Letters to the Editor

Patients with Mild MitralStenosis vs. Mildly SymptomaticPatients with Severe MitralStenosis: An ImportantDistinction

To the Editor

The recent article by Fawzy et al. [1] reporting ontheir excellent results of percutaneous balloon mitralvalvuloplaty (PBMV) in mildly symptomatic orasymptomatic patients with severe mitral stenosis(MS) is reminiscent of a somewhat similar circum-stance that exists in patients with atrial septal defect(ASD). Young patients with ASD are usually asymp-tomatic despite the existence of a large left-to-rightintracardiac shunt. The current recommendation isearly closure of any sizable ASD as soon as the diag-nosis is established, regardless of symptoms [2]. Thispolicy is universally adopted so as to prevent prob-lems that adults with unoperated ASD face, namely,pulmonary hypertension [2], left ventricular dysfunc-tion [3], serious atrial tachy-arrhythmias [4], andthromboembolism [5,6]. With the introduction of thesuccessful and safe percutaneous approach in recentyears [7,8], there is no longer any reason for not clos-ing any ASD.Therefore, in mildly symptomatic or even asympto-

matic patients with severe MS, its correction should beperformed before the patients become definitely symp-tomatic, in order to prevent the development of atrialfibrillation, irreversible pulmonary hypertension,increasing valvular and/or subvalvular fibrosis and/orcalcification, and mitral insufficiency. With the intro-duction of PBMV, which carries a high success rate ina large patient population [9], low morbidity and mor-tality [9,10], and excellent long-term results [11–13],in comparison with the surgical approach, there is noreason for any delay in recommending such a proce-dure in minimally symptomatic or even asymptomaticpatients with severe MS.One should make a distinction between patients with

mild MS and patients with mild symptoms and severeMS. Although the use of PBMV in patients with mildMS is still controversial [14], its use in mildly sympto-

matic patients with severe MS should no longer be anissue.

Tsung O. Cheng, MDDepartment of Medicine,

The George Washington University Medical Center,Washington, DC

REFERENCES

1. Fawzy ME, Shoukri M, Hassan W, Badr A, Hamadanchi A,

ElDali A, Buraiki JA. Immediate and long-term results of percu-

taneous mitral balloon valvotomy in asymptomatic or minimally

symptomatic patients with severe mitral stenosis. Cathet Cardio-

vasc Intervent 2005;66:297–302.

2. Cheng TO. The International Textbook of Cardiology. New

York: Pergamon; 1987. p 431.

3. Epstein SE, Beiser GD, Goldstein RE, Rosing DR, Redwood

DR, Morrow AG. Hemodynamic abnormalities in response to

mild and intense upright exercise following operative correction

of an atrial septal defect or tetralogy of Fallot. Circulation

1973;47:1065–1075.

4. Cheng TO. Atrial septal defect repair. Cleveland Clin J Med

2001;68:174.

5. Cheng TO. Early thromboembolism following atrial septal

defect repair. J Thorac Cardiovasc Surg 1990;99:758.

6. Cheng TO. Stroke after repair of atrial septal defect. Ann Thorac

Surg 2000;69:981.

7. Cheng TO. Coexistent atrial septal defect and mitral stenosis

(Lutembacher syndrome): an ideal combination for percutaneous

treatment. Cathet Cardiovasc Intervent 1999;48:205–206.

8. Cheng TO. No incision is even better than minimal incision car-

diac surgery for atrial septal defects. J Cardiol 2000;36:141.

9. Chen CR, Cheng TO,for the Multicenter Study Group. Percuta-

neous balloon mitral valvuloplasty using Inoue technique: a mul-

ticenter study of 4832 patients in China. Am Heart J 1995;

129:1197–1204.

10. Cheng TO. Percutaneous balloon mitral valvuloplasty: the why,

the when, the what and the which. Cathet Cardiovasc Diagn

1996;37:353–354.

11. Chen CR, Cheng TO, Chen J-Y, Huang Y-G, Huang T, Zhang

B. Long-term results of percutaneous balloon mitral valvulo-

plasty for mitral stenosis: a follow-up study to 11 years in 202

patients. Cathet Cardiovasc Diagn 1998;43:132–139.

12. Cheng TO. Long-term results of percutaneous balloon mitral

valvuloplasty using the Inoue balloon catheter technique. Circu-

lation 2000;101:e91.

13. Cheng TO, Chen CR. Late results of percutaneous balloon

mitral valvuloplasty: the Chinese experience. Circulation 2000;

102:e18.

14. Cheng TO, Holmes DR, Jr. Percutaneous balloon mitral valvulo-

plasty by the Inoue balloon technique: the procedure of choice

for treatment of mitral stenosis. Am J Cardiol 1998;81:624–628.

DOI 10.1002/ccd.20594

Published online 8 January 2006 in Wiley InterScience (www.

interscience.wiley.com).

' 2006 Wiley-Liss, Inc.

Catheterization and Cardiovascular Interventions 67:326–328 (2006)

Diastolic Coronary ArteryCompression in a CardiacTransplant Recipient: Treatmentwith a Stent

To the Editor

Our case of diastolic coronary artery compression hadevidence of ischemia in the distribution of the index vesselas evidenced by stress myocardial perfusion imagingstudy, in addition to abnormal fractional flow reserve. Thisischemia improved following intra-coronary stenting, asevidenced by a follow-up perfusion scan. The Figure 2pressure tracing [1] was included to depict compression ofthe vessel during diastole, a unique feature of our case.Supra-systemic pressure was recorded by the transducer ofthe PressureWire (Radi Medical, Uppsala, Sweden) whenpositioned at the site of compression. Dr. Angelini raisesan important question about the generation of a supra-sys-temic pressure by the intra-arterial transducer, and con-cludes that these high pressure recordings are artifacts. Wedo not agree with his assessment. Figure 1 in his letter wascreated by finger tapping on the sensor of the PressureWireand demonstrates features suggestive of an artifact, such assharp peaks. We believe that the pressure recordings in ourpatient were representative of ‘‘extrinsic compressiveforces’’ acting on the coronary artery segment and werereal pressure waveforms. The peak of our pressure tracingis not a spike, but instead represents an intravascular wave-form. Also, we were able to obtain these waveformsrepeatedly and reproducibly by moving the position of thetransducer across the area of compression, which wouldnot be likely with an artifact.The transducer incorporated in the PressureWire has a

piezo-electric membrane that is a flat structure inside acylindrical guide-wire. A pressure is generated when a

force is exerted on the membrane. This force, however,is not limited by the arterial pressure head. An analogyto this is inflating a blood pressure cuff to suprasystemiclevels and inhibiting blood flow. The site of blood pres-sure cuff inflation will have a pressure exceeding the sys-temic blood pressure. Another analogy is the ability toachieve suprasystemic diastolic pressures during infla-tion of an IABP.A transducer is fundamentally measuring force and

depicting it as a pressure wave-form. The relationbetween force and pressure is as follows:

Pressure ¼ Force=Area

The area of compression being small, the extrinsiccompressive force generated a pressure significantlyhigher than the aortic pressure in our case, and thesame was recorded repeatedly and reproducibly in ourpatient. We believe that the term ‘‘extrinsic compres-sive force’’ describes this phenomenon appropriately.

Ravi Garg, MDAllen Anderson, MDNeeraj Jolly, MDSection of CardiologyDepartment of MedicineUniversity of ChicagoChicago, IL

REFERENCE

1. Garg R, Anderson A, Jolly N. Diastolic coronary artery compres-

sion in a cardiac transplant recipient: treatment with a stent.

Catheter Cardiovasc Interv 2005;65:271–275.

DOI 10.1002/ccd.20611

Published online 11 January 2006 in Wiley InterScience (www.

interscience.wiley.com).

Myotic Aneurysms After Sirolimus-Eluting Coronary Stenting

To the Editor

We read with great interest the paper by Singh et al.[1] describing a patient who developed a mycoticaneurysm of the left anterior descending coronaryartery after sirolimus-eluting stent (SES) implantation.We have previously reported [2] a strikingly similarcase of a patient suffering a fatal cardiac infectionafter SES. Although this dreadful complication isextremely rare, the description of these two cases fur-

ther emphasizes the potential risk of SES in bluntingthe local responses to bacterial infection. Of interest,in both patients the cause was a Staphylococcus aureusinfection and the clinical presentation persisting feverand progressive malaise without a clear origin (vegeta-tions ruled out by echocardiography). In addition, aftera prolonged regimen of cloxacillin and gentamicin, theinfection appeared to be under clinical control in the

Received 1 September 2005; Revision accepted 13 October 2005

DOI 10.1002/ccd.20587

Published online 8 January 2006 in Wiley InterScience (www.

interscience.wiley.com).

Letters to the Editor 327

two cases. This, however, was a false appreciationwith major clinical consequences. In the report bySingh et al. [1], the patient suffered from an acutemyocardial infarction on the culprit vessel and angiog-raphy revealed multiple massive mycotic aneurysmsarising from the proximal part of the SES, which even-tually required surgical bypass grafting. Alternatively,our patient developed a severe pericardial effusion thatinitially was drained with apparent success. However,2 days later he died suddenly. The cardiac origin of thesepsis was confirmed when S. aureus was cultivated fromthe pericardial fluid. Although we strongly suggested thepossibility of a ruptured coronary aneurysm/abscess, thispossibility could not be confirmed due to the lack ofnecropsy examination [2]. Nevertheless, we believe thatthe case reported by Singh et al. [1] closes the pathophy-siological gap confirming our initial suspicion. Accord-ingly, it is highly likely that a ruptured coronary aneur-ysm caused the death of our patient, whereas thrombosiswithin the mycotic aneurysm (or in the resulting SESmalapposition) led to the myocardial infarction in thepatient described by Singh et al [1].Despite the dramatic capacity of SES to reduce the

rate of restenosis the possibility of rare, SES-related,local problems has been well established. First, therequirement of a prolonged dual antiplatelet regimen––to avoid the risk of SES thrombosis––is widely accepted[3]. Second, local hypersensitivity has been documentedin some patients suffering complications after SES im-plantation [4]. Third, the occurrence of ‘‘acquired’’ latemalapposition in some patients suggest a continuous in-teraction of SES with the vessel wall promoting vesselremodeling [5,6]. This could further increase the risk ofSES thrombosis. Finally, the two cases discussed herefurther suggest the possibility of an enhanced risk of in-fection due to the local immunosuppressive activity of

sirolimus. Owing to the catastrophic consequences ofSES infection, a high index of suspicion is mandatory. Inthis setting, immediate confirmation of diagnosis, eitherby invasive or noninvasive techniques, and an urgentaggressive management is required.

Fernando Alfonso, MDRaul Moreno, MDJorge Vergas, MD

San Carlos University HospitalMadrid, Spain

REFERENCES

1. Singh H, Singh C, Aggarwal N, Dugal JS, Kumar A, Luthra M.

Mycotic aneurysm of the left anterior descending artery after

sirolimus-eluting stent implantation: A case report. Cath Cardio-

vasc Inter 2005;65:282–285.

2. Alfonso F, Moreno R, Vergas J. Fatal infection after rapamycin

eluting coronary stent implantation. Heart 2005;91:e51.

3. McFadden EP, Stabile E, Regar E, Cheneau E, Ong AT, Kinnaird T,

Suddath WO, Weissman NJ, Torguson R, Kent KM, Pichard AD,

Satler LF, Waksman R, Serruys PW. Late thrombosis in drug-

eluting stents after discontinuation of platelet therapy. Lancet 2004;

364:1519–1521.

4. Virmani R, Guagliumi G, Farb A, Musumeci G, Grieco N, Motta

T, Mihalesik L, Tespili M, Valsecchi O, Kolodgie FD. Localized

hypersensitivity and late coronary thrombosis secondary to a siro-

limus-eluting stent: should we be cautious? Circulation 2004;109:

701–705.

5. Degertekin M, Serruys PW, Tanabe K, Lee CH, Sousa JE,

Colombo A, Morice MC, Ligthart JM, de Feyter PJ. Long-term

follow-up of incomplete stent apposition in patients who received

sirolimus-eluting stents for the novo coronary lesions. An intra-

vascular ultrasound analysis. Circulation 2003;108:2747–27450.

6. Stabile E, Escolar E, Weigold G, Weissman NJ, Satler LF,

Pichard AD, Suddath WO, Kent KM, Waksman R. Marked

malapposition and aneurysm formation after sirolimus-eluting

coronary stent implantation. Circulation 2004;110:e47–e48.

328 Letters to the Editor