occasionally tumor growth arrests spontaneously.4 Weights range from 8 to 175 g with a mean between 50 and 60 g.8 Work by Malekzadeh and Roberts suggests that myxomas grow on average 1.8 cm or 14 g each year. 49

The classic triad of myxoma clinical presentation is intracardiac obstruction with congestive heart failure (67%), signs of embolization (29%), systemic or constitutional symptoms of fever (19%) and weight loss or fatigue (17%), and immunologic manifestations of myalgia, weakness, and arthralgia (5%), with almost all patients presenting with one or more of these symptoms.27

Cardiac rhythm disturbances and infection occur less frequently. Myxomas in the left atrium tend to mimic mitral valvular heart disease. Large myxomas may interfere with mitral leaflet closure and produce mitral regurgitation. Syncopal episodes occur in some patients and are thought to result from the temporary occlusion of the mitral orifice.35,50,52

Right atrial myxomas can produce a clinical picture of right heart failure with signs and symptoms of venous hypertension,


including hepatomegaly, ascites, and dependent edema. The tumor simulates tricuspid valve stenosis by partially obstructing the valve orifice.35,50-52 Systemic embolization occurs in 30% to 40% of patients.2,4,35,50,51 Because the majority of myxomas are left-sided, approximately 50% of embolic episodes affect the central nervous system owing to both intracranial and extracranial vascular obstruction.

Surgical removal of all varieties of myxomas is the treatment of choice. Echocardiography is very useful for the diagnosis and evaluation of myxomas. The sensitivity of 2-D echocardiography for myxomas is 100%.53

Color flow and spectral Doppler are useful to evaluate functional obstruction to LA emptying. Transthoracic echocardiography usually provides all the information for surgical resection, but transesophageal echocardiography provides the best information concerning tumor size, location, mobility, and attachment.54-55 Transesophageal echocardiography detects tumors as small as 1–3 mm in diameter.56 Additionally, intraoperative transesophageal echocardiography post-tumor excision is indicated to identify any residual tumor fragments prior to leaving the operating room. Recurrence of nonfamilial sporadic myxomas is approximately 1% to 4%.4,57,58 Many large series report no recurrent tumors.44,57,59,60 The disease-free interval averages about 4 years and can be as brief as 6 months.57 Most recurrent myxomas occur within the heart, in the same or different cardiac chambers, and may be multiple.35,61,62

The extent to which patients should be subjected to long-term echocardiographic surveillance after myxoma resection is not standardized.

It would seem prudent to closely follow patients who are treated initially for multicentric tumors, those whose tumors are removed from unusual locations, tumors believed to have been incompletely resected, and those with abnormal DNA genotype.

Other benign cardiac tumors

Lipomas, papillary fibroelastomas, and rhabdomyomas are

the most common benign tumors.

Papillary fibroelastoma

Papillary fibroelastomas are rare, primary benign cardiac tumors that are most frequently located in the cardiac valves or adjacent endocardium (Figure 7).63


64

Maryam Esmaeilzadeh

A

BFigure 7. Papillary fibroelastoma of the tricuspid valve; transthoracic subcostal view (A) and transesophageal view (B) showing large fibroelastoma attached to atrial surface of the anterior tricuspid valve leaflet (arrows)

Fibroelastomas are usually found by chance in post-mortem examinations. It is now known that they are capable of producing the obstruction of th e flow, particularly the coronary ostial flow, and may embolize to the brain and produce stroke.64-66 They are usually asymptomatic until a critical event occurs. The prompt detection of papillary fibroelastomas is, therefore, of great importance. They are

potential causes of systemic emboli, stroke, myocardial infarction, and sudden death.67-69 Right-sided localization is even rarer.70 In order of frequency, they are the third primary cardiac tumors after myxomas and lipomas.71

Papillary fibroelastomas represent 7.9% of benign primary cardiac tumors in adults.63 Approximately, 90% of primary fibroelastomas arise from the valvular tissue, most commonly from the aortic or mitral valves.72,73

In a study including 162 patients with papillary fibroelastomas, the age ranged from 5 to 86 (mean 60±16 years).74 They may be single or multiple occurring more frequently on the ventricular surface of the semi lunar valve and on the atrial surface of atrioventricular valves and may be pedunculated with some mobility.75,76 The tricuspid valve is most affected in children and the mitral and aortic valves in adults.76 On gross anatomical examination, they resemble a sea anemone, consisting of multiple fingerlike fronds. The pathogenesis of papillary fibroelastomas remains under discussion, but several possible explanations have been reported, including previous mechanical damage to the endothelium, iatrogenic factors, organizing thrombi, and a latent infectious mechanism due to cytomegalovirus.72,77,78

With the advent of echocardiography, an increasing number of papillary fibroelastomas have been diagnosed. Typical echocardiographic features include the following:

1. Round, oval, or irregular appearance, with well-demarcated borders and a homogenous texture.

2. Small mobile stalks in 50%. Those with stalks are mobile.74,79

Sun et al. found that 99% of papillary fibroelastomas were <20mm in the largest diameter.74 The largest reported one is 53 mm.80 Even though papillary fibroelastomas are classified as benign cardiac tumors, they often cause systemic embolic events such as cerebrovascular stroke and more rarely myocardial infarction.81 This occurs because of their very friable and soft texture as well as the creation of thrombi on their surface, which may later become embolic. Echocardiography is a reliable means of evaluating the extent and anatomic attachment of these very small tumors, but many go undetected. There are no significant characteristics that enable the differentiation of fibroelastomas from degenerative valve disease. Surgical excision may be indicated in patients with large, mobile, left-sided tumors. Surgical removal of right-sided papillary fibroelastomas in asymptomatic patients is indicated only for large mobile tumors. The presence of a patent foramen ovale with a sizable right to left shunt is an additional consideration for right-sided fibroelastomas. Asymptomatic patients with small left-sided non-mobile (no stalk) fibroelastomas are usually observed. However, fibroelastomas 1 cm, especially if mobile, should be considered for excision, including in patients with other cardiovascular diseases, young patients with low risk of surgery, and those with a high cumulative risk for embolization.74



Rhabdomyoma

Rhabdomyomas are the most common cardiac tumors of infants and young children. They usually present during the first few days after birth. They are thought to be a myocardial hamartoma rather than a true neoplasm.82

They have a strong association with tuberous sclerosis, a familial neurologic syndrome characterized by hamartomas, epilepsy, mental retardation, sebaceous adenomas, and skin lesions. One study indicated that 80% of patients with cardiac rhabdomyomas had tuberous sclerosis, and 60% of patients with tuberous sclerosis younger than 18 years had cardiac rhabdomyomas.83 The exceptional patient is one with a solitary, single rhabdomyoma who does not have or develop tuberous sclerosis. Over 90% of rhabdomyomas are multiple and occur with approximate equal frequency in both ventricles.83-85

The atrium is involved in fewer than 30% of patients. Pathologically, these tumors are firm, gray, and nodular and tend to project into the ventricular cavity. The most common presentation is heart failure caused by tumor obstruction of the cardiac chambers or valvular orifice flow. Clinical findings may mimic valvular or subvalvular stenosis. Arrhythmias, particularly ventricular tachycardia and sudden death, may be a presenting symptom.

Atrial tumors may produce atrial arrhythmias.86 When associated with mechanical complications such as outflow tract obstruction, surgical excision may be indicated. However, surgical intervention is usually not necessary in the asymptomatic patient.87,88

Fibroma

Fibromas are the second most common benign cardiac tumors, with over 83% occurring in children; most are diagnosed by age 2 years. These tumors are solitary, occur exclusively within the left ventricle and the ventricular septum, and are typically intramural.24 They commonly invade the septum, anterior apex, and free wall; and may appear as markedly disproportionate, irregular hypertrophy.

They affect both sexes equally. Fibromas are non-encapsulated, firm, nodular, gray-white tumors that can become bulky. Calcium deposits or bone may occur within the tumor and occasionally are seen in radiography. These tumors are histologically benign but frequently have a malignant course. The majority of fibromas produce symptoms through chamber obstruction, interference with contraction accounting for lethal ventricular dysrhythmia, and intractable heart failure associated with dyspnea and fatigue.89-91

Depending on size and location, they may interfere with valve function, obstruct flow paths, or cause sudden death from conduction disturbances in up to 25% of patients.92

Fibromas localized to the apex can be confused with thrombus

or true apical hypertrophy, but perhaps can be distinguished by their abnormal texture. Intracardiac calcification on chest roentgenograms suggests the diagnosis, which is confirmed by echocardiography. Although successful surgical resection is common now, these tumors can be extensively infiltrative, and it is not always possible to completely remove the tumor and partial removal is only palliative and may cause further myocardial dysfunction92,93 Successful, complete excision is curative.93,94

Children with extensive fibromas have been treated by cardiac transplantation.90,95,96

Lipoma

Lipomas are well-encapsulated tumors composed of mature fat cells, and may occur anywhere in the heart (Figure 8).2

Figure 8. Lipoma; parasternal long-axis view showing a very large encapsulated mass in the left atrioventricular groove (arrow)

The most common sites affected are the left ventricle, right atrium, and interatrial septum.24 They may occur at any age and have no sex predilection. Lipomas are slow growing and may attain considerable size ( 4 kg) before producing obstructive or arrhythmic symptoms.97 Many are asymptomatic and are discovered incidentally on routine chest roentgenogram, echocardiogram, or at surgery or autopsy.98,99

Subepicardial and intrapericardial lipomas tend to compress the heart, may be associated with pericardial effusion, and present as cardiac or mediastinal enlargement on chest radiograph. Subendocardial tumors may produce chamber obstruction. Lipomas lying within the myocardium or septum


66

can produce arrhythmias or conduction abnormalities.100,101

Large tumors that produce severe symptoms should be resected. These tumors are not known to recur.

Lipomatous hypertrophy of the interatrial

septum

Although lipomas are true neoplasms, lipomatous hypertrophy is a non-encapsulated accumulation of mature adipose tissue within the atrial septum.2 This abnormality, more common than cardiac lipomas, tends to be quite large ( 7 cm), favors the right atrium, and is a common finding in women who are elderly and obese as an incidental finding during a variety of cardiac imaging procedures.60,102

Echocardiographers should recognize this lesion by its characteristic dumbbell shape, the result of sparing of the fossa ovalis (Figure 9) with the preponderance of fat typically in the superior portion of the septum. When the atrial septum is massively infiltrated by fat, the amount of adipose tissue in other parts of the heart is always increased, particularly the right ventricle epicardial surface. The main problem is differentiation from a cardiac neoplasm.103

Figure 9. Lipomatous hypertrophy of interatrial septum; typical dumbbell shape, the result of sparing of the fossa ovalis (arrow)

Magnetic resonance imaging is reliable in the characterization of fat if diagnostic issues remain.104,105

Various arrhythmias and conduction disturbances have been attributed to its presence, but a definite cause-and-effect relationship has not been established.102 Arrhythmias or heart block are considered by some as an indication for resection, but data are lacking as to the long-term benefits from resection.106

Angiomas, teratomas, and mesotheliomas of the atrioventricular node and endocrine tumors are extremely rare, representing less than 7% of all cardiac tumors.26

Angiomas are vascular tumors, and myocardial contrast echocardiography has been particularly useful in determining their vascular nature.107-109

Hemangioma

Primary hemangiomas of the heart were first described in 1893. Mc Allister reviewed 533 primary tumors and cysts of the heart and pericardium, of which 15 (2.8%) were hemangiomas.110 They are rare benign primary cardiac tumors, with less than 100 cases described in the current cardiac literature.111

The origin of hemangiomas is uncertain; they are thought to be either true neoplasms or hamartomas. These tumors can be localized in any part of the heart and pericardium. They are commonly found in the interventricular septum or the atrioventricular node, where they can cause complete heart block and sudden death. In a previous review of 56 cases of cardiac hemangiomas, 36% were found in the right ventricle, 34% in the left ventricle, 23% in the right atrium, and the rest on the interatrial septum (Figure 10) and in the left atrium.112 Histological patterns that have been described include capillary hemangiomas, cavernous hemangiomas, hemangioendotheliomas, and intramuscular hemangiomas.113

Hemangiomas can present in any age group with a mild predominance in females. The symptomatology depends on the anatomic location and extension of the tumor. Although most cardiac hemangiomas are discovered incidentally, they may cause dyspnea, palpitation, atypical chest pain, arrhythmia, and pericardial effusion.114

A

Maryam Esmaeilzadeh


BFigure 10. Cavernous Hemangioma; transthoracic subcostal (A) and transesophageal bicaval (B) views demonstrating large homogenous mass in interatrial septum bulging into right atrium (arrows)

Echocardiography is usually the initial imaging modality and has an 81% accuracy rate in detecting cardiac tumors. Cardiac catheterization studies (particularly ventricular angiograms) can help to diagnose a cardiac tumor in 40% of cases by revealing an intracavitary filling defect. The classic finding on coronary arteriography is a vascular blush. Recently CT and MR have been used in preoperative diagnosis and in the evaluation of extra cardiac extension and myocardial involvement.115 Preoperative diagnosis of cardiac hemangiomas occurs in a minority of cases. The long-term prognosis is favorable after adequate surgical resection. Unresectable tumors have a poor prognosis and may lead to sudden death due to arrhythmias.

Teratoma

Cardiac teratomas are rare tumors that usually present in infants and young children but sometimes occur in adults.116

About 80% of the tumors are benign and the remainders have microscopic or clinically malignant cells.117

Teratomas are usually found in the mediastinum. Rarely intracardiac, they are usually within the pericardial space. Teratomas have elements of all 3 germ cell layers, and can have skin, hair, and muscle. Large bloody pericardial effusions causing hemodynamic compromise are a well-described presentation of these uncommon tumors.118,119 Fetal echocardiography has been useful in identifying mediastinal

masses causing cardiac compression, with associated accumulations of pericardial fluid.

Mesothelioma of the atrioventricular node

Mesotheliomas of the atrioventricular node, also termed polycystic tumors, Purkinje tumors, or conduction tumors, are mentioned in the pathologic classification of tumors. They are relatively small, multicystic tumors that arise in proximity to the atrial ventricular node and may extend upward into the bundle of His.2

Mesotheliomas are associated with heart block, ventricular fibrillation,120 and sudden death. Cardiac pacing alone does not prevent subsequent ventricular fibrillation. Surgical excision has been reported.121

Pheochromocytoma

Cardiac pheochromocytomas arise from the chromaffin cells of the sympathetic nervous system and produce excess amounts of catecholamines, particularly norepinephrine. Approximately 90% of pheochromocytomas are in the adrenal glands. Fewer than 2% arise in the chest. These tumors predominantly affect young and middle-aged adults with an equal distribution between the sexes. Approximately 60% occur in the roof of the left atrium. The remainder involve the interatrial septum or anterior surface of the heart. The patients usually present with symptoms of uncontrolled hypertension. These tumors are usually located by scintigraphy and CT or MRI.122,123 Cardiac catheterization with differential blood chamber sampling is sometimes necessary.124 Because these tumors are vascular and may be near major coronary arteries, coronary arteries angiography is advised. After the tumor is located, it should be removed. Transplantation has been performed for unresectable tumors. Complete excision produces cure.122-124

Primary malignant tumors

Approximately, 25% of primary cardiac tumors are malignant; and of these, about 75% are sarcomas. McAllister’s survey of cardiac tumors found the most common to be angiosarcomas (31%), rhabdomyosarcomas (21%), malignant mesotheliomas (15%), and fibrosarcomas (11%).2 Primary malignant cardiac tumors are sporadic, showing no inherited linkage.

Sarcomas most commonly occur in patients between the ages of 30 and 50 years, are unusual in children, are typically found in the right heart chambers, and occur equally in men and women.24 There are several reports of sarcomas developing around surgically implanted Dacron grafts or



68

prosthetic valves, both in the heart and in other peripheral vascular sites.125-128 Cardiac sarcomas are characteristically very aggressive tumors and, once diagnosed, are associated with a downhill course. They grow rapidly, and death is usually the result of widespread infiltration of the myocardium or extensive distant metastasis. Sarcomas may cause right heart failure as a result of obstruction anywhere in the right heart inflow/outflow tract; penetration into the pericardial space and subsequent pericardial effusion may occur. Dysrhythmia is common. Cardiac findings are determined by the location of the tumor. Chest X-ray may be abnormal and even show a mass lesion, but the definite diagnosis is usually made via echocardiography.129,130 The echocardiographic characteristics of sarcomas are not specific, but sarcomas may attach at any site in the chamber, and many are sessile. A heterogeneous mass lesion in the right heart associated with dysrhythmia or conduction disturbance should include sarcoma in the differential. Right atrial lesions are more frequently malignant (usually angiosarcomas) than left-sided lesions (usually myxomas, but when malignant are often malignant fibrous histiocytomas). If malignancy is suspected, chest CT or MRI may suggest histology and provide detailed anatomy and help in staging and assessing resectability. Unfortunately, primary cardiac malignancy may grow to a large size prior to detection and involve portions of the heart not amenable to resection. Palliative medical therapy can be attempted with radiation therapy. Whether the tumor is primary or secondary, the decision to resect is based on the tumor size and location and an absence of metastatic spread.

Angiosarcoma

Angiosarcomas are two to three times more common in men than women and have a predilection for the right heart. Eighty percent arise in the right atrium.131-133 These tumors tend to be bulky and aggressively invade adjacent structures, including the great veins, tricuspid valve, right ventricular free wall, interventricular septum, and right coronary artery.132 Obstruction and right heart failure are not uncommon. Unfortunately, most of these tumors have spread by the time of presentation, usually to the lung, liver, and brain.131 Without resection, 90% of the patients are dead within 9 to 12 months after diagnosis despite radiation or chemotherapy.42,134

Malignant fibrous histiocytoma

Malignant fibrous histiocytomas are the most common soft-tissue sarcomas in adults. They are characterized histologically by a mixture of spindle cells, polygonal cells resembling histiocytes, and malignant giant cells. The cell of

origin is the fibroblast or histioblast.129-135 They usually occur in the left atrium and often mimic myxomas. Their tendency to metastasize is not as prominent as that of angiosarcomas. Several reports exist with rapid symptomatic recurrence after incomplete resection despite chemotherapy.

Rhabdomyosarcoma

Rhabdomyosarcomas do not evolve from rhabdomyoma and occur equally in the sexes. The tumors are multicentric in 60% of patients and arise from either ventricle. These tumors frequently invade cardiac valves or interfere with valve function because of their intracavitary bulk. These tumors are aggressive and may invade the pericardium. Surgical excision of small tumors may be rational but local and distant metastasis and poor response to radiation or chemotherapy limit survival to less than 12 months in the majority of these patients.94,116,117,130,136,137

Lymphomas

Lymphomas may, albeit rarely, arise from the heart.138

Most of these tumors respond to radiation and chemotherapy. Even when complete resection is not possible and incomplete resection is performed to relieve acute obstructive systems, radiation and chemotherapy have allowed for up to 3-year survival in selected patients.

Metastatic tumors

Whereas primary tumors of the heart are rare, cardiac metastases have been described in up to 20% of patients with malignancies of other organ systems.2,5,9,139 Secondary neoplasms are 20 to 40 times more common than primary cardiac malignancies.4,26,140 No malignant tumor preferentially metastasizes to the heart, with the possible exception of malignant melanomas, which involve the heart in up to 50% of patients.141 Cardiac lesions develop in up to 50% of patients with leukemia.5 Other cancers that commonly involve the heart include breast, lung, lymphoma, melanoma, and various sarcomas.2,142,143 Metastasis involves the pericardium, epicardium, myocardium, and endocardium.2,9

Cardiac metastases are encountered typically in patients with widespread systemic tumor dissemination; even in this setting, the heart may still be spared tumor deposition because of vigorous cardiac contractility and rapid coronary blood flow. The tumors that most commonly manifest cardiac metastasis are lung, breast, ovarian, kidney, leukemia, lymphoma, esophageal, and, as noted, melanoma.24,26

Although solid intracardiac metastasis from melanomas is well described, the most common cardiac extension of

Maryam Esmaeilzadeh


melanomas is subclinical and manifests as “charcoal” heart, with tumor studding the pericardial surface.144

Metastasis can reach the heart through hematogenous spread via coronary arteries, lymphatic channels, direct extension from adjacent lung, breast, esophageal and thymic tumors, and from the sub-diaphragmatic vena cava.24

Pericardial metastasis occurs more often than myocardial invasion by direct extension of thoracic cancer. The most common symptom is pericardial effusion with and without cardiac tamponade. The effusion may contain solid material adherent to the visceral or parietal pericardium; these masses may be tumors or may be clotted blood. Unfortunately, routine cytological examinations of the fluid are associated with a false-negative rate of perhaps as high as 20%.145

Recurrent effusions are common, and pericardial window may be necessary. Solid pericardial metastasis that extends into cardiac chambers can be very aggressive, with the tumor expanding rapidly and causing significant hemodynamic derangement, including obstruction to cavity emptying and filling. Chemotherapy and tumor resection or debulking may alleviate symptoms and prolong survival. Occasionally, patients develop refractory arrhythmias or congestive heart failure.24 Echocardiography is particularly useful for the diagnosis of pericardial effusion, irregular pericardial thickening, or intracavitary masses interfering with the blood flow.

Right atrial extension of sub-diaphragmatic

tumors

Both benign and malignant abdominal and pelvic tumors can extend to the heart through the inferior vena cava. Wilms’ tumors (common in children), uterine leiomyosarcomas, and hepatomas may also metastasize to the heart by the inferior vena cava. Of all the tumors that metastasize to the heart via the inferior vena cava, renal cell carcinomas (hypernephroma) are the most common. Up to 10% of renal cell carcinomas invade the inferior vena cava, and up to 43% of patients with this tumor demonstrate right atrium involvement.146,147

Their point of origin and extension into the inferior vena cava usually can distinguish these metastases from the typical myxomas, and this attachment is best imaged in the subcostal plane. Radiation and chemotherapy are not effective in relieving the obstruction of the blood flow. If the kidney can be fully removed as well as the tail of the tumor thrombus, survival can approach 75% at 5 years.92,148,149

Intravascular leiomyomatosis

The most commonly reported benign tumor with inferior vena cava intracardiac extension is intravascular leiomyomatosis of pelvic or uterine origin (Figure 11).

Figure 11. Intracardiac leiomyomatosis; transesophageal view of intracardiac leiomyomatosis invading right atrium (RA) by dilated inferior vena cava (IVC). Tumor is heterogeneous in appearance and abuts superior border of IVC (arrow).

Leiomyomatosis, a rare uterine tumor, is defined as the extension into the venous channels of a histologically benign smooth muscle tumor. As cardiac involvement is present in up to 10% of cases, it may be misdiagnosed as a primary cardiac tumor or venous thrombus-in-transit.150 It was first reported by Birch-Hirschfield in 1897,151 and the first case report in the English literature was published by Marshall and Morris in 1959.152 It generally occurs in women aged between 28 and 80 years old, most patients being middle-aged women.153

The patients often have a history of hysterectomy, or may have symptoms due to uterine fibroids. Cardiac involvement presents typically with right-sided congestive symptoms. There are, however, other presentations like syncope due to obstruction at the tricuspid valve. Rarer manifestations that have been reported include a high output state, secondary thrombosis with Budd-Chiari syndrome, massive ascites, sudden death, and systemic embolism. Metastasis to lungs and lymph nodes has been reported, and pulmonary nodules have been described.

The most important condition in the differential diagnosis is thrombus-in-transit, which appears as elongated mobile masses of venous casts and gives a ‘‘popcorn’’ appearance within the cardiac chambers.150

Other tumors such as renal cell carcinoma and hepatomas may extend into the right-sided cardiac chambers via the inferior vena cava. Tumor removal may necessitate sternotomy as well as laparotomy.151 If the tumor is extensive, a two-stage operation may be needed.152 Recurrence after the surgical removal of the cardiac tumor is not unusual and can occur up to 15 years after surgery. Echocardiography may be useful for detecting cardiac recurrence and monitoring tumor growth.



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Carcinoid syndrome

The carcinoid syndrome (flushing, gastrointestinal hypermotility with secretory diarrhea, bronchospasm associated with wheezing, and carcinoid heart disease) results from circulating humoral substances secreted by the carcinoid tumor.154 Patients with primary carcinoid tumors of the ileum who have liver metastasis develop the distinctive lesions of the heart. These lesions are always located on the right and occasionally on the left side of the heart. When the primary carcinoid tumor is of a pulmonary bronchus, the carcinoid valvular lesions may be limited to the left-sided valves. In this setting, the liver may be tumor free.155

Carcinoid valve lesions are characterized by plaque-like, fibrous endocardial thickening that causes retraction and fixation of the tricuspid and pulmonary valve leaflets.

Tricuspid regurgitation is a nearly universal finding; tricuspid stenosis, pulmonary regurgitation, and pulmonary stenosis may also occur.154 The lesion occurs nearly entirely on the downstream (ventricular) side of the septal and posterior tricuspid leaflets. On the anterior tricuspid leaflet, the deposits can occur on both sides, which results in the adherence of the leaflet to the underlying mural endocardium and in significant valvular incompetence and occasionally some degree of stenosis.154 The dominant pulmonic valve lesion tends to be stenosis. Carcinoid is the only condition in which both right-sided valves are uniformly involved, and the lesions are pulmonary stenosis and tricuspid regurgitation. The typical valve morphology is of rigid leaflets fixed in a semi-open position.

Surgical replacement of dysfunctional valves is described, but the mortality appears to be fairly high.156,157

Cardiac cysts

Although cardiac cysts are not true neoplasms, they are occasionally found within the heart and pericardium. The most common cysts are pericardial cysts, echinoccocal (hydatid) cysts, and blood cysts.

Echinococcosis

Hydatid disease is a parasitic infestation caused by the larvae of the tape form echinococcus. Cardiac involvement is rare, with a reported occurrence between 0.2- 2% of all hydatid diseases.158-161 Primary involvement of the heart usually occurs in 50% of cases via the coronary arteries. Secondary involvement of the heart occurs from the hydatid disease of the adjacent organs, such as lungs or from the dome of the liver. The left ventricle is affected most often

(50-70%), followed by right ventricle pericardium (15-20%), and interventricular septum (5-15%).159,161,162

Symptoms, signs, and potential complications depend on the location and the size of the cysts.158 Rupture, dysrhythmia, heart failure, and emboli are common and can result in death.158,159,163 Echocardiography, CT, and MRI might be used for the diagnosis. Transesophageal echocardiography shows the cystic nature of the mass, but sometimes the echolucent and multi-septated nature of lesions may be absent. Echocardiography cannot be used to differentiate hydatid cysts from congenital pericardial lesions. Computed tomography and MRI are superior to surrounding tissues. Calcifications are best seen on CT.158,163,164

The differential diagnosis of cardiac hydatid disease, other cystic masses, and tumor-like lesions of the heart such as myocardial aneurysms, pericardial cysts, and pleuropericardial masses should always be considered. Operation is the treatment of choice.165-169

Pericardial cysts

Pericardial cysts are rounded echolucent structures typically adjacent to the right atrium. The diagnosis can be made on chest radiograph. Pericardial cysts are usually asymptomatic, but can become quite large and cause compression of the right atrium and right ventricle and the surrounding mediastinal structures, including the bronchus and esophagus. Operation is indicated when significant symptoms dominate the clinical picture.170-173

Blood cysts

Blood cysts are congenital cysts typically found on the closure lines of the valvular endocardium. They appear as well-circumscribed masses with thin walls and an echolucent core. They are rare in adults, and only a few reports of prospective echocardiographic diagnosis are available. Careful echocardiographic monitoring of the cysts for changes in size and for the assessment of changes in cardiac function may be appropriate, and operation may be indicated when the cysts are noted to cause cardiac dysfunction.174-177

Conclusion

Echocardiography is the procedure of choice for the evaluation of intracardiac masses. Echocardiography should, therefore, be meticulously applied and data cautiously interpreted. The appropriate knowledge of and careful attention to cardiac anatomy, use of multiple scan planes, and application of clinical information are mandatory for the diagnosis.

Maryam Esmaeilzadeh


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173. Antonini-Canterin F, Piazza R, Ascione L, Pavan D, Nicolosi GL. Value of transesophageal echocardiography in the diagnosis of compressive, atypically located pericardial cysts. J Am Soc Echocardiogr 2002;15:192-194.174. Pelikan HMP, Tsang TSM, Seward JB. Giant blood cyst of the mitral valve. J Am Soc Echocardiogr 1999;13:1005-1007.175. Nkomo V, Miller FA. Eustachian valve cyst. J Am Soc Echocardiogr 2001;14:1224-1226.176. Sim EKW, Wong ML, Tan KT, Sim SK. Blood cyst of the tricuspid valve. Ann Thorac Surg 1996;61:1012-1013.177. Prasad A, Callahan MJ, Malouf JF. Acquired right atrial blood cyst: a hitherto unrecognized complication of cardiac operation. J Am Soc Echocardiogr 2003;16:377-378.



76


*Corresponding Author: Kyomars Abbasi, Assistant Professor of Cardiac Surgery, Tehran University of Medical Sciences, Tehran Heart Center,

North Kargar Street, Tehran, Iran. 1411413138. Tel: +98 21 88029256. Fax: +98 21 88029256. E-mail: [email protected].

Original Article

Coronary Artery Bypass Grafting Combined with Total

Occlusion of Internal Carotid Artery

Kyomars Abbasi, MD*, Shapour Shirani, MD, Mohsen Fadaei Araghi, MD, Abbasali Karimi, MD, Hossein Ahmadi, MD, Seyed Hesameddin Abbasi, MD, Naghmeh Moshtaghi, MD

Tehran Heart Center, Medical Sciences/University of Tehran, Tehran, Iran.

Received 10 October 2007; Accepted 19 January 2008

Abstract

Background: The presence of significant carotid stenosis in coronary artery bypass grafting (CABG) patients increases

the risk of either transient ischemic attack or stroke. However, there is a dearth of data on the risk for patients with unilateral

total occlusion of the carotid artery. We herein report our results of cardiac surgery in patients with unilateral total occlusion

of the carotid artery.

Methods: We examined 10,000 patients who underwent carotid artery duplex scanning before CABG or other cardiac

procedures between January 2001 and September 2006 at Tehran Heart Center. The occlusions were detected via carotid

Doppler screening and were confirmed through conventional or MR angiography. Among these patients, 15 (0.15%) patients

had unilateral total occlusion of the internal carotid artery, and all of them underwent elective cardiac surgery. During

cardiopulmonary bypass, the mean arterial pressure was maintained at above 60 mmHg with vasopressure drugs and

increasing flow pump.

Results: There were 4 patients with left and 11 patients with right carotid occlusions. Four patients had a history of

cerebrovascular accident. The mean cross-clamp time (min) and perfusion time (min) was 50.7±17.3 and 94.2±26.7,

respectively. The mean graft number was 4.1±0.9. One of these patients expired intraoperatively because of low cardiac

output. In one (6.66%) patient, postoperative cerebrovascular accident occurred on the contralateral side of the totally

occluded region. All the patients recovered uneventfully.

Conclusion: Our results suggest that CABG can be performed in patients with unilateral total occlusion of the internal

carotid artery without ipsilateral stroke using our strategies.


Keywords: Coronary artery bypass grafting • Internal carotid artery • Occlusion

Introduction

Coexistence of symptomatic coronary artery disease and significant carotid artery stenosis ranges from 3.4% to 22%.1

Stroke incidence after open heart coronary artery bypass

grafting (CABG) is estimated at between 0.8% and 6%, which is relatively high when compared to the decreasing rates of other perioperative complications.2 The presence of


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Kyomars Abbasi et al

significant carotid stenosis in CABG patients increases the risk of either transient ischemic attack (TIA) or stroke from 1.9 to 9.2.3 There is, however, precious little information in the existing literature about the risk for patients with total occlusion of the carotid artery.4 In the past two decades, the high-risk potential for neurologic dysfunction after CABG in patients with concomitant carotid stenosis has been a real challenge for surgeons in terms of determining which operative sequence offers the highest freedom from cardiac or cerebral complications.1

Previous studies vary widely in reporting perioperative stroke frequencies for patients with internal carotid artery (ICA) occlusion or stenosis. Some of these reports have shown no increase in the risk of ipsilateral stroke in patients with an occluded ICA undergoing CABG,5-7 whereas others have reported an increased frequency (15%) of perioperative transient ischemia or cerebrovascular accident (CVA).8

In 1992, Berens et al.9 reported their results with routine carotid duplex scanning (CADS) for all cardiac surgical patients aged 65 years or older; the risk of stroke was 10.9 percent for unilateral carotid artery occlusion.

There is, therefore, no recommended strategy for these patients. We report our results of cardiac surgery in patients with total occlusion of the carotid artery.

Methods

Perioperative and postoperative data were collected prospectively in all 12,000 patients who underwent CADS, as the initial screening procedure for cerebrovascular disease, before elective CABG or other elective cardiac procedures between January 2001 and September 2006 at Tehran Heart Center. Preoperative CADS was successfully performed in 10,000 (83.3%) patients, 15 (0.15 %) of whom had total occlusion of the ICA.

Carotid Doppler was carried out by an expert radiologist, who had practiced Doppler studies on a daily basis for over 5 years. The device used was a Logic 5 Expert GE with linear 7.5 MHZ and convex 3.75 MHZ transducers. A standard protocol based on the Nicolaides criteria was applied to all the patients.10 MRA was done preoperatively for the patients diagnosed with total occlusion of the carotid in their carotid Doppler.

Patient data included the following variables: age, sex, hypertension, hypercholesterolemia (whether the patient had a history of hypercholesterolemia diagnosed and or treated by a physician and or patient had been assured previously of a. TG>200, b. LDL 130, c. HDL<30, d. admission cholesterol>200 mg/dl), diabetes mellitus (defined as a history of diabetes, regardless of the duration of the disease or need for anti-diabetic agents), mean of ejection fraction, history of CVA or TIA, number of grafts, aortic cross-clamp time, perfusion time, and perioperative stroke (defined as

a persistent focal or multifocal neurologic deficit that was explained by the ischemia of the brain or brain stem from the time of surgery until the 30th postoperative day and confirmed by computed tomography (CT) scan). During cardiopulmonary bypass, the mean arterial pressure was maintained at above 60 mmHg with vasopressure drugs and increasing flow pump. Only mortality and morbidity resulted by the total occlusion of the ICA in the patients were considered

Results

From among 10,000 patients who underwent CADS before cardiac surgery, 15 patients (10 men and 5 women at a mean age of 65±8.9 years) had unilateral total occlusion of the ICA. The mean ejection fraction was 48±10.9 (mean±SD). There were 4 patients with left and 11 patients with right carotid occlusions. Significant carotid stenosis ( 50%)contralateral to the occluded ICA was detected in 2 patients, for whom surgical treatment for cerebrovascular lesions was not necessary because there were no ischemic signs. Of these 15 patients, 12 (80%) had hypertension, 11 (73.3%) had diabetes mellitus and hypercholesterolemia, and 4 (26.6%) had a history of CVA or TIA, with CVA occurring on the same side as the total occlusion of the ICA in 3 of them. The baseline characteristics of the patients are depicted in Table 1.

Table 1. Patients’ characteristics*

ICA occlusion 15 (0.15)

Age (y) 65±8.9

Male/female 10/5

Graft numbers 4.21±0.8

Cross clamp time (min) 50.7±17.3

Perfusion time (min) 94.2±26.1

Hypertension 12 (80)

Diabetes 11 (73.3)

Hypercholesterolemia 11 (73.3)

Ejection fraction (%) 48±10.9

*Data are presented as mean±SD. Numbers in parenthesis show the related percentageICA, Internal carotid artery

One patient underwent mitral valve repair and the other 14 patients had CABG, all the procedures being elective. There was one (6.66%) intraoperative death due to low cardiac output. Atrial fibrillation (AF) was detected in 2 (13.33%) patients. Perioperative stroke was observed in one (6.66%) patient; in this case with total occlusion in the right ICA, brain ischemic stroke occurred 36 hours after surgery because of emboli in the left internal capsule. On the other hand, postoperative CVA occurred on the contralateral side of the total occlusion region. The surgical procedures and


Coronary Artery Bypass Combined …

outcomes for these 15 patients are summarized in Table 2. Postoperative CT scan was performed for all the patients. In our study, all the patients recovered uneventfully, because no mortality or morbidity occurred as a result of the total occlusion of the ICA.

Discussion

There is limited information available regarding the morbidity and mortality of patients with an occluded ICA undergoing CABG, with the reported perioperative stroke rate ranging from 4.8% to 23.1%.11

Ischemic stroke can be subdivided into at least 4 categories: large-artery disease, small-artery disease, cardio-embolic disease, and cryptogenic.12,13

Atherosclerosis and thrombosis are important components of large-artery disease in vessels such as the carotid and vertebral arteries.14 Embolic events from the atherosclerosis of the carotid artery are well documented as a major contributing factor in the development of stroke.15 Cerebral embolism is

considered the most frequent cause of a perioperative stroke. However, embolism from a carotid stenosis triggered by the surgical procedure may be rather unusual in contrast to embolism from the aortic arch. More likely, carotid stenosis may induce cerebral infarction via hemodynamic compromise during cardiopulmonary bypass. Be that as it may, risk of hemodynamic infarction distal to carotid stenosis is linked to impaired cerebral autoregulation. Therefore, the incidence of perioperative stroke even in severe carotid disease may be increased only in patients with an exhausted cerebral vasodilatative response to low perfusion pressure.16

Mickleborough et al.17 showed that the incidence of perioperative stroke among CABG patients who had unilateral ICA occlusion was 16.6%. In their study of CABG patients, Brener et al.8 examined 32 patients who had an occluded carotid artery and demonstrated the incidence of perioperative stoke to be 15.6%. Schwartz et al.18 studied 21 CABG patients who had an occluded carotid artery; the perioperative stroke rate in this study was 4.8%.

Table 2. Summary of clinical information and results

Case No Age (y) Sex Symptom CADS Surgery Number of grafts Outcome (stroke)

1 77 M - rt-ICA occlusion CABG 5 No deficit

2 61 F - lt-ICA occlusion Mitral valve repair No deficit


4 63 F - rt-ICA occlusion CABG 3 No deficit

5 76 M OCI rt-ICA occlusion CABG 4 No deficit



8 62 F - lt-ICA occlusion CABG 4 No deficit

9 74 M - rt-ICA occlusion CABG 4 Expire


11 55 M TIA rt-ICA occlusion CABG 5 No deficit

12 70 M - lt-ICA occlusion CABG 5 No deficit


14 58 M - lt-ICA occlusion CABG 4 No deficit


CADS, Carotid artery duplex scanning; rt, Right; ICA, Internal carotid artery; CABG, Coronary artery bypass graft; lt, Left; OCI, Old cerebral infarction; TIA, Transient ischemic attack

A recent study by Dashe et al.19 included 25 CABG patients having an occluded carotid artery; their incidence of perioperative stroke was 8%. In a study by Tunio et al.,11

among the 61 CABG patients with occluded carotid artery,

the perioperative stroke rate was 6.5% and the mortality rate was 8.6%. This suggests that patients with ICA occlusions are indeed more prone to perioperative stroke and mortality.

Conversely, Faggioli et al.,5 and Barnes et al.,6 reported


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Kyomars Abbasi et al

no increase in the risk of ipsilateral stroke in patients with an occluded ICA who underwent CABG. In our study, new neurological events did not occur in any patients and all of them recovered uneventfully. Our results showed that CABG can be performed without ipsilateral stroke in patients with unilateral total occlusion of the ICA. Nevertheless, there is still no consensus about the rate of stroke after CABG with ICA occlusion, and the management of these patients is still controversial.

Patients with contralateral carotid occlusion are intuitively considered a higher surgical risk for multiple reasons, e.g. reduced collateral circulation during carotid clamping, cerebral hemorrhage secondary to hyperperfusion syndrome, and the overall advanced status of the vascular disease.20

In general, the mechanisms that cause neurological complications in CABG are thought to be multifactorial. Embolization of the atherosclerotic debris from the ascending aorta and carotid artery and events related to cerebral hypoperfusion are posited as the major causes of stroke in CABG patients.7,21-23 Low perfusion could also be an important factor in these patients. When there is insufficient collateral supply, ICA occlusion can decrease the perfusion pressure in the ipsilateral hemisphere; the altered circulatory state may be sufficient to produce severe ischemia in the most distal borderline area, with eventual watershed infarction.12

Therefore, perioperative care is important, particularly maintaining perfusion pressure in the area that supplies the occluded ICA and maintaining adequate perfusion pressure during surgery and postoperative course. It seems that all the patients in our study had an adequate collateral supply, which preserved the cerebral flow to the occluded areas; that could explain why none developed neurological disorders.

Conclusion

In conclusion, among 10,000 patients, 15 (0.15%) cases had total occlusion of the ICA. Ipsilateral cerebrovascular accident occurred in none. According to our study, CABG can be performed with no risk of the development of ipsilateral stroke if adequate perfusion pressure is maintained intra and postoperatively. In our study, despite an adverse risk profile in most patients, a favorable outcome was achieved.

Finally, it remains difficult to decide the most appropriate strategy for patients with unilateral total occlusion of the ICA and much work is needed before we can declare any sound and reliable method.

Acknowledgments

We would like to thank Mrs. Neda Karimi for her assistance with data entry and Miss Monirsadat Akhlaghi for typing the manuscript. This study was approved and supported by Tehran Heart Center, Tehran University of Medical Sciences.

References

1. Dylewski M, Canver CC, Chanda J, Darling RC 3rd, Shah DM. Coronary artery bypass combined with bilateral carotid Endarterectomy. Ann Thorac Surg 2001;71:777-782.2. Ozatik MA, Göl MK, Fansa I, Uncu H, Küçüker SA, Küçükaksu S, Bayazit M, Sener E, Ta demir O. Risk factors for stroke following coronary artery bypass operations. J Card Surg 2005;20:52-57.3. Goldberg RJ, Gore JM, Alpert JS, Osganian V, de Groot J, Bade J, Chen Z, Frid D, Dalen JE. Cardiogenic shock after acute myocardial infarction. Incidence and mortality from a community-wide perspective, 1975 to 1988. N Engl J Med 1991;325:1117-1122. 4. Suematsu Y, Nakano K, Sasako Y, Kobayashi J, Kitamura S, Takamoto S. Conventional coronary artery bypass grafting in patients with total occlusion of the internal carotid artery. Heart Vessels 2000;15:256-262.5. Faggioli GL, Curl GR, Ricotta JJ. The role of carotid screening before coronary artery bypass. J Vas Surg 1990;12:724-731. 6. Barnes RW, Liebman PR, Marszalek PB, Kirk CL, Goldman MH. The natural history of asymptomatic carotid disease in patients undergoing cardiovascular surgery. Surgery 1981;90:1075-1083. 7. Breslau PJ, Fell G, Ivey TD, Bailey WW, Miller DW, Strandness DE Jr. Carotid arterial disease in patients undergoing coronary artery bypass operations. J Thorac Cardiovasc Surg 1981;82:765-767.8. Brener BJ, Brief DK, Alpert J, Goldenkranz RJ, Parsonnet V. The risk of stroke in patients with asymptomatic carotid stenosis undergoing cardiac surgery: a follow-up study. J Vas Surg 1987;5:269-279. 9. Berens ES, Kouchoukos NT, Murphy SF, Wareing TH. Preoperative carotid artery screening in elderly patients undergoing cardiac surgery. J Vasc Surg 1992;15:313-321. 10. Nicolaides AN, Shifrin E, Bradbury A. Angiographic and duplex grading of internal carotid stenosis: can we overcome the confusion? J Endovasc Surg 1996;3:158-165. 11. Tunio AM, Hingorani A, Ascher E. The impact of an occluded internal carotid artery on the mortality and morbidity of patients undergoing coronary artery bypass grafting. Am J Surg 1999;178:201-205.12. Hunt JL, Fairman R, Mitchell ME, Carpenter JP, Golden M, Khalapyan T, Wolfe M, Neschis D, Milner R, Scoll B, Cusack A, Mohler ER 3rd. Bone formation in carotid plaques. A clinicopathological study. Stroke 2002;33:1214-1219. 13. Sacco RL. Risk factors, outcomes, and stroke subtypes for ischemic stroke. Neurology 1997;49:S39-S44. 14. Sacco RL, Kargman DE, Gu Q, Zamanillo MC. Race-ethnicity and determinants of intracranial atherosclerotic cerebral infarction: the Northern Manhattan Stroke Study. Stroke 1995;26:14-20. 15. Silvestry FE, Tarka EA, Mohler ER. Echocardiographic and vascular ultrasound evaluation of cerebrovascular ischemic events. ACC Curr J Rev 1998;6:79-81. 16. Schoof J, Lubahn W, Baeumer M, Kross R, Wallesch CW, Kozian A, Huth C, Goertler M. Impaired cerebral autoregulation distal to carotid stenosis/occlusion is associated with increased risk of stroke at cardiac surgery with cardiopulmonary bypass. J Thorac Cardiovasc Surg 2007;134:690-696. 17. Mickleborough LL, Walkerm PM, Yakagi Y, Ohashi M, Ivanov J, Tamariz M. Risk factors for stroke in patients undergoing CABG. J Thorac Cardiovasc Surg 1996;112:1250-1258. 18. Schwartz LB, Bridgman AH, Keiffer RW, Wilcox RA, McCann RL, Tawil MP, Scott SM. Asymptomatic carotid stenosis and stroke in patients undergoing cardiopulmonary bypass. J Vasc Surg 1995;21:146-153. 19. Dashe JF, Pessin MS, Murphy RE, Payne DD. Carotid occlusive disease and stroke risk in coronary artery bypass graft surgery. Neurology 1997;49:678-686. 20. Aburahma AF, Robinson P, Holt SM, Herzog TA, Mowery NT. Perioperative and late stroke rates of carotid endarterctomy contra lateral to carotid artery occlusion. Stroke 2000;31:1566-1571.


21. Gardner TJ, Horneffer PJ, Manolio TA, Pearson TA, Gott VL, Baumgartner WA, Borkon AM, Watkins L Jr, Reitz BA. Stroke following coronary artery bypass grafting: a ten-year study. Ann Thorac Surg 1985;40:574-581. 22. Aranki SF, Rizzo RJ, Adams DH, Couper GS, Kinchla NM, Gildea JS, Cohn LH. Single-clamp technique: an important adjunct to myocardial and cerebral protection in coronary operations. Ann Thorac Surg 1994;58:296-302. 23. Lynn GM, Stefanko K, Reed JF 3rd, Gee W, Nicholas G. Risk factors for stroke after coronary artery bypass. J Thorac Cardiovasc Surg 1992;104:1518-1523.

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*Corresponding Author: Mohammad Hasan Namazi, Associate Professor of Cardiology, Shaheed Modarres Hospital, Cardiovascular Research

Center, Saadat abad, Tehran, Iran. 1998734383. Tel: + 98 21 22083106. Fax: +98 21 22083106. Email: [email protected].

Original Article

Prevention of Atrioventricular Block During Radiofrequency

Ablation by Pace Mapping of Koch’s Triangle

Mohammad Hasan Namazi, MD*, Hassan Kamalzadeh, MD, Morteza Safi, MD, Reza Karbasi Afshar, MD, Mohammad Reza Motamedi, MD, Habibollah Saadat, MD, Hossein Vakili, MD

Modarres Hospital, Shaheed Beheshti University of Medical Sciences, Tehran, Iran.

Received 9 September 2007; Accepted 19 January 2008

Abstract

Background: Complete atrioventricular block (AV block) is a serious complication of slow pathway ablation therapy

in the treatment of atrioventricular nodal re-entrant tachycardia (AVNRT). The present study was aimed at determining

whether the electroanatomical pace mapping of Koch’s triangle could significantly improve the safety, efficiency, and efficacy

of selective slow pathway ablation in the treatment of AVNRT.

Methods: A total number of 124 patients were selected to be studied consecutively for radiofrequency (RF) ablation

therapy in the treatment of AVNRT. The subjects were divided into two groups: one, designated Group 1, to serve as the con-

trol group, and the other, designated Group 2, to serve as the study group. Conventional fluoroscopic slow pathway ablation

was performed on the Group 1 subjects (n=66), with the Group 2 subjects receiving slow pathway ablation therapy guided

by pace mapping of Koch’s triangle. The slow pathway ablation in Group 2 (n=58) was performed with regard to the pace

mapping data obtained on the basis of the St-H interval in the anteroseptal (AS), midseptal (MS), and posteroseptal (PS)

regions of Koch’s triangle. The anterograde fast pathway (AFP) location was determined based on the shortest St-H interval

obtained by stimulating the anteroseptal (AS), midseptal (MS), and posteroseptal (PS) aspects of Koch’s triangle.

Results: In the Group 2 subjects, AFP location was AS in 50 (86.2%) of the cases, MS in 7 (12%) of the cases, and PS in

1 case (1.7%). One patient with posteroseptal AFP was administered retrograde fast pathway ablation therapy. One patient

in the control group (Group 1), representing 1.5% of the group, developed persistent AV block in the course of the treatment,

but none of the subjects in the study group (Group 2) developed any complications.

Conclusion: It was concluded that an atypical fast pathway location is conducive to the development of atrioventricular

block in the ablation therapy in AVNRT, with pace mapping of Koch’s triangle having the capacity to eliminate the risk of any

such complication developing. It follows that it helps to identify the AFP location before ablation therapy is administered in

AVNRT, thereby improving the safety of the treatment.


Keywords: Tachycardia, atrioventricular nodal reentry • Atrioventricular block • Catheter ablation

Introduction

Catheter ablation is an invasive procedure currently used in the treatment of atrioventricular nodal re-entrant

tachycardia (AVNRT). Slow pathway catheter ablation in AVNRT has an extremely high success rate, about 100%,


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Mohammad Hasan Namazi et al

with only a 0.5% to 2% risk of causing second or third-degree atrioventricular (AV) block.1-3 The risk of this complication arising is low, but, when it occurs, it may not be tolerated, especially by young patients, as it may lead to a life-threatening arrhythmia. The proximity of the location of the fast pathway to the compact atrioventricular node and the bundle of His can cause inadvertent AV block during slow pathway ablation in AVNRT. In other cases, the cause of the block could not be determined, as the energy is delivered to the posterior aspect of Koch’s triangle, far from the usual site of the anterograde fast pathway and that of the AV node.4 AV block generally occurs during RF delivery or within 24 hours after the procedure.

In this study, patients with atypical fast pathway location (in the midseptal [MS] or posteroseptal [PS] areas) were identified by pace mapping of Koch’s triangle before ablation therapy administration. Ablation therapy was performed using the conventional slow pathway method in the control group (designated Group 1, n=66) and after pace mapping of Koch’s triangle in the study group (designated Group 2, n=58). In this article, the occurrence of persistent AV block in the two groups during or after administering catheter ablation is examined and compared.

Methods

Catheter ablation therapy was performed by two separate medical groups on 124 patients presenting with the typical form of AVNRT, referred to Modarres Hospital in Tehran, Iran, from September through February 2007. The diagnosis of typical AVNRT was based on a number of specific criteria including:

1- Initiation of the tachycardia after AH interval jump during atrial pacing

2- Earliest retrograde atrial activation in tachycardia at the bundle of His

3- HA interval in tachycardia less than the HA interval with ventricular pacing

4- Atrial and reciprocating tachycardia excludedThe 66 patients in Group 1 were administered the

conventional slow pathway ablation therapy, while the 58 Group 2 patients received slow pathway ablation therapy with regard to the data obtained by pace mapping of Koch’s triangle.

Routine laboratory tests, as well as transthoracic echocardiography and 12-lead ECG were performed for all the subjects. Any anti-arrhythmic medication was discontinued for at least five half lives before conducting the study. All the subjects arrived at the electrophysiology (EP) lab in a fasting state. Three quadripolar electrode catheters (with 5 mm inter-electrode distances) and one decapolar

catheter were inserted in the high right atrium, the bundle of His region, the right ventricular apex, and the coronary sinus, in that order, via the right and left common femoral veins. The stimulation protocol involved atrial and ventricular pacing, and extra stimulation, which was performed on all the subjects. The specific location for RF energy delivery was identified, either through the conventional method or by pace mapping of Koch’s triangle, and the radiofrequency (RF) energy was delivered accordingly. The temperature control was preset at 60˚ and the maximum power at 50 watts. For the 66 patients in Group 1, conventional slow pathway ablation was performed, with the 58 patients in the study group (Group 2) receiving ablation therapy under the guidance of pace mapping of Koch’s triangle.

In Group 1, conventional slow pathway ablation was performed by positioning the catheter in the right anterior oblique view near the coronary sinus ostium. It was positioned in the zone of low frequency, fractionated, electrocardiogram recording (as described by Haissaguerre et al.) or potentially as described by Jackman et al. (sharp and late atrial electrocardiogram following a low amplitude atrial electrocardiogram during sinus rhythm).2,3 If the application was unsuccessful, the catheter was repositioned progressively higher along the tricuspid annulus in an attempt to ablate the slow pathway (anatomical approach).

In Group 2, pace mapping of Koch’s triangle data was obtained first, before the ablation therapy was administered. Pace mapping was performed by stimulating the site near the bundle of His, in the anteroseptal (AS) region of Koch’s triangle, where the fast pathway is normally located, followed by the stimulation of the midseptal (MS) and posteroseptal (PS) aspects of Koch’s triangle. A short St-H interval was normally recorded in the anterosuperior region of Koch’s triangle, defined as the fast pathway region. The longest St-H interval, on the other hand, is defined as the slow pathway area. The ablation catheter was inserted into the AS region, where the highest His deflection was recorded, for stimulation. During the continuous pacing, the ablation catheter was withdrawn slowly until the atrium was captured (Figure 1). The 2-3 first captured beats were used for the St-H assessment, whereby the shortest St-H interval was selected. For the PS stimulation, the ablation catheter was inserted in front of the coronary sinus ostium. For the MS region stimulation, the area between the AS and PS aspects of Koch’s triangle was stimulated. For locating the site of retrograde fast pathway, the right ventricle was paced; and the ventriculoatrial (VA) interval in the AS, MS, and PS areas was calculated. In cases where the fast pathway was found to be located in the AS region, slow pathway ablation was performed using the conventional approach. In patients with the fast pathway located in the MS region, radiofrequency


Prevention of Atrioventricular Block During ...

ablation was performed strictly in the PS area. In cases where the anterograde (antegrade) fast pathway conduction was found to be in the PS region, retrograde fast pathway ablation was performed in the AS area. Persistent AV block was defined in cases where the block occurred during ablation and was found not to have cleared within 24 hours after the procedure was completed. The block was defined as transient second or third-degree in cases where the AV block occurred during ablation but cleared before the patient left the EP lab. The results of the ablation treatment of both groups are summarized in Table 1.

Table 1. The results of slow pathway ablation in conventional (group 1) and those patients who underwent pace mapping of Koch’s triangle (group 2)

VariableGroup 1

(n=66)

Group 2

(n=58)

Procedure time (min)*

Time RFA (sec)*

Transient block

Permanent block

Successful ablation

80.3±27.6

186.6±165.9

1(1.5%)

1(1.5%)

100%

86.4±36.6

228.8±222.1

0

0

98.3%

*Data are presented as mean±SD

The results are expressed as mean values±standard deviation (SD) for the continuous variables. The results were analyzed via the chi-square test or Fischer’s exact test, and the Mann-Whitney U Test was employed to compare the two groups. For statistical analysis, SPSS version 13 computer software was used. For all the tests, a P value of less than 0.05 (P<0.05) was considered statistically significant.

Figure 1. Pace mapping of A: anteroseptal (AS), B: midseptal (MS) and C: posteroseptal (PS) portion of Koch’s triangle. Stimulation to His interval

was performed at AS, MS and PSp

A

B

C

Results

Group 1 consisted of 22 males and 44 females at an average age of 48±13.1 years, as compared with Group 2 comprised of 13 males and 45 females at an average age of 45.5±13.7 years.

In Group 2, AVNRT was induced in all the subjects (with or without Isoprel infusion). Among the 58 subjects in Group 2, the anterograde fast pathway location was in the AS region in 50 cases (designated Subgroup A), in the MS region in 7 cases (designated Subgroup B), and in the PS region in one case (designated Subgroup C). The results of Koch’s triangle stimulation in Group 2 subjects are summarized in Tables 2-4.


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Table 2. The results of pace mapping of Koch’s triangle in three subgroups of patients*

Subgroup A (n=50)

Subgroup B (n=7)

Subgroup C (n=l)

Anteroseptal (ms) 8 1.5±24.2 103.7±46.5 64

Midseptal (ms) 97.6±26.5 77.4±36.2 98

Posteroseptal (ms) 120.8±31.2 117.1±32.6 44


Subgroup A, patients in whom anterograde fast pathway was in anteroseptal region of Koch’s triangle; Subgroup B, patients in whom anterograde fast pathway was in midseptal region of Koch’s triangle; Subgroup C, patients in whom anterograde fast pathway was in posteroseptal region of Koch’s

triangle

Table 3. Comparison of procedure and ablation times between subgroups of patients*

Subgroup No of cases Procedure time (min)

Ablation time (sec)

A 50 86.9 ±37.9 230.5 ±224.9

B 7 77.1± 23.6 142.9 ±49.6

C 1 120 746


Subgroup A, patients in whom anterograde fast pathway was in anteroseptal region of Koch’s triangle; Subgroup B, patients in whom anterograde fast pathway was in midseptal region of Koch’s triangle; Subgroup C, patients in whom anterograde fast pathway was in posteroseptal region of Koch’s

triangle

Table 4. St-H interval in patients who underwent pace mapping of Koch’ triangle*

Region of Koch’s triangleMean(msec)

Minimum(msec)

Maximum(msec)

Anteroseptal 83.8±28.2 45 200

Midseptal 95.2±28.1 44 176

Posteroseptal 119.1±32.4 44 220


Patients that presented with antegrade fast pathway (AFP) in the MS or PS regions were notified of the significant risk of atrioventricular block occurring in the course of the ablation therapy. One patient did not respond to slow pathway ablation despite having the AFP location in the AS region. It can be attributed to the slow pathway LA extension. In all the cases in Group 1, slow pathway ablation was successfully performed using the conventional method. Persistent first-degree AV block occurred in one (1.7%) of the Group 2 subjects with the AFP location in the PS area, whereby retrograde fast pathway ablation was administered in the AS region. Persistent AV block occurred in one (1.5%) of the Group 2 subjects, for whom a permanent pace maker was implanted. Transient second-degree AV block occurred in another patient in Group 1. The differences in persistent AV block did not represent a statistically significant difference between the groups. Similarly, differences in the mean procedure time, mean ablation time, and the gender and age

differences were not statistically significant.

Discussion

Slow pathway catheter ablation in the treatment of AVNRT carries the risk of causing complete atrioventricular block. It is most likely due to causing injury to the atrial inputs to the posterior aspect of the AV node, the bundle of His, or both the slow and the fast pathways, in the course of the treatment. It is not feasible to predict with certainty this complication arising in individual cases. The rate of the junctional rhythm during ablation has been shown to be a reliable indicator of impending AV block.5 If the VA block occurs during the junctional rhythm, it is more applicative; it is a highly sensitive but not specific indicator. A study by Hintringer et al. showed only 23% of episodes of VA block during junctional rhythm to be associated with impaired antegrade conduction in a group of 58 patients. Although the occurrence of retrograde block with junctional rhythm has low specificity, it is not to be neglected, and the radiofrequency delivery is to be stopped at once when it occurs. Also, an interval of less than 20 milliseconds between the ablation atrial electrogram and the His atrial electrogram has been described as being predictive of AV block with RF. On the other hand, A/V ratio, presence of slow pathway potential, atrial electrogram fractionation, and the number of RF lesions were considered not to be predictive of AV block. Pietro Delise et al. showed the anterograde fast pathway to be abnormally located in the MS or PS region, or otherwise unable to conduct in an anterograde manner, in about 10% of patients with AVNRT.1

It has been postulated that atrioventricular node morphology is quite variable in humans.6 It accounts for the possibility of AV block during slow pathway ablation. In a study by Denise et al., 909 consecutive patients were administered radiofrequency ablation for the treatment of AVNRT. The subjects were divided into two groups designated Group 1 (n=487) and Group 2 (n=422); Group 1 was assigned to undergo conventional slow pathway ablation, while Group 2 was assigned to undergo ablation therapy guided by pace mapping of Koch’s triangle, which located the anterograde fast pathway interval, based on the shortest St-H interval. It was obtained by stimulating the anteroseptal, midseptal, and posteroseptal aspects of Koch’s triangle. In Group 2 subjects, the AFP was anteroseptal in 384 (91%) of the cases, midseptal in 33 cases (7.8%), and posteroseptal or absent in 5 cases (1.2%). Of the 33 patients with midseptal AFP, slow pathway ablation was performed in 32 patients strictly in the posteroseptal area. Of the 5 patients with posteroseptal or absent AFP, on the other hand, retrograde fast pathway ablation was performed in 3 cases, with 2 patients declining treatment. Persistent second to third-degree AV block was induced in 7 (1.4%) of the cases in Group 1 versus none being induced in Group 2 (P=0.032).4 In our study, slow pathway ablation in all the cases with midseptal and posteroseptal AFP location, 7 and 50 in number respectively, was performed in the PS region. The ablation procedure took longer in the Group 2

Mohammad Hasan Namazi et al


subjects than that in the Group 1 cases, but this difference in time was not statistically significant. In addition, in cases where the slow pathway was in the MS region (Subgroup B), the procedure time and the ablation time were less than those of the Subgroup A cases. It suggests that when the slow pathway is near the fast pathway (as in Subgroup B), it is more sensitive to RF energy than when it is further away from it (as in Subgroup A).

Transient AV block was detected in one of the patients in Group 1 versus none in Group 2. Permanent (third-degree) AV block occurred in one patient in Group 1, again with no cases found in Group 2. Persistent first-degree AV block occurred in one patient in Group 2 after retrograde fast pathway ablation, but the block did not show any progression in the first 4-week follow-up.

This study has weaknesses on several grounds rendering it to some extent inconclusive. They include its having been conducted in a single-blind non-randomized manner. Furthermore, the small number of subjects (especially in Subgroup C) does not allow drawing firm conclusions regarding the efficacy of pace mapping of Koch’s triangle in averting AV block in all patients with AVNRT on the basis of the results obtained.

Conclusion

The present study concluded that an atypical location of fast pathway is conducive to complete AV block occurring as a result of catheter ablation in the treatment of AVNRT. Pace mapping of Koch’s triangle can reveal any such abnormalities and may be useful in guiding ablation, thereby avoiding AV block. It greatly improves the safety of radiofrequency ablation therapy in AVNRT through identifying the exact location of anterograde fast pathway, thus guiding the ablation therapy. It can greatly diminish the likelihood of AV block occurring in the course of the treatment. It is, however, worthy of note that the total number of the subjects studied being small, it is mandatory that further trials be made to allow a more definitive conclusion to be reached.

Acknowledgments

With special thanks to the cardiovascular research center of Shaheed Beheshti University of Medical Sciences and nurses of the catheterization laboratory of Shaheed Modaress Hospital (Mohammad Reza Samadi, Arash Babak, Masume Valanparast).

This study was approved and supported by Shaheed Beheshti University of Medical Sciences.

References

1. Delise P, Sitta N, Zoppo F, Corò L, Verlato R, Mantovan R, Sciarra L, Cannarozzo P, Fantinel M, Bonso A, Bertaglia E, D’Este D. Radiofrequency ablation of atrioventricular nodal reentrant tachycardia; The risk of intra-procedural, late and Long-term atrioventricular block. The Veneto Region multicenter experience. Ital Heart J 2002;3:715-720.2. Haissaguerre M, Gaita F, Fischer B, Commenges D, Montserrat P, d’Ivernois C, Lemetayer P, Warin JF. Elimination of atrioventricular nodal reentrant tachycardia using discrete slow potential to guide application of radiofrequency energy. Circulation 1992;85:2162-2175.3. Jackman WM, Beckman KJ, McClelland JH, Wang X, Friday KJ, Roman CA, Moulton KP, Twidale N, Hazlitt HA, Prior MI, et al. Treatment of supraventricular tachycardia due to atrioventricular nodal reentry by radiofrequency catheter ablation of slow-pathway conduction. New Engl J Med 1992;327:313-318.4. Delise P, Sitta N, Bonso A, Coro’ L, Fantinel M, Mantovan R, Sciarra L, Zoppo F, Verlato R, Marras E, D’Este D. Pace mapping of Koch’s triangle reduces risk of atrioventricular block during ablation of atrioventricular nodal reentrant tachycardia. Pacing Clin Electrophysiol 2005;16:30-35.5. Hintringer F, Hartikainen J, Davies DW, Heald SC, Gill JS, Ward DE, Rowland E. Prediction of atrioventricular block during radiofrequency ablation of the slow pathway of the atrioventricular node. Circulation 1995;92:3490-3496.6. Inoue S, Becker AE. Posterior extensions of the human compact atrioventricular node. A neglected anatomic feature of potential clinical significance. Circulation 1998;97:188-193.

Prevention of Atrioventricular Block During ...


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*Corresponding Author: Abbasali Karimi, Associate Professor of Cardiac Surgery, Tehran Heart Center, North Kargar Street, Tehran, Iran. 1411713138.

Tel: +98 21 88029721. Fax: +98 21 88029724. Email: [email protected].

Original Article

Repair Versus Replacement for Ischemic Mitral Regurgitation

Hakimeh Sadeghian, MD, Abbasali Karimi, MD*, Mehran Mahmoodian, MD, Hossein Ahmadi, MD, Seyed Hesameddin Abbasi, MD

Tehran Heart Center, Medical Sciences / University of Tehran, Iran.

Received 27 September 2007; Accepted 19 January 2008

Abstract

Background: This study was undertaken to compare the outcome in patients with moderate to severe ischemic mitral

regurgitation (IMR) undergoing coronary artery bypass grafting (CABG) with either mitral valve repair or mitral valve

replacement.

Methods: Between March 2002 and February 2005, 49 consecutive patients (mean age: 62.84±8.42 years; mean Euro-

SCORE: 10.03±3.12) with coronary artery disease and moderate to severe IMR underwent CABG plus mitral valve replace-

ment or mitral valve repair. The patients with annulus dilatation were more likely to undergo repair. The mean follow-up

period was 18.89±2.1 months.

Results: 40.8% of the patients underwent CABG plus mitral valve replacement, and 59.2% had CABG concomitant with

mitral valve repair. The total rate of mortality in our population was 14.9% (7 patients) including 10.3% (3 patients) early

mortalities; all the deceased patients were in the repair group. Both groups had a similar EuroSCORE, but more patients in

the repair group had a recent episode of unstable angina (65.5% vs. 35.0%, respectively; P=0.035) and diabetes mellitus

(44.8% vs. 10.0%, respectively; P=0.009). After the follow-up period, in the repair group, 11.5% had no features of Mitral

regurgitation (MR); while 50% had mild MR, 23.1% moderate MR, 11.5% moderately severe MR, and 3.8% severe MR.

Overall, 68.9% had no or mild MR, which we defined as successful repair, and 31.1% had moderate to severe MR. Success of

repair and mortality were not statistically related to preoperative ejection fraction (39.2±7.8% vs. 32.5±8.5%; P=0.057).

Conclusion: Early mortality was higher in the repair group than that in the replacement group, but this may have been due

to the higher frequency of diabetes mellitus and unstable angina in the former group. Future studies are required to determine

the benefit of repair versus replacement concomitant with CABG in IMR patients.


Keywords: Mitral regurgitation • Ischemia • Heart valve

Introduction

In moderate to severe ischemic mitral regurgitation (IMR), the use of mitral valve repair versus mitral valve replacement along with coronary artery bypass grafting (CABG) is controversial. Patients undergoing mitral valve repair may have a reduced incidence of thromboembolism and reduced necessity for anticoagulation compared with patients undergoing mitral valve replacemen.1 Other advantages of

mitral valve repair over replacement include greater freedom from endocarditis and better preservation of left ventricular function.2 These advantages have been investigated when degenerative mitral valve disease exists in isolation. The use of mitral valve repair in ischemic mitral regurgitation (IMR) is, however, controversial. IMR is a disease of myocardium,3

and while some authors believe that myocardial infarction


90

Hakimeh Sadeghian et al

(MI) always precedes IMR,3 others believe that IMR is caused by coronary artery disease (CAD) and not necessarily by MI.4

Surgical treatment of IMR is associated with a high operative mortality rate and poor long-term survival.5 Choosing a most appropriate surgical treatment to maximize the survival for these patients is complicated by the inconsistent classification schemes and a paucity of long-term data to compare valve repair versus replacement in this group of patients.5 In this study, we compare the mid-term outcome in patients with IMR undergoing CABG with either mitral valve repair or mitral valve replacement.

Methods

The present retrospective study was performed in the cardiothoracic surgery registry of Tehran Heart Center, which is a single-center registry containing demographic and clinical features, previous medical antecedents such as risk factors and procedural details, and follow-up data.

Between March 2002 and February 2005, 49 consecutive patients with moderate to severe Mitral regurgitation (MR) (2+ to 4+) and coronary artery disease (CAD) who underwent CABG plus mitral valve replacement or mitral valve repair were identified from the cardiothoracic surgery registry of Tehran Heart Center Surgery Data Base. Moderate to severe IMR was defined as MR grade II or IV on echocardiography or ventriculograghy. Mitral valve regurgitation due to rheumatism or myxomatous degenerative disease was excluded from the study population, but patients with IMR and concomitant senile calcification or prolapse or rupture of chordae secondary to MI were included. EuroSCORE was used before surgery to estimate the risk of mortality after CABG. The choice between mitral valve replacement and mitral valve repair was based on the surgeons’ discretion; be that as it may, the patients with annulus dilatation were more likely to undergo repair (P=0.088). It is deserving of note that EuroSCORE is a simple, objective, and up-to-date system for assessing heart surgery, soundly based on one of the largest, most complete, and accurate databases in European cardiac surgical history.6

A preoperative echocardiography was performed for all the patients. Transesophageal echocardiography (TEE) was employed to detect the severity and mechanism of MR when needed. The assessment of MR severity was based on a number of variables (Table 1). MR was defined as ischemic if associated with persistent wall motion abnormality and no significant organic mitral valve disease. IMR was further subdivided into four major mechanisms of regurgitation: 1- Annulus dilation, 2- Restriction of the posterior mitral leaflet, 3- Prolapse of each leaflet, and 4- Rupture of the cord. Post-pump intraoperative TEE was used in the repair group; and if there was more than mild to moderate MR, mitral valve replacement was performed. 93.2% of the study population had postoperative or follow-up echocardiography. The mean follow-up period was 18.89±2.1 months.

Table 1. Assessment of the mitral regurgitation severity

RV (ml) ERO (cm2) MR jet (% LA)

I Mild <30 <0.2 <15

II 30-44 0.2-0.29 15-30

III 45-59 0.3-0.39 35-50

IV Severe 60 >0.4 >50

RV, Regurgitation volume; ERO, Effective regurgitation orifice (cm2); MR, Mitral regurgitation; % LA, percentage of left atrial area encompassed by the mitral regurgitation jet with color flow Doppler imaging

The preoperative, operative, and postoperative data were collected prospectively in the division’s clinical database and confirmed by reviewing the actual medical records. Statistical analysis was performed with the SPSS statistical package (SPSS Version 13.0). All the continuous variables were expressed as mean±SD and the dichotomous variables as frequencies. The categorical variables were compared using the chi-square test, and the continuous variables were compared using Student’s t-test. P values 0.05 were considered statistically significant. Also, the ordinal variables were compared using the nonparametric Mann-Whitney or Willcoxon signed ranks tests.

Results

The patient characteristics of the 49 participants undergoing mitral valve repair or replacement are depicted in Table 2. In our patients, the causal mechanisms of IMR consisted of the following conditions: annulus dilatation (66.7%), restriction of posterior mitral leaflet (40%), prolapse of both leaflets (11.1%), prolapse of anterior mitral leaflet or posterior mitral leaflet (6.7%), and rupture of cords (2.2%) (Table 3).Table 2. Patients’ characteristics*

MVR(n=20)

MV Repair (n=29)

P value

Age (y) (mean±SD) 63.89±8.17 62.07±8.68 0.48

Female 7(35.0) 7(24.1) 0.41

Hypertension 4(20.0) 8(27.6) 0.54

Diabetes mellitus 2(10.0) 13(44.8) 0.009

Recent MI 2(10.0) 3(10.6) 0.96

Recent UA 7(35.0) 19(65.5) 0.035

CHF 4(20.0) 4(13.8) 0.56

Renal insufficiency (Cr>1.5 mg/dl)

3(15.0) 7(24.1) 0.43

*Numbers in parenthesis show the related percentagesMVR, Mitral valve replacement; MV, Mitral valve; MI, Myocardial infarction; UA, Unstable angina; CHF, Congestive heart failure; Cr, Creatinine



Table 3. Mechanism and etiology of mitral regurgitation*

AllPatients

MVR(n=20)

MV Repair (n=29)

P value

Annulus dilation 30(66.7) 10 (33.3) 20 (66.7) 0.088

Restriction of PML 18 (40) 7 (38.8) 11 (61.2) 0.71

Prolapse of AML 3(6.7) 1(33.3) 2 (66.7) 0.74

Prolapse of PML 3 (6.7) 1 (33.3) 2 (66.7) 0.74

Both leaflets prolapse

5 (11.1) 2 (40.0) 3 (60.0) 0.91

Posterior cordal rupture

1 (2.2) 1 (100) 0 -

Calcification of PML

1 (2.2) 1 (100) 0 -

Calcification of AML

1 (2.2) - 1 (100) -

*Numbers in parenthesis show the related percentagesMVR, Mitral valve replacement; MV, Mitral valve; PML, Posterior mitral leaflets; AML, Anterior mitral leaflets

Of these participants, 20 (40.8%) underwent mitral valve replacement and 29 (59.2%) underwent repair. In the repair group, 65.5% underwent annuloplasty, 27.6% other reconstruction techniques concomitant with annuloplasty, and 6.9% reconstruction techniques without annuloplasty. The mean age of the patients in both groups was similar (63.89±8.18 years in the replacement group vs. 62.11±8.68 years in the repair group; P=0.48), but there were more female patients undergoing mitral valve replacement. The proportions of female gender, history of prior MI, and hypertension were not significantly different between the two groups. More patients in the repair group had a recent episode of unstable angina (65.5% vs. 35.0%; P=0.035), and the frequency of diabetic patients was significantly higher among the patients undergoing repair (44.8% vs. 10.0%; P=0.009). More patients in the repair group suffered from annulus dilatation, but the number was not statistically significant (76.9% vs. 52.6%; P=0.088). The mean of left ventricular ejection fraction (LVEF) was not statistically significantly different between two groups (39.5±8.3 in the replacement group vs. 36.2±8.3 in the repair group; P=0.19).

The difference in EuroSCORE between mitral valve repair and mitral valve replacement was not statistically expressive (10.2±2.9 in the replacement group vs. 9.9±3.3 in the repair group; P=0.80). All the patients in both groups underwent concomitant CABG with a similar number of grafts (P=0.116) (Table 4).

Table 4. Severity of disease

MVR(n=20)

MV Repair(n=29)

P value

Ejection Fraction (%)* 39.47±8.27 36.25±8.35 0.19

Concomitant CABG 20 29

Number of grafts n (%) 0.11

0-1 4(22.3) -

2 - 2(7.4)

3 8(44.4) 11(40.7)

4 5(27.8) 9(33.3)

5-6 1(5.6) 5(18.5)

EuroSCORE* 10.16±2.88 9.93±3.33 0.80

DLVD (mm)* 53.51±13.61 56.13±15.17 0.56

SLVD (mm)* 42.53±9.44 40.48±13.54 0.63

*Data are presented as mean±SDMVR, Mitral valve replacement; MV, Mitral valve; CABG, Coronary artery bypass grafting; DLVD, Diastolic left ventricle dimension; SLVD, Systolic left ventricle dimension

It must be noted that the perioperative use of intra-aortic balloon pump (IABP) was higher in the repair group, but it was only a trend (24.1% vs. 5.0%; P=0.075).The total rate of mortality in our population was 14.9% (7 patients), including 10.3% (3 patients) early mortalities. All the deceased patients were among those in the repair group. It is noteworthy that 12 patients (25.5%) had EF 30%, and 2 (18.2%) of these patients died. Mortality was not statistically related to preoperative EF (34.3±8.9% vs. 38.4±8.4%; P=0.24), diastolic LV dimensions (55.5±4.9 vs. 54.0±15.1 mm; P=0.84), and systolic LV dimensions (37.0±5.3 vs. 41.1±12.2 mm; P=0.51), and nor was it related to MR severity (P=0.23), postoperative MR in the repair group (P=0.58), and history of recent unstable angina (P=0.029). However, the deceased patients had lower LV ejection fraction in the follow-up period, but it must be considered as a trend (32.0±4.8% in the mortality group vs. 36.6±10.4% in the others; P=0.098). A history of preoperative use of IABP was more frequent in the deceased cases compared with the living patients (42.9% vs. 12.5%, respectively; P=0.049). EuroSCORE was not different between the deceased and the living (10.9±1.9 vs. 9.9±3.4; P=0.46). After the follow-up period, in the repair group, 11.5% had no features of MR, while 50% had mild MR, 23.1% moderate MR, 11.5% moderately severe MR, and 3.8% severe MR. There were only two crossovers from repair to replacement: one of them because of severe MR and the other because of severe mitral stenosis. Overall, 68.9% had no or mild MR, which we defined as successful repair and 31.1% had moderate to severe MR. MR severity and LVEF in postoperative and follow-up echocardiography are shown in Tables 5 and 6.


92

Table 5. Mitral regurgitation (MR) severity by Transthoracic echocardiography (TTE)*

Severity of MR Preoperative Postoperative TTE Follow-up TTE

0 0 9.5 15.8

1+ 0 52.4 47.4

2+ 34.5 28.6 21.1

3+ 62.1 9.5 10.5

4+ 3.4 0 5.3*Data are presented as percentage

Table 6. LVEF in postoperative and follow-up echocardiography*

MVR(n=20) MV repair(n=29)

Preoperative EF (%) 39.47±8.27 36.25±8.35

Postoperative EF (%) 36.56±10.60 36.14±11.75

Follow-up EF (%) 39.06±8.45 40.91±9.70

*Data are presented as mean±SDLVEF, Left ventricular ejection fraction; MVR, Mitral valve replacement; MV, Mitral valve; EF, Ejection fraction

Preoperative LVEF was slightly higher in the successful repair cases; it was, however, not statistically significant (39.2±7.8% vs. 32.5±8.5%; P=0.057). Success of repair was not related to diastolic LV dimensions (58.9±8.5 vs. 54.1±24.2 mm; P=0.68), systolic LV dimensions (44.0±12.0 vs. 39.3±19.9 mm; P=0.63), severity of MR (P=0.65), and surgical methods of repair (P=0.31).

Discussion

Our early and total mortality rates, all of which occurred in the mitral valve repair group, were 10.3% and 14.9%, respectively. These mortality rates are comparable with those in other studies: 15% in the Tavakoli et al.,7 14.6% in the Dion et al.,8 9.3% in the Cohn et al.,9 and 9.2% in the Hendren et al.10 studies. Akins and colleagues11 and Enriquez-Sarano and associates12 found that repair was associated with reduced hospital mortality; nevertheless, the view was not corroborated by other authors.2,13,14 In the Gillinov’s study,5

the 30-day and one-year mortality rates were 6% and 18% in the repair group and 19% and 44% in the replacement group in IMR patients, respectively. In contrast, the rate of mortality was higher in our repair group, which may have been secondary to the greater frequency of diabetes mellitus and unstable angina in the patients comprising this group, although the total mean EuroSCORE of both groups was similar. In addition, the etiology of MR in our patients was ischemia; and according to Gillinov et al., these patients had a poor prognosis.5 We found that a history of preoperative use of IABP was a predictor of mortality. Hendren et al.10 also reported that a preoperative use of IABP was associated with increased operative mortality. In the Tavakoli et al. study,7 the

only independent risk factors for early mortality were IABP and chronic obstructive pulmonary disease (COPD). In line with the Hausmann et al. study;15 the postoperative LVEF during our follow-up period had a trend of being effective in mortality, and mortality was higher in patients with more severe LV dysfunction after surgery.

Repair was successful in 61.5% of our patients, and only 2 patients underwent reoperation. Our results indicated that the success of repair was not related to preoperative ejection fraction, severity of mitral valve regurgitation, techniques of repair, or diastolic and systolic LV dimensions. In another study by Gillinov et al., approximately 70% of the patients were predicted to benefit from repair; the benefit lessened or was negated if an internal thoracic artery graft was not used, if a lateral wall motion abnormality was present, or if the MR jet pattern was complex. Freedom from repair failure at 5 years in the said study was 91%.5 Grossi EA et al. clearly presented lower short-term complications or death rates in patients with mitral valve reconstruction compared with mitral valve replacement patients, while noting that five-year complication-free survival rates were higher in patients undergoing mitral valve repair.16

We found that mortality in patients with severe LV systolic dysfunction (LVEF 30%) and moderate to severe MR was about 18.2%. Similarly, Bishay et al. reported 11% one-year mortality and 14% two-year mortality rates for patients with LVEF<35% and MR for those who underwent mitral valve replacement or repair.17 In our study, the patients with higher preoperative LVEF had slightly more successful repair; it was, however, not statistically significant (as a trend) and may have been due to the relatively small number of cases. We could not find any relationship between success of repair and diastolic and systolic LV dimensions, MR severity, and techniques of repair. Gillinov et al. reported that the benefit of repair was lessened in the presence of lateral wall motion abnormality or complex jets of MR.

Conclusion

Early mortality was higher in the repair group in spite of the similarity observed in the mean EuroSCORE of both repair and replacement groups. However, this high mortality in the repair group may have been due to the higher frequency of diabetes mellitus and unstable angina in its patients. Future studies are required to determine the benefit of repair versus replacement concomitant with CABG in IMR patients. Furthermore, future prospective randomized trials would help us to evaluate the success of mitral valve repair and factors influencing this success.

Hakimeh Sadeghian et al


Acknowledgments

The authors wish to thank Dr Ali Ghaforian, Dr Sirous Jahangiri, Dr Mohammad Majd (Tehran Heart Center) and Mrs. Neda Soltanian for their assistance. This study was approved and supported by Tehran Heart Center, Tehran University of Medical Sciences.

References

1. Perrier P, DeLoache A, Chauvaud S. Comparative evaluation of mitral valve repair and replacement with Starr, Bjork, and porcine valve prostheses. Circulation 1984;70:187.2. Gillinov AM, Faber C, Houghtaling PL, Blackstone EH, Lam BK, Diaz R, Lytle BW, Sabik JF 3rd, Cosgrove DM 3rd. Repair versus replacement for degenerative mitral valve disease with coexisting ischemic heart disease. J Thorac Cardiovasc Surg 2003;125:1350-1362.3. Gorman RC, Gorman III JH, Edmuns H. Ischemic mitral regurgitation. In: Cohn LH, Edmunds LH, eds. Cardiac Surgery in the Adult. 2nd ed. New York: McGraw-Hill; 2003. p. 751-769. 4. Gillinov AM, Cosgrove DM. Mitral valve repair. In: Cohn LH, Edmunds LH, eds. Cardiac Surgery in the Adult. 2nd ed. New York: McGraw-Hill; 2003. p. 933-949. 5. Gillinov AM, Wierup PN, Blackstone EH, Bishay ES, Cosgrove DM, white J, Lytle BW, McCarthy PM. Is repair preferable to replacement for ischemic mitral regurgitation? J Thorac Cardiovasc Surg 2001; 122:1125-1141.6. Nashef SAM, Roques F, Michel P, Gauducheau E, Lemeshow S, Salamon R. European system for cardiac operative risk evaluation (EuroSCORE). Eur J Cardiothorac Surg 1999;16:9-13.7. Tavakoli R, Weber A, Brunner-La Rocca H, Bettex D, Vogt P, Pretre R, Jenni R, Turina M. Results of surgery for irreversible moderate to severe mitral valve regurgitation secondary to myocardial infarction. Eur J Cardiothorac Surg 2002;21:818-824.8. Dion R, Benetis R, Elias B, Guennaoui T, Raphael D, Van Dyck M, Noirhomme Ph, Van Overschelde JL. Mitrale valve procedure in ischemic regurgitation. J Heart Valve Dis 1995;4:S124-131.9. Cohn LH, Rizzo RJ, Adams DH, Couper GS, Sullivan TE, Collins JJ, Aranki SF. The effect of pathophysiology on the surgical treatment of ischemic mitral regurgitation: operative and late risks of repair versus replacement. Eur J Cardiothorac Surg 1995;9:568-574.10. Hendren WG, Nemec JJ, Lytle BW, Loop FD, Taylor PC, Stewart RW, Cosgrove III DM. Mitral valve repair for ischemic mitral insufficiency. Ann Thorac Surg 1991;52:1246-1252.11. Akins CW, Hilgenberg AD, Buckley MJ, Vlahakes GJ, Torchiana DF, Daggett WM, Austen WG. Mitral valve reconstruction versus replacement for degenerative or ischemic mitral regurgitation. Ann Thorac Surg 1994;58:668-675.12. Enriquez-Sarano M, Schaff HV, Orszulak TA, Tajik AJ, Bailey KR, Frye RL. Valve repair improves the outcome of surgery for mitral regurgitation. A multivariate analysis. Circulation 1995;91:1022-1028.13. Sand ME, Naftel DC, Blackstone EH, Kirklin JW, Karp RB. A comparison of repair and replacement for mitral valve incompetence. J Thorac Cardiovasc Surg 1987;94:208-219.14. Cohn LH, Couper GS, Kinchla NM, Collins JJ Jr. Decreased

operative risk of surgical treatment of mitral regurgitation with or without coronary artery disease. J Am Coll Cardiol 1990;16:1575-1578.15. Hausmann H, Siniawski H, Hotz H, Hofmeister J, Chavez T, Schmidt G, Hetzer R. Mitral reconstruction and mitral valve replacement for ischemic mitral insufficiency. J Card Surg 1997;12:8-14.16. Grossi EA, Goldberg JD, LaPietra A, Xiang Y, Zakow P, Sussman M, Delianides J, Culliford AT, Eposito RA, Ribakove GH, Galloway AC, Colvin SB. Ischemic mitral valve reconstruction and replacement: Comparison of long-term survival and complications. J Thorac Cardiovasc Surg 2001;122:1107-1124.17. Mohty D, Orszulak TA, Schaff HV, Avierinos JF, Tajik JA, Enriquez-Sarano M. Very long-term survival and durability of mitral valve repair for mitral valve prolapse. Circulation 2001;104:I1-17.



94


Original Article

Intracardiac Shunts and Role of Tissue Doppler Imaging in

Diagnosis and Discrimination

Mohammad Asadpour Piranfar, MD1, Mersedeh Karvandi, MD1*, Arash Mohammadi Tofigh, MD2

1Taleghani Hospital, Shahid Beheshti University of Medical Sciences, Tehran, Iran.2Imam Hussein Hospital, Shahid Beheshti University of Medical Sciences, Tehran, Iran.

Received 20 October 2007; Accepted 25 January 2008

Abstract

Background: Obesity is a common risk factor for morbidity and mortality after cardiac surgery. However, the relationship

between obesity and postoperative risk has not been fully defined.

Methods: A prospective study of 1015 consecutive patients undergoing isolated coronary artery bypass grafting (CABG)

was carried out. Body mass index (BMI) was used as the measure of obesity and was categorized as normal weight (BMI=20-

25) and obese (BMI>25 and<35). The preoperative, operative, and postoperative risk factors as well as the complication and

in-hospital death rates were compared between the two groups.

Results: Of the 1015 patients, 40% had a normal weight and 49% were obese. Compared with the normal-weight group, the

obese group had a significantly higher incidence of diabetes mellitus (P=0.007) and lower arterial partial pressure of oxygen

(PaO2) (P=0.03). The normal-weight patients had a higher New York Heart Association (NYHA) Functional Class (P=0.03)

and were at a higher risk for emergent surgery (P=0.003) or reoperation (P=0.002). Among the postoperative complications,

respiratory complications (P=0.027) were more frequent in the obese patients. The duration of mechanical ventilation

(P=0.001), the incidence of arrhythmia (P=0.011), low cardiac output syndrome (P=0.001), reintubation (P=0.001), and

neurological complications (P=0.003) were significantly higher in the normal-weight patients. Obesity was associated with

a lower risk of reoperation for bleeding (P=0.032). There were no significant differences in infective complications, length of

intensive care unit (ICU) stay, total length of stay in hospital, and operative mortality between the groups.

Conclusion: In the patients undergoing isolated CABG procedures, obesity did not increase the risk of

operative mortality and morbidity with the exception of respiratory complications. The normal body weight

patients were at a higher risk for complications than were the obese patients. Therefore, obese patients may safely

undergo CABG without previous weight reduction if due attention is paid to minimize respiratory complications.


Keywords: Echocardiography, Doppler • Diagnostic imaging • Congenital heart defect

*Corresponding Author: Mersedeh Karvandi, Cardiologist, Shahid Beheshti University of Medical Sciences, Taleghani Hospital, Velenjak Street, Evin

Street, Tehran, Iran. 1617763141. Tel: +98 21 22932846. Fax: +98 21 22403561. E-mail: [email protected].

Introduction

The right ventricle (RV) is a structurally and functionally complex chamber. This chamber propels systemic venous

blood returning from the right atrium through the pulmonary vascular bed and maintains hemodynamic stability.1-3 An


96

Mohammad Asadpour Piranfar et al

assessment of RV function is highly important in patients with congenital heart disease. The loss of RV contractile function and pulmonary dysfunction is the main cause of exercise intolerance in patients with congestive heart failure. RV dysfunction may also cause serious problems in maintaining an adequate cardiac output after surgical correction of congenital heart disease. Tissue Doppler imaging (TDI) has provided a new insight into RV function assessment.4-7 The purpose of this investigation was to evaluate RV systolic and diastolic functions via TDI for the discrimination of RV pressure overload from RV volume overload.

Methods

Twenty patients (12 female, average age 45±17 years) with echocardiographic signs of pulmonary hypertension (pulmonary artery systolic pressure [PASP]>70mmHg, pulmonary vascular resistance [PVR]>4 WOOD), and right-to-left or bidirectional shunt (8 patients with primum type atrial septal defect [ASD], 5 patients with patent ductus arteriosus [PDA], 3 patients with common atrio-ventricular [AV] canal, and 4 patients with inlet ventricular septal effect [VSD]) were enrolled as group I. Another 20 patients (10 female, average age 32±15 years) without echocardiographic signs of significant pulmonary hypertension (PVR<2 WOOD, 30<PASP<50 mmHg) and left-to-right shunt (7 patients with secundum type ASD, 5 patients with sinus venous type ASD, 5 patients with perimembranous VSD, and 3 patients with small PDA) were enrolled as group II. The third group consisted of 20 healthy subjects (10 female, mean age 35±16) enrolled as controls (PASP<30). The shunt direction was evaluated by the presence of pulmonary hypertension and contrast echocardiography. Exclusion criteria were hemodynamically significant left-sided valvular heart disease, left ventricle systolic dysfunction, and any rhythm other than sinus rhythm. All the patients underwent standard echocardiography and TDI. RV ejection fractions (RV EF) were estimated using Simpson’s or modified Simpson’s methods.6

We used a commercially reliable ultrasound system (GE Vivid Seven) equipped with a multi frequency phased array transducer and pulsed Doppler tissue imaging technique for transthoracic echocardiography (TTE). All the patients were in stable hemodynamic condition, and tracings were recorded during end expiration. The tricuspid annulus systolic and diastolic velocities and the time interval were acquired in apical 4-chamber views at the junction of the right ventricle free wall and the anterior leaflet of the tricuspid valve via TDI. The acoustic power, filter, and gain were adjusted for detecting myocardial velocities. All the recordings were made at a sweep speed of 50 and 100 mm/s with a simultaneous

superimposed ECG.8,9 The peak systolic (Sa) and 2 diastolic waves: early (Ea) and atrial contraction (Aa), the time between the end of Sa and the beginning of Ea (isovolumic relaxation time [IVRT]), the time between the end of Aa and the beginning of Sa (isovolumic contraction time [IVCT]), and ejection time (duration of Sa) were obtained by placing a sample volume with a fixed length of 0.5 cm at the junction of the RV free wall and the anterior leaflet of the tricuspid valve in the 2-D four chamber view via DTI (Figure 1).10,11

Figure 1. Illustration of pulsed tissue Doppler imaging of tricuspid valve S wave, peak systolic velocity at the anterior leaflet of tricuspid valve; E wave, peak early diastolic velocity at the anterior leaflet of tricuspid valve; A ware, a positive wave toward the left atrium at late diastole; IVRT, the time between the end of S wave and the beginning of E wave; IVCT, the time between the end of A wave and the beginning of S wave

The myocardial performance index (MPI) was calculated as (a-b/b), where a is the interval from the onset of IVCT to the end of IVRT and b is the ventricular ejection time (Figure 2).12

Figure 2. Myocardial performance index was calculated as (a-b/b) E wave, peak early diastolic velocity at the anterior leaflet of tricuspid valve; IVCT, Isovolumic contraction time; IVRT, Isovolumic relaxation time; S wave, peak systolic velocity at the anterior leaflet of tricuspid valve

A commercially available statistical program (SPSS


Intracardiac Shunts and Role of Tissue Doppler …

10.1 and 11.1) was used. Pearson’s correlation and linear regression were plotted to show certain relationships.

A P-value less than 0.05 was considered significant. For the assessment of inter-observer variability, the mean value of the first observer was compared with that of the second observer, who was unaware of the first observer’s result. The mean difference between their measurements was calculated, and the percentage of the variability was derived as the absolute difference between the measurements divided by the mean of the two observations. Intra-observer variability was also calculated using this method. Receiver-operator characteristic curves were analyzed to select the optimal cut-off values. The study protocol was approved by the Institutional Review Board of Shahid Beheshti University of Medical Sciences, Tehran, Iran.

Results

PASP was calculated according to the values obtained from the echocardiographic studies of the right heart (tricuspid regurgitation peak gradient [TRPG] + right atrium pressure [RAP]) except in the patients that were catheterized. In these patients, PASP was directly measured. RAP was estimated by the diameter of the inferior vena cava and respiratory response. For the evaluation of pulmonary vascular resistance, the following formula was employed:

[TR peak velocity/RVOT (VTI)]×10, where TR is tricuspid regurgitation, RVOT is right ventricular outflow tract, and VTI is time-velocity integral. The different diagnoses of the patients in group I (bidirectional or right-to-left shunt) and group II (left-to-right intracardiac shunt) are listed in Table 1.

The basic characteristics and standard echocardiographic parameters of the groups are listed in Table 2. In groups I and II, left ventricle ejection fractions were within normal limits. The patients with pulmonary hypertension (group I)

had a high incidence of lower RV ejection fraction and lower RV stroke volume. On the other hand, RV stroke volume and RV ejection fraction in the patients with left-to-right shunt (group II) were much higher than those in the other groups.

The analysis of the tissue Doppler parameters showed that Sa and Aa velocities in group II (left-to-right shunt) were greater than Sm in group I (bidirectional or right-to-left shunt) and the control group (III) ( P< 0.0001, P=0.018).

IVCT, IVRT, and MPI in group I were greater than those in the other two groups (P <0.0001).

Ea velocity in group I was lower than that in the other two groups (P <0.0120).

Sa/Ea in group II was significantly greater than that in the other two groups (P<0.0001).

MPI/Sa in group I was significantly greater than that in the other two groups (P<0.0001).

Sa/IVRT and Sa/IVCT in group II were significantly greater than those in the other two groups (P<0.0001).

In the patients with left-to-right shunt (group II), the RV Sa/Ea value was>1.25 with a sensitivity of 80% and specificity of 75%.

In the patients with right-to-left or bidirectional shunt (group I), the MPI/Sa value was >0.045 with a sensitivity of 85% and specificity of 83%.

In the patients with left-to-right shunt, Sa/IVRT was> 0.23 with a sensitivity of 80% and specificity of 80%.

In the patients with left-to-right shunt (group II), Sa/IVCT was >0.24 with a sensitivity of 83% and specificity of 84%.

The RV Sa/Ea value >1.25, Sa/IVRT value >0.23, and Sa/IVCT value >0.24 were useful to identify left-to-right shunt (RV volume overload) from right-to-left or bidirectional shunt (RV pressure overload); and the MPI/Sa value >0.045 was useful to identify right-to-left shunt or bidirectional shunt (RV pressure overload) from left-to-right shunt (RV volume overload).

Table 1. Diagnosis of patients with left to right shunt and bidirectional or (right to left) shunt

Groups Diagnosis

Right to left or bidirectional shunt Inlet VSD4

Common AV Canal3

PDA5

Primum ASD8

Left to right shuntPerimembranous VSD

5Sinus venous ASD

5Secondum ASD

7Small PDA

3

VSD, Ventricular septal defect; AV, Atrio-ventricular; PDA, Patent ductus arteriosus; ASD, Atrial septal defect


98

Table 2. Basic characteristics and echocardiographic parameters of the three groups

P valueGroup III

(control group)N=20

Group II(left to right shunt)

N=20

Group I(Right to left or bidirectional shunt)

N=20Variable

0.050035+1632+1545+17Age (y)

-10/1010/108/12Men/women

< 0.000160+555+553+3LV EF (%)

0.001044+1247+1735+17RV EF (%)

0.000121+840+1082+11PASP (mmHg)

< 0.0050<1.7<2>4PVR (wood)

< 0.000113+215.5+311+3 RV Sa (cm/s)

0.012012+311.5+3 10.5+3RV Ea (cm/s)

0.018011+4 14+411+4/5 RV Aa (cm/s)

< 0.000163+955+1668+20RV IVCT (ms)

< 0.000160+1356+1683+25RV IVRT (ms)

< 0.00010.4+0.050.44+0.160.57+0/2RV MPI

< 0.00011.081.341.04RV Sa/Ea

< 0.00010.030.0380.054RV MPI/Sa (cm/s)

< 0.00010.200.280.16RV Sa/IVCT(cm/s²)

< 0.00010.200.270.13RV Sa/IVRT (cm/s²)

< 0.0050~1>1.4**<1Qp/Qs

*Data are presented as mean±SD**In PDA cases Qs/Qp >1.4LV, Left ventricle; EF, Ejection fraction; RV, Right ventricle; PASP, Pulmonary arterial systolic pressure; PVR, Pulmonary vascular resistance; Sa, Peak systolic; Ea, Early contraction; Aa, Atrial contraction IVCT, Isovolumic contraction time; IVRT, Isovolumic relaxation time; MPI, Myocardial performance index; Qp/Qs, pulmonary to systemic flow

on RV MPI. The prolongation of IVRT and IVCT, obtained by tissue Doppler from the lateral annulus of the tricuspid valve, was correlated with pulmonary hypertension. It seems that RV MPI/Sa>0.045 can be used to identify RV pressure overload with an acceptable sensitivity and specificity.

There were, however, some limitations in our study. There was a significant age difference between those in group 1 and the ones in the other two groups. We believe that this is because of the late appearance of right-to-left shunt and the longer time it requires to manifest itself. In group 2, we had three cases of small PDA. In these cases, we studied ratio of systemic flow to pulmonary (Qs/Qp) instead of Qp/Qs, which was more than 1.4/1 at all times. On the other hand, only in these cases we had an LV volume overload and not RV volume overload, although the shunt direction was still left-to-right. One more limiting factor in the present study was our low sample volume.

Conclusion

We conclude that an evaluation of MPI-Sa, Sa/Ea wave, MPI/Sa wave, Sa/IVCT, and Sa/IVRT values via TDI can be useful in the discrimination between RV pressure overload and RV volume overload.

Mohammad Asadpour Piranfar et al

Discussion

Diastolic RV dysfunction (lower tricuspid valve peak E velocity in TV inflow, lower E/A velocity, and prolonged RV IVRT and IVCT) and systolic RV dysfunction (lower TV peak S wave) have been demonstrated in patients with pulmonary hypertension and in those with symptomatic congestive heart failure, even in the absence of pulmonary hypertension, suggestive of a potential role for ventricular interdependence in impaired RV filling.13 It must be noted that significant pulmonary hypertension leads to increased IVRT, IVCT, and MPI and a decreased S wave velocity. The present study was designed to assess the potential of TDI for the provision of new information to enable a differentiation between right-to-left shunt (RV pressure overload) and left-to-right shunt (RV volume overload).

According to the Frank- Starling law, a larger heart volume increases the initial length of the muscle fibers, which increases cardiac contractility and stroke volume. This can explain why RV Sa was much larger in the RV volume overload group than that in the other groups.

MPI was defined as the sum of IVRT and IVCT divided by ejection time [(IVRT+IVCT)/ ET].

However, pure RV volume overload had no significant effect


Acknowledgments

We wish to thank all the echocardiography ward staff of Taleghani Hospital and Lavasani Heart Center for their assistance and support. This study was supported by Shahid Beheshti University of Medical Sciences.

References

1. Burgess MI, Mogulkoc N, Bright-Thomas RJ, Bishop P, Egan JJ, Ray SG. Comparison of echocardiographic markers of right ventricular function in determining prognosis in chronic pulmonary disease. J Am Soc Echocardiogr 2002;15:633-639. 2. D’Alonzo GE, Barst RJ, Ayres SM. Survival in patients with primary pulmonary hypertension. Results from a national prospective registry. Ann Intern Med 1991;115:343-349. 3. Yetman AT, Freedom RM, McCrindle BW. Outcome in cyanotic neonates with Ebstein’s anomaly. Am J Cardiol 1998;81:749-754. 4. Meluzin j, Spinarova L, Hude P, Krejci J, Kincl V, Panovsky R, Dusek L. Prognostic importance of various echocardiographic right ventricular functional parameters in patients with symptomatic heart failure. J Am Soc Echocardiogr 2005;18:435-444. 5. Dokainish H, Abbey H, Gin K, Ramanathan K, Lee PK, Jue J. Usefulness of tissue Doppler imaging in the diagnosis and prognosis of acute right ventricular infarction with inferior wall acute left ventricular infarction. Am J Cardiol 2005;95:1039-1042. 6. Miller D, Farah MG, Liner A, Fox K, Schluchter M, Hoit BD. The relation between quantitative right ventricular ejection fraction and indices of tricuspid annular motion and myocardial performance. J Am Soc Echocardiogr 2004;17:443-447. 7. Moustapha A, Lim M, Saikia S, Kaushik V, Kang SH, Barasch E. Interrogation of the tricuspid annulus by Doppler tissue imaging in patients with chronic pulmonary hypertension: implications for the assessment of right-ventricular systolic and diastolic function. Cardiology 2001;95:101-104.8. Sutherland GR, Hatle L. Pulsed Doppler myocardial imaging. A new approach to re¬gional longitudinal function? Eur J Echocar¬diogr 2000;1:81-83.9. Garcia- Fernandez MA, Azevedo J, Moren M, Bermejo J, Perez-Castellano N, Puerta P, Desco M, Antoranz C, Serrano JA, García E, Delcán JL. Regional diastolic function in ischemic heart disease using Pulsed wave Doppler tis¬sue imaging. Eur Heart J 1999;20:496-505.10. Meluzin J, Spinarova L, Bakala J, To-man J, Krejci J, Hude P, Kara T, Soucek M. Pulsed Doppler tissue imaging of the velocity of tricuspid an¬nular systolic motion. Eur Heart J 2001;22:340-348.11. Alam M, Wardell J, Andersson E, Samad B, Nordlander R. Characteristics of mitral and tricuspid annular velocities determined by Pulsed wave Doppler tissue imaging in healthy subjects. J Am soc Echocardiogr 1999;12:618-628.12. Yilmaz R, Celik S, Baykan M, Orern C, Kasap H, Durmus I, Erdol C. Pulsed wave tissue Doppler-derived myocardial performance index for the assessment of left ventricular thrombus formation risk after acute myocardial infarction. Am heart J 2004;48:1102-1108. 13. Yuc C, Sanderson J, Chan S. Right Ven-tricular diastolic dysfunction in heart failure. Circulation 1996;93:1509-1514.


100


*Corresponding Author: Mahdi Najafi, Assistant Professor, Tehran Heart Center, North Kargar Street, Tehran, Iran 14111713138. Tel: +98 21 88029256.

Fax: +98 21 88029256. E-mail: [email protected].

Original Article

Quality of Life in Coronary Artery Disease: SF-36 Compared

to WHOQOL-BREF

Mahdi Najafi, MD*, Mehrdad Sheikhvatan, MD, Ali Montazeri, MD, Seyed Hesameddin Abbasi, MD, Mahmood Sheikhfatollahi, MSc

Tehran Heart Center, Medical Sciences/University of Tehran, Tehran, Iran.

Received 15 October 2007; Accepted 10 December 2007

Abstract

Background: The Short Form Health Survey (SF-36) and WHO Quality of Life-BREF (WHOQOL-BREF) questionnaires

are two common tools to assess changes in quality of life (QOL) over the course of treatment, especially in patients with coro-

nary artery disease (CAD). However, the value of these two instruments among CAD patients has not been studied and com-

pared. The objective of the present study was; therefore, to compare the SF-36 with the WHOQOL-BREF in these patients.

Methods: Between May and September 2006, patients with a final diagnosis of CAD who were candidates for isolated

coronary artery bypass grafting (CABG) and hospitalized in Tehran Heart Center were randomly divided into two groups of

268 patients (for assessment of QOL with the SF-36) and 275 patients (for assessment of QOL with the WHOQOL-BREF).

The correlations between the WHOQOL-BREF domains and SF-36 subscales, in addition to those between the SF-36 com-

ponents summary scores and WHOQOL-BREF domains, were examined with Pearson’s correlation coefficients.

Results: The correlations between the physical, psychological, and social domains of the WHOQOL-BREF and physical

functioning, mental health, and social functioning of the SF-36 were weak with Pearson’s correlation coefficients of 0.015,

-0.036, and 0.042, respectively (r<0.3). There were also poor correlations between the physical component summary of the

SF-36 and physical domain of the WHOQOL-BREF (r=0.001), and between the mental component summary of the SF-36

and mental domain of the WHOQOL-BREF (r=-0.082).

Conclusion: The correlation between the two questionnaires of the SF-36 and WHOQOL-BREF in the evaluation of QOL

in CAD patients is weak.


Keywords: Quality of life • Coronary artery disease • Iran

Introduction

In clinical practice, quality of life (QOL) assessments will assist clinicians in making judgments about the areas in which a patient is most affected by disease and in making treatment decisions. In most countries, treatments aimed at improving QOL through palliative care, for example, can be

both effective and inexpensive.1

Several instruments are available to assess changes in QOL over the course of treatment, especially in patients with coronary artery disease (CAD). The Short Form Health Survey (SF-36) questionnaire is one of the most widely generic


102

Mahdi Najafi et al

health status instruments used extensively in cardiac patient populations, and some studies have investigated longitudinal changes in QOL with this questionnaire.2-5 It includes a global evaluation of health and covers eight dimensions of health including limitations in physical functioning, usual role activities, social functioning related to health problems, and vitality.6

Another questionnaire widely used to assess generic health status is the WHO Quality of Life-BREF (WHOQOL-BREF) questionnaire. It defines QOL as participants’ perceptions of their position in life in the context of the culture and value systems in which they live and in relation to their goals, expectations, standards, and concerns. The recognition of the multidimensional nature of QOL in the WHOQOL-BREF is based on the four domains of physical health activities, namely daily living, psychological bodily image and appearance, social and personal relationships, and environmental-financial resources.7

The value of the SF-36 has been previously compared with that of other generic questionnaires in patients with CAD. Some studies have concluded that the SF-36 is the most appropriate generic instrument to assess the QOL of cardiac patients.8 In a study by Motamed et al. in Iran, the SF-36 was reported to be an appropriate tool for assessing health perceptions of the Iranian general population with acceptable reliability and validity.9 Additionally, a study by Nedjat et al. demonstrated good-to-excellent reliability and acceptable validity of the WHOQOL-BREF in various groups of subjects in Iran.10

However, the value of these two instruments among CAD patients has not been studied and compared. The objective of the present study was; therefore, to compare the SF-36 with the WHOQOL-BREF in patients with CAD.

Methods

Between May and September 2006, patients with a final diagnosis of CAD who were candidates for isolated coronary artery bypass grafting (CABG) and hospitalized in Tehran Heart Center were randomly divided into two groups of 268 patients (for assessment of QOL with the SF-36) and 275 patients (for assessment of QOL with the WHOQOL-BREF). Before the interview, the research assistants obtained a written informed consent from the participants and, thereafter, administered a computer-assisted structured questionnaire so as to obtain personal and health information. Through these interviews, QOL was measured using eight subscales and also two physical (PCS) and mental (MCS) component summary scores of the SF-36 in the first group and four domains of the WHOQOL-BREF in the second group. Our methodology necessitated transforming the domain scores of both questionnaires to a 0 to 100-point scale, with a higher score on these questionnaires indicating a better QOL. The patients’ medical history and clinical manifestations were collected via interviews (by a trained nurse) and physical examinations (by a physician).

The results were reported as mean±standard deviation

(SD) for the quantitative variables and percentages for the categorical variables. The two groups were compared using the Student’s t-test or Mann-Whitney U test (whenever the data did not appear to be normally distributed) for the continuous variables. We calculated Pearson’s correlation coefficients between the physical, psychological, and social domains of the WHOQOL-BREF and physical functioning, mental health, and social functioning of the SF-36, respectively. We also calculated these correlations between the PCS of the SF-36 and the physical domain of the WHOQOL-BREF, and between the MCS and the psychological domain of the WHOQOL-BREF so as to verify whether all correlations were positive in direction and substantial in magnitude (0.30 or higher), as recommended by Ware.11 The data analyzer was anonymous, and data collection and processing were approved by the institutional review board of our heart center. P values of 0.05 or less were considered statistically significant. All the statistical analyses were performed using SPSS version 13 (SPSS Inc., Chicago, IL, USA)

Results

All the 543 respondents completed the QOL questionnaires. The mean age of the study population in the SF-36 and WHOQOL-BREF groups were 59.7±9.0 and 59.8±9.0 years, respectively, with the majority of the respondents in the two groups being male (Table 1).

Table1. Participants’ characteristics*

CharacteristicsST-36 group

(n=275)WHOQOL-BREF

group(n=268)

Male 73.5 73.3

Age (y) 59.7±9.0 59.8±9.0

Body mass index 27.2±4.4 26.6±4.3

Family history of CAD 44.7 46.0

Current cigarette smoking 36.7 37.5

Alcohol using 11.3 11.6

Opium using 14.2 14.9

Diabetes mellitus 42.2 42.4

Hyperlipidemia 66.2 68.0

Hypertension 48.7 49.1

Cerebrovascular accident 4.0 4.4

Peripheral vascular disease 20.4 20.3

Myocardial infarction 48.7 49.1

Previous PTCA 2.7 2.3

Functional class:

I 33.6 33.5

II 50.7 51.3

III 15.7 15.3

Ejection fraction (%) 49.3±9.7 49.6±9.5

Euroscore 2.5±3.5 2.3±2.2

Number of coronary involvement

One 3.7 3.6

Two 22.4 23.3

Three 73.9 73.1

*Data are presented as percentage or mean±SDCAD, Coronary artery disease; PTCA, Percutaneous transluminal coronary angioplasty


Quality of life in coronary artery disease …

Among the various sub-scales of the SF-36, the role limitation-physical and social functioning sub-scales reached the lowest and highest values, respectively. Similarly, the lowest and highest values in the WHOQOL-BREF were for the physical functioning and social functioning domains, respectively (Table 2).Table 2. The statistical measures of the various dimensions of the SF-36 and WHOQOL-BREF questionnaires

Item Mean Standard Deviation

Minimum Maximum

SF-36

Physicalfunctioning

65.4 24.2 5 100

Role limitation-physical

35.5 39.5 0 100

Bodily pain 72.0 31.4 0 100

General health 69.6 17.1 20 100

Vitality 69.4 22.1 10 100

Social functioning 76.5 25.2 13 100

Role limitation-emotional

62.1 40.2 0 100

Mental health 67.5 20.7 8 100

SF-36 Summary

Physicalcomponent score

62.2 19.9 14 99

Mental component score

69.0 19.6 14 98

WHOQOL-BREF

Physical domain 56.3 10.4 25 81

Psychologicaldomain

58.0 11.4 13 88

Social domain 59.2 16.9 0 94

Environmental domain

56.4 14.1 6 100

The mean physical, mental, and social component scores were different between the SF-36 and the WHOQOL-BREF (P<0.001). Also, the means of the PCS and MCS domains of the SF-36 were higher than those of the physical and psychological components of the WHOQOL-BREF, respectively (P<0.001) (Table 3).

Table 3. The mean of the SF-36 subscales and WHOQOL-BREF domains

Characteristics Score P value

Physical functioning (SF-36) 65.4±24.2<0.001

Physical domain (BREF) 56.3±10.4

Mental health (SF-36) 67.5±20.7<0.001

Psychological domain (BREF) 58.0±11.4

Social functioning (SF-36) 76.5±25.2<0.001

Social domain (BREF) 59.2±16.9

Physical component score (SF-36) 62.2±19.9<0.001

Physical domain (BREF) 56.3±10.4

Mental component score (SF-36) 69.0±19.6<0.001

Psychological domain (BREF) 58.0±11.4*Data are presented as mean±SD

The correlations between the physical, psychological, and social domains of the WHOQOL-BREF and physical functioning, mental health, and social functioning of the SF-36 were weak with Pearson’s correlation coefficients of 0.015, -0.036, and 0.042, respectively (r<0.3). We also found poor correlations between the PCS of the SF-36 and the physical domain of the WHOQOL-BREF (r=0.001), and between the MCS and mental domain of the WHOQOL-BREF (r=-0.082).

Discussion

The designers of the WHOQOL-BREF believe that for epidemiological surveys, this questionnaire can allow detailed QOL data to be gathered on a particular population, facilitating the understanding of diseases and the development of treatment methods. They also believe in developing a QOL assessment that would be applicable cross-culturally.12

Furthermore, the SF-36 was constructed to survey health status in medical outcome studies and designed for use in clinical practice and research, health policy evaluations, and general population surveys.13 Be that as it may, it has hitherto not been clear which of these two questionnaires is appropriate and applicable among patients with CAD.

Moreover, a number of instruments have been designed to examine specifically the impact of angina, myocardial infarction, or heart failure on QOL. Examples include the Seattle Angina Questionnaire,14 the Quality of Life after Myocardial Infarction,15 and Minnesota Living with Heart Failure16 questionnaires.

The agreement between the SF-36 and the WHOQOL-BREF has been examined in some studies and in different fields. Huang et al. in a national survey on 11440 persons indicated that the correlations were weak among the subscales of both instruments and concluded that the SF-36 and WHOQOL-BREF appeared to measure different constructs so that the SF-36 measured health-related QOL, while the WHOQOL-BREF measured global QOL.17

However, in another study by Hsiung on patients with HIV infection, both the WHOQOL-BREF and the SF-36 were reliable and valid health-related QOL instruments in these patients.18 In the present study, we found poor correlations across the subscales of the two questionnaires among CAD patients. It seems that the reliability and validity of these two questionnaires for the evaluation of QOL in patients with variant diseases may be different. The SF-36 has been used in angina, myocardial infarction, heart failure,19 and in patients with recent myocardial infarction. It has also been demonstrated to be a sensitive tool for detecting improvement of QOL after active cardiac intervention.20,21 Transversal studies have shown that the SF-36 is a valid and reliable instrument for detecting differences between groups defined by age, sex, socio-economic status, and clinical condition.22 Also, in a study


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among the Iranian population, the Persian version of the SF-36 performed well and the findings suggested that it was a reliable and valid measure of QOL among the general population.23

Therefore, it can be concluded that SF-36 is an applicable tool for the evaluation of QOL in patients with CAD.

In addition, some studies on patients with heart disease have indicated that the reliability or validity of the WHOQOL-BREF for the evaluation of QOL in CAD patients is low, with a few claiming that even national QOL questionnaires have higher values than does the BREF questionnaire. The Zhao et al. study on patients with congestive heart failure showed that the Chinese QOL instrument had better criterion validity than did the WHOQOL-BREF.24 In a population-based study in Germany, relatively low correlations were found between demographic characteristics (age and sex) and the WHOQOL-BREF domain scores.25 Also some studies have highlighted the low reliability of the BREF questionnaire in different domains. In a study conducted in Iran, Nejat et al. reported that the reliability of this questionnaire in the domain of social functioning was lower than 70%.26 One study in Hong Kong estimated this reliability at 59%.27 In a study by Izutsu in Bangladesh, the reliability of this questionnaire in both physical and social domains was low and equal to 59% and 28%, respectively.28 Also, in the World Health Organization study in 23 countries, the reliability of its social domain in 16 countries was lower than 70%.29

Conclusion

It seems that the WHOQOL-BREF has less application than does the SF-36 or special questionnaires for the evaluation of CAD patients. Nonetheless, more studies are needed for the determination of the reliability and validity of the WHOQOL-BREF compared with other applicable questionnaires among these patients.

Acknowledgments

This research project was supported by Medical Sciences/University of Tehran. We wish to thank all the researchers who took part in this study for their kind assistance, especially Dr. Shahin Akhondzadeh and Dr. Soheil Saadat, for their valuable technical assistance.

References

1. Olweny CLM. Quality of life in developing countries. J Palliat Care 1992;8:25-30.2. Rumsfeld JS, MaWhinney S, McCarthy M Jr, Shroyer AL, VillaNueva CB, O’Brien M, Moritz TE, Henderson WG, Grover FL, Sethi GK, Hammermeister KE. Health-related quality of life as a

predictor of mortality following coronary artery bypass graft surgery. JAMA 1999;281:1298-1303.3. Bosworth HB, Siegler IC, Olsen MK, Brummett BH, Barefoot JC, Williams RB, Clapp-Channing NE, Mark DB. Social support and quality of life in patients with coronary artery disease. Qual Life Res 2000;9:829-839.4. Brown N, Melville M, Gray D, Young T, Munro J, Skene AM, Hampton JR. Quality of life four years after acute myocardial infarction: short form 36 scores compared with a normal population. Heart 1999;81:352-358.5. Jette DU, Downing J. Health status of individuals entering a cardiac rehabilitation program as measured by the medical outcomes study 36-item short-form survey (SF-36). Phys Ther 1994;74:521-527.6. Ware JE Jr, Kosinski M, Bayliss MS, McHorney CA, Rogers WH, Raczeck A. Comparison of methods for the scoring and statistical analysis of SF36 health profile and summary measures. Med Care 1995;33:264-279.7. Harper A, Power M. Development of the World Health Organization WHOQOL-BREF Quality of Life Assessment. Psychol Med 1998; 28:551-558.8. Dempster M, Donnelly M. Measuring the health related quality of life of people with ischemic heart disease. Heart 2000;83:614-644.9. Motamed N, Ayatollahi AR, Zare N, Sadeghi-Hassanabadi A. Validity and reliability of the Persian translation of the SF-36 version 2 questionnaire. East Mediterr Health J 2005;11:349-357. 10. Nedjat S, Montazeri A, Holakouie K, Mohammad K, Majdzadeh R. Psychometric properties of the Iranian interview-administered version of the World Health Organization’s Quality of Life Questionnaire (WHOQOL-BREF): A population-based study. BMC Health Services Research 2008;8:61. 11. John E. Ware Jr. On health status and quality of life assessment and the next generation of outcomes measurement. Interview by Marcia Stevic and Katie Berry. J Healthc Qual 1999;21:12-17. 12. Kuyken W, Orley J, Hudelson P, Sartorius N. Quality of life assessment across cultures. Int J Ment Health 1994;23:5-27.13. Ware JE Jr, Sherbourne CD. The MOS 36-item short-form health survey (SF-36). I. Conceptual framework and item selection. Med Care 1992;30:473-483.14. Spertus JA, Winder JA, Dewhurst TA, Deyo RA, Prodzinski J, McDonell M, Fihn SD. Development and evaluation of the Seattle Angina Questionnaire: a new functional status measure for coronary artery disease. J Am Coll Cardiol 1995;25:333-341.15. Oldridge N, Guyatt G, Jones N, Crowe J, Singer J, Feeny D, McKelvie R, Runions J, Streiner D, Torrance G. Effects of quality of life with comprehensive rehabilitation after acute myocardial infarction. Am J Cardiol 1991; 67:1249-1256.16. Rector TS, Kubo SH, Cohn JN. Patients’ self-assessment of their congestive heart failure: content, reliability, and validity of a new measure, the Minnesota Living with Heart Failure Questionnaire. Heart Failure 1987;3:198-209.17. Huang IC, Wu AW, Frangakis C. Do the SF-36 and WHOQOL-BREF measure the same constructs? Evidence from the Taiwan population. Qual Life Res 2006;15:15-24. 18. Hsiung PC, Fang CT, Chang YY, Chen MY, Wang JD. Comparison of WHOQOL-BREF and SF-36 in patients with HIV infection. Qual Life Res 2005;14:141-150. 19. Brown N, Melville M, Gray D, Young T, Munro J, Skene AM, Hampton JR. Quality of life four years after acute myocardial infarction: short form 36 scores compared with a normal population. Heart 1999;81:352-358.

Mahdi Najafi et al


20. Thompson DR, Yu CM. Quality of life in patients with coronary heart disease. I: assessment tools. Health Qual Life Outcome 2003;1:42.21. Yu CM, Li LSW, Ho HH, Lau CP. Long-term changes in exercise capacity, quality of life, body anthropometry, and lipid profiles after a cardiac rehabilitation program in obese patients with coronary heart disease. Am J Cardiol 2003;91:321-325. 22. Failde I, Ramos I. Validity and reliability of the SF-36 Health Survey Questionnaire in patients with coronary artery disease. J Clin Epidemiol 2000;53:359-365. 23. Montazeri A, Goshtasebi A, Vahdaninia M, Gandek B. The Short Form Health Survey (SF-36): translation and validation study of the Iranian version. Qual Life Res 2005;14:875-882. 24. Zhao L, Liang KF, Liu FB. Psychometric properties of the Chinese quality of life instrument in patients with chronic heart failure. Zhongguo Zhong Xi Yi Jie He Za Zhi 2006;26:784-787.25. Trompenaars FJ, Masthoff ED, Van Heck GL, Hodiamont PP, De Vries J. Content validity, construct validity, and reliability of the WHOQOL-BREF in a population of Dutch adult psychiatric outpatients. Qual Life Res 2005;14:151-160. 26. Nejat S, Montazeri A, Holakouie Naieni K, Mohammad K, Majdzadeh SR. The World Health Organization quality of Life (WHOQOL-BREF) questionnaire: Translation and validation study of the Iranian version. Scientific Journal of School of Public Health and Institute of Public Health Research 2004;4:1-12.27. Leung KF, Wong WW, Tay MS, Chu MM, Ng SS. Development and validation of the interview version of the Hong Kong Chinese WHOQOLBREF. Qual Life Res 2005;14:1413-1419.28. Izutsu T, Tsutsumi A, Islam A, Matsuo Y, Yamada HS, Kurita H, Wakai S. Validity and reliability of the Bangla version of WHOQOL-BREF on an adolescent population in Bangladesh. Qual Life Res 2005;14:1783-1789.29. Skevington SM, Lotfy M, O’Connell KA. The World Health Organization’s WHOQOL-BREF quality of life assessment: psychometric properties and results of the international field trial. A report from the WHOQOL group. Qual Life Res 2004;13:299-301.

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*Corresponding Author: Soheila Dabiran, Assistant Professor of Community Medicine, Tehran University of Medical Sciences, Faculty of Medicine,

Keshavarz Bldv, Tehran, Iran. Tel: +98 21 66439463. Fax: +98 21 66919206. E-mail: [email protected].

Original Article

An Echocardiographic Study of Heart in a Group of Male

Adult Elite Athletes

Soheila Dabiran, MD1*, Parichehr Tutunchi, MD1, Amir Sasan Tutunchi, MSc2, Gholam-hasan Khosravi, MD1, Ahmad Mohebi, MD3, Hamidreza Goodarzynejad, MD4

1Faculty of Medicine, Medical Sciences/University of Tehran, Tehran, Iran.2Hamedan University of Medical Science, Hamedan, Iran.3Shaheed Rajaie Cardiovascular Medical and Research Center, Tehran, Iran.4Tehran Heart Center, Medical Sciences/University of Tehran, Tehran, Iran.

Received 10 September 2007; Accepted 17 December 2007

Abstract

Background: Severe and prolonged physical training is associated with morphological and physiological cardiac chang-

es, often termed as the “athlete’s heart”. Echocardiographic features peculiar to elite Iranian athletes have not been previ-

ously described. The aim was to examine the echocardiographic characteristics of highly trained Iranian athletes involved

in three different sports.

Methods: We studied cardiac morphology and function as assessed by rest echocardiography in 50 elite adult male ath-

letes referring to a university hospital in Tehran between February 2001 and March 2006. Resting ejection fraction, inter-

ventricular septal wall thickness (IVSWT), left ventricular posterior wall thickness (LVPWT), left ventricular internal end

diastolic dimension (LVEdD), left ventricular internal systolic dimension (LVIsD), left ventricular (LV) mass, and relative

wall thickness (RWT) were measured. The control group consisted of 50 age- and weight-matched normal healthy men.

Results: Of the athletes, 38 were engaged in predominantly dynamic (running and soccer) and 12 in predominantly static

(weightlifting) sports. The overall mean LVEdD (51.06±5.49mm) and IVSWT (10.24±1.43mm) were higher in the athletes

than those in the normal subjects. The mean of IVSWT in the 38 endurance-trained athletes was significantly more than that

of the 12 strength-trained athletes (11.1 mm vs. 10.3 mm, P<0.05). LVEdD was also greater in the endurance-trained ath-

letes, but the difference was not statistically significant (51.2 mm vs. 50.6 mm).

Conclusion: Our results of higher LVEdD and IVSWT in Iranian male athletes are in line with previous re-

ports. To generalize the results, we require more studies with larger sample sizes (with female athletes included).


Keywords: Echocardiography • Athletics • Sport • Heart

Introduction

Cardiac enlargement in athletes was initially described at the end of the 16th century by Henschen.1 Regular physical training in athletes leads to cardiac enlargement through a


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Soheila Dabiran et al

combination of left ventricular (LV) cavity enlargement (dilatation) and increased wall thickness (hypertrophy). Athlete’s heart is a condition characterized by changes in cardiac function and morphology associated with intense physical training.2 Physiological changes from training include an increased stroke volume and decreased heart rate,3 whereas morphological changes include increased LV cavity dimension, wall thickness, and LV mass.2,4,5

Standard Doppler echocardiography has been widely used to identify the athlete’s heart and to distinguish it from LV pathologies.6-10 Morganroth et al.11 were the first to postulate that two different morphological forms of athlete’s heart can be distinguished: strength-trained heart and endurance-trained heart. According to their theory, aerobic isotonic sports with a high dynamic component (e.g. running) stimulate LV hypertrophy and cavity dilatation (eccentric), while resistance or isometric training (e.g. weight lifting) stimulates hypertrophy with normal cavity dimensions (concentric). Endurance-trained athletes are presumed to demonstrate eccentric LV hypertrophy, characterized by an unchanged relationship between LV wall thickness and LV radius (i.e. ratio of wall thickness to radius), whereas strength-trained athletes are presumed to demonstrate concentric LV hypertrophy, which is characterized by an increased ratio of wall thickness to radius .

Although the morphology of athlete’s heart and the impact of various sports on cardiac structure have been recently investigated by several authors,5,8,12,13 few data are presently available about the possible impact of racial differences in the response of the heart to certain physical training, as part of the normal physiological adaptation process.

On these grounds, we were prompted to utilize echocardiography to evaluate the LV function at rest in a group of highly trained Iranian athletes.

Methods

Between February 2001 and March 2006, 50 elite adult male athletes (mainly competing at an international level and national title holders) in three different sports, namely running, weightlifting, and soccer, were included in the study. All the athletes, who had a minimum average of 10 hours per week exercise activity, underwent a routine physical examination and electrocardiography as part of their evaluation for selection into the national teams. At the time of the present investigation, the athletes had been engaged in systematic training for at least the previous 2 months in national training camps or had been examined up to one week after the end of national competitions to avoid reconditioning effects. Exclusion criteria were a history of coronary artery disease, arterial hypertension, and valvular disease. The study group consisted of 22 soccer players, 16 runners, and 12 weightlifters. We categorized the athletes as 38 predominantly endurance-trained (sum of runners and soccer players) and 12 predominantly strength-trained

(weightlifters) athletes. The control group consisted of 50 pair-matched for age, and weight normal healthy men, none of whom exercised over 2 hours per week. Informed consent was obtained from the athletes and the control group.

The echocardiographic studies were performed with a Contron Sigma Iris (Contron Medical, Pans France Instrument), equipped with a 2.5 MHz transducer. Standard transthoracic, i.e. two-dimensional guided and M mode examinations were performed, with the participants positioned at 30º left lateral position. Measurements were taken from “frozen” M mode tracings obtained using two-dimensional guiding in the long axis parasternal view, with the ultrasound beam perpendicular to the ventricular walls. Internal LV diameter, interventricular septal wall thickness (IVSWT), and left ventricular posterior wall thickness (LVPWT) were measured at end diastole and end systole as recommended by the American Society of Echocardiography.14 Relative wall thickness was calculated by dividing the sum of the IVSWT and LVPWT by left ventricular internal end diastolic dimension (LVEdD), and ejection fraction was calculated by cross-sectional echocardiography.15 LV mass was measured by both the American Society of Echocardiography (ASE)criteria and the Cornell-Penn convention:

LV mass (Penn formula) =1.04 ([LVEdD+LVPWT+IVSWT]3- [LVEdD]3)-13.6 g

LV mass (ASE method)=0.8 (1.04 ([LVEdD+LVPWT+IVSWT]3- [LVEdD]3))+ 0.6 g

Left atrial (LA) diameter was measured at the end of atrial diastole at the parasternal long axis view by M-mode. A single cardiologist blind to the participant’s training group took three measurements of each parameter, and the average was calculated.

The continuous data are expressed as mean±SD, and the discrete variables are shown as percentages. The statistical analyses were performed using the independent sample t-test, univariate analysis of variance (ANOVA) test with post hoc, and Chi-square test. A P value<0.05 was considered statistically significant.

Results

The characteristics of the athletes and control cases at rest are depicted in Table 1. The athletes and control groups were matched in terms of mean age, sex, and weight.

Table 1. Athletes and control groups characteristics*

VariableAthletes (n=50)

Control(n=50)

P value

Age (y) 27±5.5(20-43) 26.0±3.0(21-37) 0.26

Weight (kg) 72.6±8.4(58-69) 71.0±9.0(55-88) 0.36

LOT (y) 9.8±5.5(2-24) - -

*Data are presented as mean±SD (min-max)LOT, Length of training

Table 2 lists the results of the echocardiographic data regarding the cardiac structure in the predominantly


An Echocariographic Study …

endurance-trained athletes including runners and soccer players in comparison to the strength-trained athletes (weightlifters) and the control group. LVPWT, IVSWT, LVEdD, and atrial dimension were significantly larger in the athletes group.Table 2. Echocardiographic measurements in endurance-trained athletes, strained athletes, and normal matched control subjects*

VariableEndurance-

trained(n=38)

Strength-trained(n=12)

Control subjects(n=50)

P value

LA diameter(mm)

34.5±3.5 32.6±2.6 30.1±0.5 < 0.05

LVEdD (mm) 51.2±5.7 50.6±5.0 47.0±4.3 < 0.01

LVIsD (mm) 33.5±4.6 31.3±2.2 30.7±4.5 NS

LVPWT (mm) 10.0±1.2 9.5±1.3 8.9±0.31 < 0.05

IVSWT (mm) 11.1±1.5 10.3±1.2 9.25±1.22 < 0.05

RWT (mm) 0.42±0.08 0.39±0.06 0.34±0.03 < 0.05

LV mass(g)[Penn formula]

255.4±55.2 230.6±45.7 148.1±6.3 < 0.01

LV mass(g)[ASE method]

204.3±44.2 184.5±36.5 143.1±6.2 < 0.01

Ejection fraction (%)

68.8±6.3 70.1±4.2 67.2±4.8 NS

*Data are presented as mean±SDLA, Left atrium; LVEdD, Left ventricular internal end diastolic dimension; LVISD, Left ventricular internal systolic dimension; LVPWT, Left ventricular posterior wall thickness; IVSWT, Interventricular septal wall thickness; RWT, Relative wall thickness; LV, Left ventricle; ASE, American society of echocardiography

The maximal value of LVEdD in the athletes was 64.5 mm. Nine of the athletes showed LVEdD above 58 mm, of whom 7 (14%) athletes were in the endurance-trained group and the rest (2.4%) were in the strength-trained group. Ejection fractions were similar in the athletes and control group, but there was a significant increase in relative wall thickness (RWT) in the athletes compared to the controls.

There was a significant difference between the 2 groups of athletes and the control subjects with respect to IVSWT (P<0.05); however, the endurance-trained athletes and strength–trained athletes did not show a significant difference regarding LVEdD (P=0738).

There was a significant difference with respect to IVSWT between the control and athletes groups (9.25±1.22mm vs. 10.94±1.43mm, P<0.05) and also between the endurance–trained athletes and strength-trained athletes (11.1±1.5mm vs. 10.3±1.2mm, P<0.05). Septal or posterior wall thickness above 12 mm were seen in 4 (8 %) of the athletes, in all of whom, except one, the septal wall to posterior wall ratio remained lower than 1.3.

In one case, the ratio was 1.41. For this reason, all of the individual’s first-degree relatives were investigated echocardiographically with respect to hypertrophic cardiomyopathy (HCM). No evidence of HCM was found; nevertheless, the athlete was advised to return for further investigation after a period of avoiding severe physical activities (reconditioning). There was no significant

relationship between LVEdD and RWT and age of the athletes or length of training.

Discussion

Physiological hypertrophy is a common feature of the “athlete’s heart”. We found a 7.91% increase in LVEdD and 15% increase in IVSWT in our athletes as compared to the control subjects. The cardiac morphological changes seen in our study in terms of LVEdD and IVSWT are similar to values reported by Maron et al.,16 who found a 10% and 15-20% increase in LVEdD and RWT; respectively, when comparing highly-trained Olympic athletes to control subjects.

The septal-to-LVPWT ratios in prior studies13,16 have almost always been found to be below 1.3, and rarely have markedly increased ratios (1.3-1.5) in some athletes been reported. Fagard17 in a meta-analysis suggested that a wall thickness more than 16 mm was very unusual in a healthy athlete and that most of the cases would be less than 13 mm.

Early echocardiographic studies showed that intense isometric (anaerobic, strength/power) exercise training led to a more concentric LV hypertrophy, which was characterized by an increase in LV mass with an augmented the ratio of wall thickness to the LV diameter,18 whereas extensive isotonic (aerobic, endurance) exercise training begot a more dominant enlargement of LV diameter.5,11,19,20 Recent studies, however, have been unable to prove such a dichotomy of the cardiac structural adaptation patterns in athletes.21-23 Some investigators have demonstrated that even very intense strength training sports will not necessarily lead to cardiac wall thickening18,24-27 or the resultant myocardial structure in strength athletes will not differ from that of endurance athletes.26-28 In our study, the group comprised of runners and soccer players did not have exceptionally thicker LV walls, and nor did the group composed of weightlifters differ from the other group of athletes with respect to the LVEdD parameter. Similar absence of difference in myocardial wall thickness between strength-trained and endurance-trained athletes has also been documented by other echocardiographic studies.27,29

Possible explanation for the discrepancy between the results of different studies might be related to the variations in training regimens (season, specificity) and usually limited statistical power to detect subtle differences.30

In the present study, we found an increased LVEdD as well as a significant increase in wall thickness and RWT in the athletes compared to the control subjects. These findings are consistent with other previous studies,5,15,31 in which the authors demonstrated a combination of LV cavity dilatation and increase in IVSWT in elite athletes. In addition, studies in other countries with different populations in regard to ethnicity or race have shown a raised mean IVSWT and LVEdD in competitive athletes compared to control groups, which is in line with our study.5,15,32,33


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Results of several studies have demonstrated that in dynamic sports, ventricular dilatation is predominantly observed rather than an increase in IVSWT.31-34 Other studies22,31 have demonstrated that in static sports, in contrast, an increase in IVSWT predominates the LV dilation. However, in the present study we found that LV dilatation and IVSWT in endurance-trained athletes were greater than those of strength-trained athletes. Therefore, we concluded that elite sports, associated with more increase in LVEdD, also resulted in a more increase in IVSWT. This finding is in line with several recent studies.4,13,33,34 Be that as it may, the results of various similar studies are controversial. The likely reason for conflicting results regarding the type of sport and pattern of hypertrophy may be related to differences in training methods, duration, and severity of champion sports in various studies. In one study, cardiac morphology changes in the “athlete’s heart” were attributed to determinants such as type of sport, gender, and possible inherited genetic factors.35

In our investigation, only 4 athletes had IVSWT above 12 mm, but in a recent study on African handball players,33 none of them showed IVSWT>12mm.

Conclusion

The present study demonstrated that highly trained Iranian athletes had increased LV mass, LVEdD, and IVSWT, which chimes in with the results of previous studies with different populations. Contrary to common belief, ejection fraction is not supra-normal in athletes. However, because our study population was limited in size and also restricted to the male gender, caution should be exercised in extrapolating our results to the whole population of Iranian athletes.

Acknowledgement

This research project was supported by Medical Sciences/University of Tehran. We are indebted to Farzan Research Institute for technical assistance and statistical analysis. The authors would like to thank the interviewers, who collected the information, and the participants, who devoted their time to the study.

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heart” assessed by echocardiography in 947 elite athletes representing 27 sports. Am J Cardiol 1994;74:802-806.5. Pluim BM, Zwinderman AH, van der Laarse A, van der Wall EE. The athlete’s heart: a Meta- analysis of cardiac structure and function. Circulation 1999;100:336-344. 6. Huston TP, Puffer JC, Rodney WM. The athletic heart syndrome. N Engl J Med 1985;4:24-32. 7. Maron BJ. Outer limits of the athlete’s heart: the effect of gender and relevance to the differential diagnosis with primary cardiac diseases. Cardiol Clin 1997;15:381-396. 8. Pelliccia A, Culasso F, Di Paolo F. Physiologic left ventricular cavity dilatation in elite athletes. Ann Intern Med 1999;130:23-31. 9. Fagard RH, Pluim BM, Zwinderman A. Athlete’s heart response. Circulation 2001;103:28-32.10. Caso P, D’ Andrea A, Galderisi M. Pulsed Doppler tissue imaging in endurance athletes: relation between left ventricular preload and myocardial regional diastolic function. Am J Cardiol 2000;85:1131-1136. 11. Morganroth J, Maro BJ, Henry WL. Comparative left ventricular dimension in trained athletes. Ann Intern Med 1975;82:521-524. 12. Fagard R. Athlet’s heart. Heart 2003;89:1455-1491. 13. Abernethy III WB, Choo JK, Hutter JR AM. Echocardiographic characteristics of professional football players. J Am Coll Cardiol 2003;41:280-284.14. Sahn DJ, De Maria A, Kislo J. Recommendations regarding quantitation in M-mode echocardiography: results of a survey of echocardiographic measurements. Circulation 1978:58:1072-1083. 15. Schiller NB, Shah P, Crowford M. Recommendations for quantization of the left ventride by two-dimensional echocardiography. J Am Echocardiogr 1989;5:358-367. 16. Maron BJ, Pelliccia A, Granara M. Reduction in left ventricular wall thickness after reconditioning in highly trained Olympic athletes. Br Heart J 1993;69:125-128. 17. Fagard RH. Athlete’s heart: a Meta-analysis of the echocardiographic experience. Int J Sport Med 1996;17:140-144. 18. Haykowsky MJ, Dressendorfer R, Taylor D, Mandic S, Humen D. Resistance training and cardiac hypertrophy: unravelling the training effect. Sports Med 2002;32:837-849. 19. Snoeckx LH, Abeling HF, Lambregts JA, Schmitz JJ, Verstappen FT, Reneman RS. Echocardiographic dimensions in athletes in relation to their training programs. Med Sci Sports Exer 1982;14:428-434.20. George KP, Wolfe LA, Burggraf GW. The ‘athletic heart syndrome’. A critical review. Sports Med 1991;11:300-330.21. Naylor LH, George K, O’Driscoll G, Green DJ. The athlete’s heart: a contemporary appraisal of the ‘Morganroth Hypothesis’. Sports Med 2008;38:69-90.22. Barbier J, Ville N, Kervio G, Walther G, Carre F. Sports-specific features of athlete’s heart and relation to echocardiographic parameters. Herz 2006;31:531-543.23. Baggish AL, Wang F, Weiner RB, Elinoff JM, Tournoux F, Boland A, Picard MH, Hutter AM Jr, Wood MJ. Training-specific changes in cardiac structure and function: a prospective and longitudinal assessment of competitive athletes. J Appl Physiol 2008;104:1121-1128. 24. Bertovic DA, Waddell TK, Gatzka CD, Cameron JD, Dart AM, Kingwell BA. Muscular strength training is associated with low arterial compliance and high pulse pressure. Hypertension 1999;33:1385-1391.25. Pelliccia A, Maron BJ, Spataro A, Proschan MA, Spirito P. The upper limit of physiologic cardiac hypertrophy in highly trained elite


athletes. New Engl J Med 1991;324:295-301. 26. Wernstedt P, Sjostedt C, Ekman I, Thuomas KA, Areskog NH, Nylander E. Adaptation of cardiac morphology and function to endurance and strength training. A comparative study using MR imaging and echocardiography in males and females. Scand J Med Sci Sports 2002;12:17-25. 27. Whyte GP, George K, Sharma S, Firoozi S, Stephens N, Senior R, McKenna WJ. The upper limit of physiological cardiac hypertrophy in elite male and female athletes: the British experience. Eur J Appl Physiol 2004;92:592-597.28. Legaz Arrese A, Serrano Ostariz E, Gonzalez Carretero M, Lacambra Blasco I. Echocardiography to measure fitness of elite runners. J Am Soc Echocardiogr 2005;18:419-42629. Iglesias Cubero G, Batalla A, Rodriguez Reguero JJ, Barriales R, Gonzalez V, De La Iglesia JL, Terrados NE. Left ventricular mass index and sports: the influence of different sports activities and arterial blood pressure. Int J Cardiol 2000;75:261-265. 30. Venckunas T, Lionikas A, Marcinkeviciene JE, Raugaliene R, Alekrinskis I, Stasiulis AA. Echocardiographic parameters in athletes of different sports. J Sports Sci Med 2008;7:151-156. 31. D’ Andrea A, Limongelli G, Caso P, Sarubbi B, Della Pietra A, Brancaccio P. Association between left ventricular structure and cardiac performance during effort in two morphologic forms of athlete’s heart. Int Cardiol 2002;86:177-184. 32. Doumbia AS, Diallo TA, Kane A, Diao M, Diop IB, Sarr M. The athlete’s heart: an echocardiographic case-control study on Senegalese athletes. Dakar Med 2003;48:92-94.33. Dzudie A, Menanga A, Hamadou B, kingne AP, Atchou G, kingne S. Ultrasonographic study of left ventricular function at rest in a group of highly trained black African handball players. Eur J Echocardiogr 2007;8:122-127.34. Dickhuth HH, RÖker K, Mayer F, KÖning D, Korsten-Reck U. Endurance training and cardial adaptation (athlete’s heart). Herz 2004;29:373-380.35. Pelliccia A, Dipaolo FM, Maron BJ. The athlete’s heart: remodelling, electrocardiogram and preparticipation screening. Cardiol Rev 2002;10:85-90.

An Echocariographic Study …


112


*Corresponding Author: Alireza Rostami, Surgical Department, second floor, Rajaee Heart Center, adjacent to Mellat Park, Valiasr Ave, Tehran, Iran.

Tel: +98 21 23922589. Fax: +98 21 22042037. Email: [email protected].

Case Report

Device-Induced Perforation of Right Atrium Following

Interventional Closure of Atrial Septal Defect (ASD)

Ramin Baghaei Tehrani, MD, Alireza Rostami, MD*, Hosein Ali Basiri, MD, Hojatollah Mortezaiian, MD

Rajaee Heart Center, Iran University of Medical Sciences, Tehran, Iran.

Received 22 September 2007; Accepted 12 November 2007

Abstract

This is a case presentation of a 26-year-old woman with a moderate-sized atrial septal secundum defect (17mm) who un-

derwent catheterism, during which an Amplatzer Septal Occluder number 26 was inserted successfully. On the second postopera-

tive day, she deteriorated and a clinical examination showed a typical tamponade. After a percutaneous aspiration of the pericar-

dial cavity and transient improvement in vital signs, a pig-tail catheter was inserted percutaneously emergently, and the patient was

transferred to the operating room in a preshock state. During the operation, an active bleeding point in the superoanterior aspect

of the right atrium near the aortic root was detected, which was repaired by direct suture and pericardial patch reinforcement. The

Amplatzer device was removed and the atrial septal defect was repaired with a pericardial patch.

A lethal complication of the interventional closure of atrial septal defect, properly treated by an emergent intervention and

operation, is presented and discussed herein.


Keywords: Atrial septal defect • Device removal • Congenital heart defect

Introduction

Atrial septal defect (ASD) is a prevalent congenital heart disease (3.78 per 10000 live births).1 Surgical treatment is safe and effective, but there are complications related to thoracotomy, bleeding, arrhythmia, post-pericardectomy syndrome, and residual defects.1 Over the years, various devices have been utilized for the closure of ASDs by interventional pediatric cardiologists. The concept of the

ASD closure device was first introduced by Ring et al. in 1976.2 The devices usually used for ASD closure are the CardioSEAL Septal Occluder, Amplatzer Septal Occluder (ASO), and Das-AngelWings Septal Occluder.2 The ASO is a device approved by the FDA for the transcatheter closure of secundum ASDs and fenestrations of the Fontan


114

Ramin Baghaei Tehrani et al.

operation.3,4

The ASO is a self-expandable, double-disc device made from a Nitinol wire mesh. Nitinol is a metal alloy used in many medical appliances. The two discs are linked together by a short connecting waist corresponding to the size of the ASD. Its closing ability is normally increased by filling the discs and the waist with polyester fabric.3

Case report

A 26-year-old woman with symptoms of palpitation and dyspnea on exertion was referred for ASD closure with the ASO. She had normal sinus rhythm on her ECG and a normal chest X-ray. Transthoracic and transesophageal echocardiography revealed a moderate-sized ASD (secundum type) 17mm in size as well as left-to-right shunt, Qp/Qs=1.8, anterosuperior rim: 2mm, posteroinferior rim: 16 mm, anteroinferior rim: 7-8mm, posterosuperior rim: 11mm, superior rim: 10mm, inferior rim: 19mm, and ejection fraction: 50%.

The patient underwent catheterism and received heparin (7500 units intravenous). The patient’s activated clotting time was not checked. An ASO number 26 was inserted successfully for the closure of the defect, and balloon sizing was performed. Transesophageal echocardiography was not available during the procedure. Aspirin and Plavix were prescribed for the patient after the procedure. She was in good physical condition for 2 days, but then a mild pericardial effusion was detected, which was confirmed by echocardiography. The effusion suddenly deteriorated, and the patient’s blood pressure decreased and her pulse rate increased. Echocardiography showed severe pericardial effusion. Before long, she was in shock. The clinical impression being that of cardiac tamponade, percutaneous aspiration of the pericardial cavity was performed, which led to a transient improvement in the patient’s vital signs. Emergently, a pig-tail catheter was inserted percutaneously. On account of the fact that the patient was bleeding continuously and was in a preshock state, she was transferred to the operating room, where via a mid-sternotomy incision her pericardial cavity was exposed and copious amounts of blood were aspirated. An active bleeding point in the superoanterior aspect of the right atrium adjacent to the aortic root was detected (Picture 1).

Picture 1. Proximity and probable erosion of posterior side of aortic root (arrow)

Cannulation of the aorta, superior vena cava and inferior vena cava was carried out after cardiopulmonary bypass had been established. The right atrium was opened, and the ASO was pulled back in its sheath and removed by the interventionist (Picture 2).

Picture 2. Perforation site (arrow)

The ASD was repaired using a pericardial patch, and the right atrial perforation was repaired by direct suture and pericardial patch reinforcement. Cardiopulmonary bypass and, subsequently, the operation were terminated


Device-induced perforation …

uneventfully. After a normal and uneventful postoperative course, the patient was discharged from hospital in good general condition.

Discussion

Reports from different parts of the world indicate that the ASO-associated cardiac perforation is a rare complication which uniquely involves the anterosuperior atrial walls and the adjacent aorta. Despite a great deal of research, the pathophysiology of this complication has hitherto remained poorly understood.4,5 It is worthy of note that the fistulisation of different cardiac chambers has also been reported.6 As reported in the literature, our patient had perforation in the anterosuperior aspect of her right atrium. There are reports of early as well as late perforations by the ASO.7,8 Patients with deficient aortic rims and/or superior rims may be at higher risk of device erosion.9,10,11 In our case, however, it seems that the rim was sufficient and a deficient rim cannot be blamed for the erosion. Oversized ASOs may increase the risk of erosion, and a device to the defect ratio of 1:1 or a device 10-20% larger than invasively measured stretched defect diameter should be chosen and implanted on the basis of the intracardiac echocardiographic data. 9,12,13 Thedefect should not be overstretched during balloon sizing,9

and the reason for cardiac perforation in our case must have been a mismatch between the size of the defect and that of the device; in other words the insertion of a large device in a small ASD. Morphologic variations of the ASD are common. Transthoracic echocardiography supplemented with transesophageal echocardiography is crucial for the determination of the ASD morphologic features, diameter, and rims, which are crucial for proper patient selection. Transesophageal echocardiography allows precise guiding and positioning of the ASO, which is essential for a safe and effective transcatheter ASD closure.11,14 In our patient, the catastrophic perforation must have occurred 2 days after the procedure because during the first 2 post-intervention days there were no abnormal findings other than mild pericardial effusion. This is a point to ponder; indeed the fact that such delayed catastrophic events may occur after such procedures renders a close observation of the patients, even those in whom the immediate results are promising, mandatory.

Conclusion

Cardiac perforation following ASD closure with the ASO is a rare complication. Transesophageal echocardiography during the interventional procedure may reduce the incidence of this complication in as much as it affords a better view of the defect rims, thereby avoiding a mismatch between the size of the device and that of the ASD.

References

1. Bialkowski J, Kusa J, Szkutnik M, Kalarus Z, Banaszak P, Bermudez-Canete R, Fernandez Pineda L, Zembala M. Percutaneous catheter closure of Atrial septal Defect. Short-term and mid-term results. Rev Esp Cardiol 2003;56:383-388.2. Bialkowski J, Karwot B, Szkutnik M, Banaszak P, Kusa J, Skalski J. Closure of atrial septal defects in children surgery versus Amplatzer [reg] device implantation. Tex Heart Inst J 2004;31:220-223.3. Sadeghpour Tabaee A, Rostami AR, Ghafari R, Sadeghpour Tabaee AH. Surgical removal of an embolized amplatzer device from left Ventricle. ICRJ 2007;1:53-57.4. Divekar A, Gaamangwe T, Shaikh N, Raabe M, Ducas J. Cardiac perforation after device closure of atrial septal defects with the Amplatzer septal occluder. J Am Coll Cardiol 2005;45:1213-1218.5. Aggoun Y, Gallet B, Acar P, Pulik M, Czitrom D, Lagier A, Laborde F. Perforation of the aorta after percutaneous closure of an atrial septal defect with an Amplatzer prosthesis, presenting with acute severe hemolysis. Arch Mal Coeur Vaiss 2002;95:479-482.6. Jang GY, Lee JY, Kim SJ, Shim WS, Lee CH. Aorta to right atrial fistula following transcatheter closure of an atrial septal defect. Am J Cardiol 2005;96:1605-1606.7. Berger F, Ewert P, Dähnert I, Stiller B, Nürnberg JH, Vogel M, von der Beek J, Kretschmar O, Lange PE. Interventional occlusion of atrial septum defects larger than 20 mm in diameter. Z Kardiol 2000;89:1119-1125.8. Preventza O, Sampath-Kumar S, Wasnick J, Gold JP. Late cardiac perforation following transcatheter atrial septal defect closure. Ann Thorac Surg 2004;77:1435-1437.9. Amin Z, Hijazi ZM, Bass JL, Cheatham JP, Hellenbrand WE, Kleinman CS. Erosion of Amplatzer septal occluder device after closure of secundum atrial septal defects: review of registry of complications and recommendations to minimize future risk. Catheter Cardiovasc Interv 2004;63:496-502.10. Sauer HH, Ntalakoura K, Haun C, Le TP, Hraska V. Early cardiac perforation after atrial septal defect closure with the Amplatzer septal occluder. Ann Thorac Surg 2006;81:2312-2313.11. Mazic U, Gavora P, Masura J. The role of transesophageal echocardiography in transcatheter closure of secundum atrial septal defects by the Amplatzer septal occluder. Am Heart J 2001;142:482-488.12. Mathewson JW, Bichell D, Rothman A, Ing FF. Absent posteroinferior and anterosuperior atrial septal defect rims: factors affecting nonsurgical closure of large secundum defects using the Amplatzer occluder. J Am Soc Echocardiogr 2004;17:62-69.13. Du ZD, Cao QL, Rhodes J, Heitschmidt M, Hijazi ZM. Choice of device size and results of transcatheter closure of atrial septal defect using the Amplatzer septal occluder. J Interv Cardiol 2002;15:287-292.14. Lin SM, Tsai SK, Wang JK, Han YY, Jean WH, Yeh YC. Supplementing transesophageal echocardiography with transthoracic echocardiography for monitoring transcatheter closure of atrial septal defects with attenuated anterior rim: a case series. Anesth Analg 2003;96:1584-1588.


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Website: http://www.pccs2008.com27-30 May 2008

Jeju, Korea (South)The Second Asia-Pacific Congress of Pediatric Cardiology

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Versailles, France61st Congress of the French Society for Thoracic and

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racic Surgery

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Woluwe, Brussels Belgium13th Congress on Cardio-Thoracic Surgery

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9 August 200828 July 2008Oslo, NorwayCardiology & Infectious Disease

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14 August 200811 August 2008Vail, CO, United

States22nd Annual Echocardiographic Symposium at Vail

14 August 200812 August 2008Venice, Italy17th International Cardiovascular Symposium

15 August 200813 August 2008Philadelphia, United

StatesEchocardiography: The Fundamentals

29 August 200817 August 2008Copenhagen,

DenmarkThe Baltic Summer School 2008: Basic and Clinical Aspects of

Cardiac Arrhythmias

3 September 200830 August 2008Munich, GermanyESC Congress 2008

5 September 20084 September 2008Beverly Hills, United

StatesControversies and Advances in the Treatment of Cardiovascular

Disease: The Eighth in the Series

7 September 20084 September 2008Atlanta, GA, United

StatesIntraoperative Echocardiography in the 21st Century

19 September 20087 September 2008San Diego, CA, United States

19th Annual Coronary Interventions

25 September 200820 September 2008Rochester, United

StatesMayo Cardiovascular Review Course for Cardiology Boards and

Recertification

26 September 200822 September 2008Las Vegas, United

StatesVIVA 2008 (Vascular InterVentional Advances) The National

Education Course for Vascular Intervention and Medicine

27 September 200825 September 2008Poznan, Spain12th International Congress of the Polish Cardiac Society

27 September 200826 September 2008Riga, LatviaNational Congress of the Latvian Society of Cardiology

27 September 200826 September 2008Thessaloniki, Greece6th Advanced Symposium on Congenital Heart Disease in the

Adult

27 September 200826 September 2008Athens, GreeceAICT 2008: Athens Interventional Cardiovascular Therapeutics

1 October 200830 September 2008Tbilisi, Georgia3rd Georgian Congress of Cardiology

7 October 20085 October 2008Bratislave, SlovakiaXIII Annual Congress of the Slovak Society of Cardiology

9 October 20087 October 2008Moscow, RussiaNational Congress of the Society of Cardiology of the Russian

Federation

11 October 20089 October 2008Bilbao, SpainAnnual Meeting of the Spanish Society of Cardiology 2008 (El

Congreso de las Enfermedades Cardiovasculares SEC 2008)

11 October 200810 October 2008Galway, IrelandIrish Cardiac Society Annual Scientific Meeting 2008

25 October 200811 October 2008Istanbul, TurkeyRheumatology & Cardiovascular Medicine



124

Information for Authors

The first three consecutive issues of ‘’The Journal of Tehran University Heart Center’’ were published under the title of ‘’The Journal of Tehran Heart Center’’ with ISSN: 1735-5370. From the fourth issue onward, however, the journal has been entitled ‘’The Journal of Tehran University Heart Center’’ with ISSN: 1735-8620.

Scope of the journal “The Journal of Tehran University Heart Center” aims to publish the highest quality material, both clinical and scientific, on all aspects of Cardiovascular Medicine. It includes articles related to research findings, technical evaluations, and reviews. In addition, it provides a forum for the exchange of information on all aspects of Cardiovascular Medicine, including educational issues. “The journal of Tehran University Heart Center” is an international, English language, peer reviewed journal concerned with Cardiovascular Medicine. It is an official journal of the Tehran University Heart Center and is published quarterly. Papers submitted to this journal which do not adhere to the Instructions for Authors will be returned for appropriate revision to be in line with the Instructions for Authors. They may then be resubmitted. Submission of an article implies that the work described has not been published previously (except in the form of an abstract or as part of a published lecture or academic thesis), that it is not under consideration for publication elsewhere , that its publication is approved by all Authors and tacitly or explicitly by the responsible authorities where the work was carried out, and that, if accepted , it will not be published elsewhere in the same form, in English or in any other language, without the written consent of the publisher.

Article CategoriesThe Journal of Tehran University Heart Center” accepts the following categories of articles:”Guest Editorial Original Article Clinical and pre-clinical papers based on either normal subjects or patients and the result of cardiovascular pre-clinical research will be Considered for publication provided they have an obvious clinical relevance. Brief communication Case reportReview Article “The Journal of Tehran University Heart Center” publishes a limited number of scholarly, comprehensive reviews whose aims are to summarize and critically evaluate research in the field addressed and identify future implications. Reviews should not exceed 5000 words.Letter to editor Letters to the editor must not exceed 500 words and should focus on a specific article published in “The Journal of Tehran University Heart Center” within the preceding 12 weeks. No original data may be included. Authors will receive pre-publication proofs, and the authors of the article cited invited to reply.

Submission of manuscriptsFour double spaced copies on 8 1/2 × 11 in. paper should be sent to: Dr. A. Karimi, Editor in Chief, “The Journal of Tehran University Heart Center”, Tehran Heart Center, North Kargar Street, Tehran, Iran 1411713138 Photocopies or good reproductions of illustrations are acceptable only on the spare copies. Included also should be a set of the electronic files of the manuscript on floppy – disk or CD-ROM. For preparation of electronic files, see the instructions herein below. Also, manuscripts can be submitted electronically via the journal’s website: http://jthc.tums.ac.ir. On-line submission allows the manuscript to be handled in electronic forms throughout the review process.

Review of manuscripts All manuscripts correctly submitted to will first be reviewed by the Editors. Some manuscripts will be returned to authors at this stage if the paper is deemed inappropriate for publication in “The Journal of Tehran University Heart Center”, if the paper does not meet submission requirements, or if the paper is not deemed to have a sufficiently high priority. All papers considered suitable by the Editors to progress futher in the review process will undergo appropriate peer review and all papers provisionally accepted for publication will undergo a detailed statistical review.

Preparation of manuscripts All submitted manuscripts must not exceed 5000 words, including References, Figure Legends and Tables. The number of Tables, Figures and References


should be appropriate to the manuscript content and should not be excessive. Authors should comply with the manuscript formatting and the ethical conventions of the “Uniform Requirements for Manuscripts Submitted to Biomedical Journals” issued by the International Committee of Medical Journal Editors (http://www.icmje.org).

Style and spelling

Authors whose first language is not English are requested to have their manuscripts checked carefully before submission. This will help expedite the review process and avoid confusion. Abbreviations of standard SI units of measurement only should be used.

Declaration of Helsinki

The Authors should state that their study complies with the Declaration of Helsinki that the locally appointed ethics committee has approved the research protocol and that informed consent has been obtained from the subjects (or their guardians).

Clinical trials

Clinical trial reports should also comply with the Consolidated Standards of Reporting Trials (CONSORT) and include a flow diagram presenting the enrollment, intervention allocation, follow-up, and data analysis with number of subjects for each (www.consort-statement.org). Please also refer specifically to the CONSORT Checklist of items to include when reporting a randomized clinical trial.

Section of the manuscript Original articles should be divided into the following sections: (1) Title page, (2) Abstract and Keywords, (3) Introduction, (4) Methods, (5) Results, (6)

Discussion, (7) Conclusion, (8) Acknowledgements, (9) References, (10) Figure legends, (11) Tables, (12) Figures.

General formatPrepare your manuscript text using a word processing package. Submissions of text in the form of PDF files are not permitted. Manuscripts should be double –spaced, including text, tables, legends and references. Number each page. Please avoid footnotes; use instead, and as sparingly as possible, parenthesis within brackets. Enter text in the style and order of the Journal. Type references in the correct order and style of the journal. Type unjustified, without hy-phenation, except for compound words. Type headings in the style of the journal. Use the TAB key once for paragraph indents. Where possible use Times New Roman for the text font and Symbol for the Greek and special characters. Use the word processing formatting features to indicate Bold, Italic, Greek, Maths, Superscript and subscript characters. Clearly identify unusual symbols and Greek letters. Differentiate between the letter o and zero, and the letters I and i and the number 1. Mark the approximate position of each figure and table. Check the final copy of your paper carefully, as any spelling mistakes and errors may be translated into the typeset version.

Title pageThe title page should include the following: (1) the title, (2) the name (s) of authors and their highest degree ( no more than 12 authors are acceptable), (3) the institution (s) where work was performed, (4) institution, and location of all authors, (5) the address, telephone number, fax number and e-mail address of the corresponding author.

AbstractAll abstracts may not contain more than 250 words and should also be submitted as a separate file. The abstract should be formatted with the following heading: (1) Background, (2) Methods, (3) Results, (4) Conclusion. A maximum of six Keywords may be submitted.

FiguresThe review process will not begin until all figures are received. Figures should be limited to the number necessary for clarity and must not duplicate data given in tables or in the text. They must be suitable for high quality reproduction and should be submitted in the desired final printed size so that reduction can be avoided. Figures should be no larger than 125 (height)×180 (width) mm (5×7 inches) and should be submitted in a separate file from that of the manuscript.

Electronic submission of figuresFigures should be saved in TIFF format at a resolution of at least 300 pixels per inch at the final printed size for colour figures and photographs, and 1200 pixels per inch for black and white line drawings. Although some other formats can be translated into TIFF format by the publisher, the conversion may alter the tones, resolution and contrast of the image. Digital colour art should be submitted in CMYK rather than RGB format, as the printing process requires colours to be separated into CMYK and this conversion can alter the intensity and brightness of colours. Therefore authors should be satisfied with the colours in CMYK (both on screen and when printed) before submission. Please also keep in mind that colours can appear differently on different screens and printers. Failure to follow these guides could result in complications and delays. Photographs: Photographs should be of sufficiently high quality with respect to detail, contrast and fineness of grain to withstand the inevitable loss of contrast and detail inherent in the printing process. Please indicate the magnification by a rule on the photograph. Colour figures: There is a special charge for the inclusion of colour figures. Figure legends: These should be on a separate, numbered manuscript sheet grouped under the heading “Legends” on a separate sheet of the manuscript after the References. Define all symbols and abbreviations used in the figure. All abbreviations and should be redefined in the legend.


126

TablesTables should be typed with double spacing, but minimizing redundant space and each should be placed on a separate sheet. Tables should be submitted, wherever possible, in portraits, as opposed to landscape, layout. Each Table should be numbered in sequence using Arabic numerals. Tables should also have a title above and an explanatory footnote below. All abbreviations and should be redefined in the Footnote.

AcknowledgementsAll sources of funding and support, and substantive contributions of individuals, should be noted in the Acknowledgements, positioned before the list of references.

Reference formatNumber references sequentially and use Arabic number in superscript to cite the reference in the text. All references should be compiled at the end of the article in the Vancouver style. Complete information should be given for each reference including the title of the article, abbreviated journal title and page numbers. All authors should be listed. Personal communications; manuscripts in preparation and other unpublished data should not be cited in the reference list but may be mentioned in parentheses in the text. Authors should get permission from the source to cite unpublished data. Titles of journals should be abbreviated in accordance with Index Medicus (see list printed annually in the January issue of Index Medicus). If a journal is not listed in Index Medicus then its name should be written out in full.

Article citation example:

Journal citation example: 1. Schroeder S, Baumbach A, Mahrholdt H. The impact of untreated coronary dissections on the acute and long-term outcome after intravascular ultrasound guided PTCA. Eur Heart J 2000;21:137-145.

Chapter citation example: 2. Nichols WW, O’Rourke MF. Aging, high blood pressure and disease in humans. In: Arnold E, ed. McDonald’s Blood Flow in Arteries: Theoretical, Experimental and Clinical Principles. 3rd ed. London/Melbourne/Auckland: Lea and Febiger; 1990. p. 398-420.

Webpage citation example: 3. Panteghini M. Recommendations on use of biochemical markers in acute coronary syndrome: IFCC proposals. eJIFCC 14. http://www.ifcc.org/ejifcc/vol14no2/1402062003014n.htm (28 May 2004). Where the date in parenthesis refers to the access date.

StatisticsAll manuscripts selected for publication will be reviewed for the appropriateness and accuracy of the statistical methods used and the interpretation of statistical results. All papers submitted should provide in their Methods section a subsection detailing the statistical methods , including the specific method used to summarize the data , the methods used to test their hypothesis testing and (if any) the level of significance used for hypothesis testing.

Conflict of interest At submission, the editors require authors to disclose any financial association that might pose a conflict of interest in connection with the submitted article. All sources of funding for the work should be acknowledged in a footnote on the title page and in the Acknowledgements within the manuscript, as should all the institutional affiliations of the authors (including corporate appointments). Other kinds of associations, such as consultancies, stock ownership or other equity interest or patent – licensing arrangements should be disclosed to the editors in the cover letter at the time of the of submission. If no conflict of interest exists, please state this in the cover letter.

ProofsPage proofs will be sent to the corresponding author. Please provide an e-mail address to enable page proofs to be sent as PDF files via e-mail. These should be checked thoroughly for any possible changes or typographic errors. Significant alterations instigated at this stage by the author will be charged to the author. It is the intention of the Editor to review, correct and publish your article as quickly as possible. To achieve this it is important that all of your corrections are returned to us in one all – inclusive mail or fax. Subsequent additional corrections will not be possible, so please ensure that your first communication is complete.


Surname:

First Name:

Hospital or Organization:

Date of subscription:

Full mail address:

P.O.BOX: Tell: Fax:

E-mail:

The annual Subscription and postage rate: 100/000 Rials for Iran and US $ 100 including postage for other countries.

Please liquidate the total amount of subscription and postal charges into:

Bank: Refah Branch Code: 1232 Account: Tehran Heart Center Account Number: 200001.28

and send the original bank slip along with duly completed form of subscription to the following address:

Tehran Heart Center,

North Kargar Street,

Tehran, Iran

1411713138

Tel: +98 21 88029702

FAX: +98 21 88029702

E-mail: [email protected]

New Subscription: Continuation of Subscription:

Subscription Form


Surname:

First Name:

Hospital or Organization:

Date of subscription:

Full mail address:

P.O.BOX: Tell: Fax:

E-mail:

The annual Subscription and postage rate: 100/000 Rials for Iran and US $ 100 including postage for other countries.

Please liquidate the total amount of subscription and postal charges into:

Bank: Refah Branch Code: 1232 Account: Tehran Heart Center Account Number: 200001.28

and send the original bank slip along with duly completed form of subscription to the following address:

Tehran Heart Center,

North Kargar Street,

Tehran, Iran

1411713138

Tel: +98 21 88029702

FAX: +98 21 88029702

E-mail: [email protected]

New Subscription: Continuation of Subscription:

Subscription Form


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