Roundtable Talk

8/6/2019 Roundtable Talk

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The Editors Roundtable: Acute Decompensated Heart Failure

Vincent E. Friedewald, MDa,*, Mihai Gheorghiade, MDb, Clyde W. Yancy, MDc,James B. Young, MDd, and William C. Roberts, MDe

Acknowledgment

This CME activity is supported by an educational grant

from Scios, Inc., Fremont, California.

Disclosure

Dr. Friedewald has no relevant financial relationships todisclose. Dr. Gheorghiade has received honoraria for speak-ing from Otsuka, Rockville, Maryland; Medtronic, Minne-apolis, Minnesota; and GlaxoSmithKline, Research Trian-gle Park, North Carolina. Dr. Roberts has receivedhonoraria for speaking from AstraZeneca, Wilmington,Delaware; Merck, North Wales, Pennsylvania; Scher-ing Plough, Kenilworth, New Jersey; Pfizer, New York,New York; and Novartis, East Hanover, New Jersey. Dr.

Yancy has received honoraria for speaking fromGlaxoSmithKline, Research Triangle Park, North Caro-lina; Novartis, East Hanover, New Jersey; consulting feesand grant/research support from AstraZeneca, Wilming-ton, Delaware; GlaxoSmithKline, Research TrianglePark, North Carolina; Scios, Fremont, California; Ni-tromed, Lexington, Massachusetts; and Medtronic, Min-neapolis, Minnesota. Dr. Young has received grant/re-search support from Abbott, Abbott Park, Illinois;Amgen, Thousand Oaks, California; AstraZeneca, Wil-mington, Delaware; GlaxoSmithKline, Research TrianglePark, North Carolina; Guidant, St Paul, Minnesota;Medtronic, Minneapolis, Minnesota; Vasogen, Missis-sauga, Ontario, Canada; and has been a Consultant forAbbott, Abbott Park, Illinois; Acorn Cardiovascular, St.Paul, Minnesota; Amgen, Thousand Oaks, California;AstraZeneca, Wilmington, Delaware; Artesian Therapeu-tics, Gaithersburg, Maryland; Boehringer Ingelheim, In-gelheim, Germany; GlaxoSmithKline, Research TrianglePark, North Carolina; Guidant, St. Paul, Minnesota;Medtronic, Minneapolis, Minneapolis; Protemix, San Di-

ego, California; Scios, Freemont, California; Sunshine,Maumee, Ohio; Vasogen, Mississauga, Ontario, Canada;and World Heart, Oakland, California.

Objectives: Upon completion of the activity, the physi-cian should be able to:

1. Categorize patients according to type of ADHF.2. Treat patients according to the type of ADHF and not

treat all patients with ADHF the same.3. Divide the treatment strategies into 3 phases during

hospitalization.4. Properly use decongesting and vasodilating agents in

patients with ADHF.5. Involve the patient as a key member of the manage-

ment team.

Introduction

One million patients are hospitalized each year with acutedecompensated heart failure (ADHF), and 20% of them arerehospitalized for this condition within 30 days of theinitial admission.1 ADHF is the most common reason forhospital admission of patients 65 years of age, and 1/2of ADHF patients 70 years of age are readmitted within90 days. More than 50,000 patients die annually fromADHF, more than any single cancer.2 In the sectionEvaluation and Management of Patients with Acute De-compensated Heart Failure in the Heart Failure Society

of America 2006 Comprehensive Heart Failure PracticeGuideline,3 only 2 of 34 recommendations carried a levelA strength of supporting evidence, highlighting theneed for much more research about ADHF. In this Edi-tors Roundtable, the faculty discusses best managementstrategies for patients with ADHF based on the limitedknowledge base.

Discussion

Dr. Friedewald: What is acute decompensated heart fail-ure (ADHF)?

Dr. Yancy: ADHF applies to 2 groups of cardiac pa-

tients: (1) patients having symptoms of heart failure (HF)for the first time, and (2) patients with exacerbated symp-toms of established HF.

Dr. Gheorghiade: I divide ADHF patients into 3 groups:(1) worsening chronic HF (70% of all cases of acute HF);(2) HF diagnosed for the first time (25%), and (3) advancedor end-stage HFpatients who do not respond to treatment(5%).

Dr. Yancy: Patients with ADHF are a heterogeneousgroup, and include many patients who do not have straight-forward left ventricular systolic dysfunction with its classicsigns and symptoms.

aAssistant Editor, American Journal of Cardiology; Clinical Professor,

Department of Internal Medicine, The University of Texas Medical School

at Houston, Houston, Texas; Visiting Professor, University of Notre Dame,

Notre Dame, Indiana; bProfessor of Medicine, Associate Chief of the

Division of Cardiology, Chief of the Cardiology Clinical Service, andDirector of the Telemetry Unit Northwestern University Feinberg School

of Medicine, Chicago, Illinois; cMedical Director, Baylor Heart & Vascular

Institute, Chief, Cardiothoracic Transplantation, Baylor University Medi-

cal Center, Dallas, Texas; dChairman, Division of Medicine, Professor,

Department of Medicine, Cleveland Clinic Lerner College of Medicine of

Case Western Reserve University, Cleveland, Ohio; eEditor-in-Chief,

American Journal of Cardiology; Director, Baylor Heart and Vascular

Institute; Dean, A. Webb Roberts Center for Continuing Medical Educa-

tion of Baylor Health Care System, Dallas, Texas. Manuscript received

March 13, 2007; accepted March 13, 2007.

*Corresponding author: Tel: 512-264-1611; fax: 512-264-7034.

E-mail address: [email protected] (V. E. Friedewald).

0002-9149/07/$ see front matter 2007 Elsevier Inc. All rights reserved. www.AJConline.orgdoi:10.1016/j.amjcard.2007.03.019


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Dr. Roberts: Are patients with cor pulmonale includedin the definition of ADHF?

Dr. Yancy: Yes, because cor pulmonale is driven by leftventricular dysfunction. Patients with ADHF often haveother co-morbid conditions, including chronic lung disease,renal insufficiency, diabetes mellitus, atrial dysrhythmias,and anemia.

Dr. Georghiade: About 40% of patients with ADHFhave diabetes mellitus; 50% have systemic arterial hyper-tension; and 30% have renal insufficiency.

Dr. Young: My criteria for ADHF include anyone goingto an urgent care center with symptoms due to HF orcomplications of HF, such as an arrhythmia or syncope.

Dr. Roberts: What about sudden weight gain?Dr. Young: I would not call that acute decompensated

HF, just worsening HF. Patients with chronic HF haveweight fluctuations of5 pounds per week, and symptomsfluctuate accordingly. Weight gain itself, however, does notinevitably lead to a need for urgent care.

Dr. Friedewald: My concern about your definition of

ADHF is some other factors often determine whether apatient seeks urgent care, such as lack of health insuranceor convenient transportation.

Dr. Roberts: I agree that a definition should not dependon where patients go after symptoms appear. They can haveacute decompensation and remain at home.

Dr. Young: The natural history of ADHF is that a badevent will eventually happen and, when it does, the patienteither seeks treatment or dies.

Dr. Yancy: Many European experts believe ADHF in-volves only patients with pulmonary edema. In NorthAmerica, however, we allow a number of different ways forADHF to be manifest.

Dr. Gheorghiade: Such heterogeneity, however,makes it difficult to do studies on these patients. We needa clearer definition of ADHF. Pulmonary edema, hyper-tension, and right-sided HF are all clinical presenta-tions. We should not confuse clinical presentation with adefinition of ADHF. ADHF classification is often donein retrospect, because it is very difficult to classify pa-tients when they are first admitted. At the time of admis-sion the clinical picture encompasses several differentprocesseshypertension, right-sided HF, and pulmonaryedema. Other parameters, like the ejection fraction,are needed to classify the patient, and they are notknown when the patient is seen for the first time. It

usually takes 24 hours before the HF patient can beclassified properly. It is important to distinguish betweenclassification, which can be done later, and mode of

presentation.Dr. Roberts: No one has mentioned etiology in the

definition of ADHF.Dr. Gheorghiade: Initially, the etiology is not impor-

tant, because a high left ventricular filling pressureis the main reason a patient with ADHF comes to thehospital. The immediate therapeutic goal is to reducethe filling pressure, regardless of whether the etiologyis acute myocardial infarction or acute aortic regur-gitation.

Dr. Roberts: Mitral stenosis is immediately correctible.Dr. Gheorghiade: Yes, but the initial goal is to reduce

congestion. As soon as the patient is stable, etiologybecomes very important, because it guides to definitivetherapy. Regardless of whether the patient has hyperten-sion or aortic valve stenosis, most deaths are due to ahigh filling pressure, not to a low cardiac output. Theimmediate therapeutic goal in ADHF is to safely improvethe left ventricular filling pressure.

Dr. Young: Heart failure is the umbrella under which areacute, decompensated, ischemic, valvular, right-sided, left-sided, and so on.

Dr. Roberts: The common denominator of ADHF issudden elevation of the left ventricular end-diastolic pres-sure?

Dr. Young: Yes.Dr. Gheorghiade: Elevation of left ventricular end-dia-

stolic pressure, however, does not have to be sudden. It canbe gradual.

Dr. Roberts: Untreated, however, it eventually reaches alevel where the symptoms are intolerable, and the result isADHF.

Dr. Gheorghiade: That is correct.Dr. Friedewald: What are the demographics of ADHF?Dr. Gheorghiade: The mean patient age is 75 years.

Forty to 50% of patients have preserved left ventricularsystolic function; 70% have a history of systemic hyperten-sion, 60% have documented coronary arterial disease; 45%are post-myocardial infarction; 30% have a history of atrialfibrillation; 40% have diabetes mellitus; and 30% havechronic obstructive pulmonary disease. Secondary mitralregurgitation is common. Although ADHF is a complexentity, the patient comes to the emergency department for asingle reason: the left ventricular filling pressure is high,causing breathlessness. Thus, the immediate treatment end

point is to eliminate dyspnea. The other abnormalities canbe treated later. About 50% of patients with ADHF presentto the hospital with reactive hypertension, which is anintermittent form of hypertension. These patients may benormotensive 6 hours later.

Dr. Roberts: You said that 40% of patients with ADHFhave diabetes mellitus, which adults essentially do not getunless they are overweight. Is that not correct?

Dr. Yancy: Yes. Patients with HF and an increased bodymass index do better than persons of normal weight.

Dr. Roberts: That is also true for patients with acutemyocardial infarction.

Dr. Friedewald: Would you expand on reactive hyper-

tension in patients with ADHF?Dr. Gheorghiade: Among 200,000 patients in The

Acute Decompensated Heart Failure National Registry(ADHERE) and other registries, 50% were hypertensiveat the time of their initial presentation. Many of the hyper-tensive patients, however, were normotensive prior to ad-mission; after admission, their pressures were often easy tocontrol and were frequently normal within 6 to 24 hours.The reason for this arterial systolic pressure reactivity isactivation of neurohormones due to the high left ventricularfilling pressure. Thus, this population should not be con-fused with patients who have a history of hypertension,because the 2 are distinctly different pathophysiological

conditions. The blood pressure cannot increase unless thereis adequate left ventricular function, so blood pressure in a

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way indicates cardiac reserve in patients with ADHF. Pa-tients with peak systolic blood pressures of 120 mm Hg atthe time of admission have a poor prognosis because theirventricles are unable to appropriately respond to increasedsympathetic tone.

Dr. Yancy: Few patients with ADHF have low bloodpressure or shock. In The Evaluation Study of Congestive

Heart Failure and Pulmonary Artery Catheterization Effec-tiveness (ESCAPE), the patients with lower blood pressureand cardiac outputs on admission did not respond well totherapy.

Dr. Young: In both The Organized Program to InitiateLifesaving Treatment in Hospitalized Patients with HeartFailure (OPTIMIZE-HF) and the ADHERE registries(50,000 and 100,000 patients, respectively), 50% had pre-served left ventricular systolic function.

Dr. Gheorghiade: Most physicians treating ADHF fo-cus on improving the cardiac output, although cardiac out-put is usually normal or high in these patients, and it is notthe major problem. The treatment goal should be to reduce

the pulmonary arterial wedge pressure, which, of course,corresponds with the left ventricular end-diastolic pressure(the filling pressure).

Dr. Roberts: If we could prevent systemic hypertension,would we also prevent most cases of HF?

Dr. Yancy: In the Systolic Hypertension in the ElderlyProject, among patients with coronary heart disease andsystolic hypertension, concomitant administration of a thi-azide diuretic plus a blocker led to an 80% reduction insubsequent HF. It is likely that treating hypertension to goal(blood pressure at least 140/90 mm Hg) would reduce theincidence of HF by 50%. There are no prospective trials,however, designed to prevent HF.

Dr. Roberts: Perhaps lipid-lowering or antihypertensivetherapy will prove to be the best anti-HF therapy.

Dr. Yancy: Statin therapy also may have a stabilizingeffect in ADHF, possibly because of its anti-inflammatoryeffect.

Dr. Young: The data on the favorable effect of statins isimpressive in HF cohorts, even when not prescribed forelevated lipids. Coupled with antihypertensive therapy, thismay be the direction we need to go to prevent symptomaticleft ventricular diastolic dysfunction.

Dr. Roberts: Do you include statins in the treatment ofpatients with idiopathic dilated cardiomyopathy?

Dr. Yancy: Yes, I do sometimes.

Dr. Gheorghiade: Heart failure may be a consequenceof hypertension, coronary arterial disease, atrial fibrillation,and diabetes mellitus, and all of them, of course, are treat-ment targets in ADHF, in addition to lowering the leftventricular filling pressure.

Dr. Roberts: Patients with increased left ventricularend-diastolic pressures who have normal-sized left ventri-cles and thick left ventricular walls are not the same aspatients with comparable end-diastolic pressures, but whohave dilated left ventricular cavities and relatively thinwalls, are they?

Dr. Gheorghiade: No, because the left ventricular end-diastolic pressure is a function of the left atrium contracting

against a stiff left ventricle.Dr. Yancy: We call a left ventricular ejection fraction

40% heart failure with preserved systolic function. Aleft ventricle with an ejection fraction of 45% lookspretty sick, a ventricle with an ejection fraction of 55%looks better, and a ventricle with an ejection fraction of70% looks great. We should differentiate, however, be-tween patients with symptomatic pulmonary congestionin the presence of a normal-sized left ventricular chamber

versus patients with symptomatic congestion and a di-lated left ventricular cavity.

Dr. Gheorghiade: I agree, but it is unusual for patientsto have preserved left ventricular systolic function and highfilling pressures, unless they have an infiltrative cardiomy-opathy (amyloidosis, for example) or systemic hyperten-sion.

Dr. Roberts: Are you talking about left ventricular wallsthat are much thicker than normal versus those ventricularwalls that are not thickened?

Dr. Gheorghiade: Primary left ventricular diastolic dys-function is a rare cause of HF. Few patients with leftventricular hypertrophic cardiomyopathy develop HF.

Dr. Roberts: You said 40 to 45% of patients with HFhad left ventricular diastolic failure.

Dr. Gheorghiade: Yes, but I said diastolic, not primarydiastolic HF. There is a difference. The ventricular wall maybe thick, but it is not primary thickening. I distinguishbetween primary diastolic dysfunction and secondary dia-stolic dysfunction. Patients with myocardial ischemia andpatients with systemic hypertension both have secondarydiastolic dysfunction. Thus, there are many patients withdiastolic HF, but it is not a primary form of diastolic HF.They have thicker ventricles, but there is not always a goodcorrelation between ventricular thickness and the presenceof diastolic HF.

Dr. Young: This is both a structural and a mechanicalphenomenon, complicated by the reality that patients withleft ventricular systolic dysfunction have varying degrees ofdiastolic dysfunction.

Dr. Roberts: But not the reverse.Dr. Young: That is correct. The one profound driver in

the process is afterload increasewhich, by definition, ishypertension. Because only recently has the importance ofdiastolic HF been recognized, therapies primarily focusingon diastolic HF have not been designed.

Dr. Roberts: What are the most common signs or symp-toms of diastolic HF?

Dr. Gheorghiade: Of patients with ADHF, 70% edema;

70% rales; 40%, a systolic precordial murmur; 40% dyspneaat rest; and 30% have jugular venous distention.

Dr. Yancy: Both the European regulatory body and theFood and Drug Administration state that the sine qua non ofADHF is dyspnea.

Dr. Friedewald: What is the natural history of ADHF?Dr. Yancy: The death rate for the hospitalized patient

with ADHF is low, but in some select, very well-definedgroups, it is as high as 20%. Even with optimal care,however, the 30-day risk of death is 10%. At 1 year from theindexed hospitalization, the risk of death is about 30%. Thedeath rate at 1 year for ambulatory class III HF patients isabout 10%. The risk of rehospitalization is 50%. There is

something about hospitalization that changes the naturalhistory, but we do not know what that is.

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Dr. Roberts: Are you saying that patients should notcome to the hospital?

Dr. Yancy: No, we assume it would even be worsewithout hospitalization.

Dr. Friedewald: Is etiology a factor in prognosis?Dr. Gheorghiade: Yes. Data from OPTIMIZE show that

myocardial ischemia carries a far worse prognosis than

primary cardiomyopathy. The mortality curve in patientswith class IV HF is linear between mortality and time.Patients hospitalized for HF resemble the post-myocardialinfarction curve, with a very high event rate in the first 60days, followed by a relatively flat curve.

Dr. Gheorghiade: Etiology is the key to proper man-agement, but not for assessing prognosis.

Dr. Yancy: The precipitating cause must be addressed ina patient with ADHF. Chronic HF trials have shown nodifference in outcomes with blockers or angiotensin-converting enzyme (ACE) inhibitors or any other evidence-based therapy as a function of the etiology of left ventriculardysfunction. Thus, therapy for HF is stratified according toleft ventricular function, not etiology.

Dr. Roberts: Many of these studies, however, do notinclude patients with severe aortic stenosis, mitral stenosis,coarctation of the aorta, and other such correctable condi-tions. It would be terrible to miss such a diagnosis.

Dr. Yancy: That is correct.Dr. Roberts: It appears that HF specialists are the car-

diac oncologists of heart disease, because you are focusedon longevity. Longevity, however, is not the orientation ofthe average cardiologist.

Dr. Gheorghiade: About 80% of patients with HF arenot seen by a cardiologist. There are studies suggesting thatcardiologists are no better in managing HF than are generalinternists.

Dr. Young: In response to Dr. Roberts assertion that HFspecialists are cardiac oncologists, I am reminded of apatient I saw this morning who was referred for inoperable3-vessel coronary arterial disease. He had well-compen-sated class I HF. He had been told by his physician that hewas going to die and that he might need a heart transplant.How long is he going to live? Although the overall prog-nosis for such patients is not good, there are categories ofHF patients who do well for decades, a fact that is some-times lost in the descriptions of high morbidity and highmortality. Such negative attitudes on the part of physicians

cause many patients with HF to go through a lot of unnec-essary psychological angst.Dr. Gheorghiade: I am reminded of a patient, a physi-

cian, who was diagnosed years ago with end-stage HF.Today, he has a normal-sized heart. I see such patientsnearly every day. Many patients with proper medical ther-apy of their HFI call them chemical, rather than mechan-ical transplantshave sufficient myocardial viability, suchthat their ejection fraction can be normalized over time.

Dr. Yancy: You are correct. HF specialists tend to thinkin 1-year and 5-year mortality constructs, much thesameas Dr. Roberts pointed outas oncologists.

Dr. Gheorghiade: But there is a huge difference. The

oncologist does not have truly life-saving therapy, whereasHF specialists do.

Dr. Roberts: What life-saving therapies are you refer-ring to?

Dr. Gheorghiade: Beta blockers, ACE inhibitors, aldo-sterone-blocking agents, cardiac resynchronization therapy,intracardiac defibrillators, perhaps statins. Although HF is acondition with a bad prognosis, we have remedies. Theproblem is that there is a huge gap between what we can do

and what is being done.Dr. Yancy: This is true with chronic HF, where we have

greatly improved therapies, but treating patients with ADHFis far less successful.

Dr. Gheorghiade: It is essential to identify the precipi-tating cause of ADHF for patients to improve. If the pre-cipitating cause is not delineated and treated, the patient willnot improve. Atrial fibrillation, infection, diabetes mellitus,anemia, all must be treated. Unfortunately, this is not beingdone nearly enough. I have seen patients with a hemoglobinof 5 mg/dl who were treated with diuretics; they will notimprove until the anemia is corrected. The same is true forcontrolling the heart rate in atrial fibrillation. The precipi-

tating cause is key to successful treatment of patients withADHF.

Dr. Friedewald: I am concerned that so few HF patientsare seen by cardiologists. I would argue that every patientwith HF should be evaluated at least once by a cardiologist.

Dr. Gheorghiade: With 1 million annual hospitaliza-tions for HF in the USA that desire is not possible.

Dr. Yancy: Outcomes for patients with HF are deter-mined more by factors, such as renal function, systemicblood pressure, and hemoglobin, than by etiology. Everypatient with heart failure should have a practitioner who hasa HF focus, even if that person is a nurse practitioner.

Dr. Roberts: What is your general workup for a patient

with first-time ADHF?Dr. Gheorghiade: I recommend a full right and left-

sided cardiac catheterization, including coronary angiogra-phy and left ventriculography.

Dr. Yancy: The guidelines recommend cardiac catheter-ization in patients with HF and angina pectoris. No morethan 5% of patients admitted to the hospital with ADHFundergo cardiac catheterization.

Dr. Roberts: What laboratory tests do you do routinelyperform?

Dr. Gheorghiade: Tests are renal function and targetorgan function, electrolytes, Doppler echocardiogram, chestradiograph, and perhaps the brain naturetic peptide (BNP).

Dr. Roberts: Why perhaps the BNP?Dr. Yancy: The role of BNP is unresolved. It is most

useful when there is diagnostic ambiguity, whether dyspnea,for example, is due to pulmonary or cardiac disease. Whenthe likelihood of lung disease is high, the BNP does nothave much diagnostic value. The BNP, however, can pro-vide unique prognostic information. Thus, while the role ofserial BNP measurements is unresolved, BNP does havevalue in cases of diagnostic ambiguity and for determiningprognosis.

Dr. Friedewald: How do you assess the mortality risk ina patient with ADHF?

Dr. Yancy: In ADHERE, 3 measurements indicated a

22% inpatient risk of death: blood urea nitrogen 37 mg/dl,systolic blood pressure 115 mm Hg, and creatinine 2.75



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mg/dl. When the blood urea nitrogen was 37 mg/dl andthe systolic blood pressure was 115 mm Hg, the risk ofinpatient death was only 2%.

Dr. Gheorghiade: The systolic blood pressure at thetime of admission is a major predictor of risk: when it is120 mm Hg, the in-hospital mortality is 7%, the post-discharge mortality is 14%, and the readmission rate is 30%,

compared to an in-hospital mortality of 1% and a post-discharge mortality of 5% when the systolic blood pressureis 115 mm Hg. Systolic blood pressure is an indicator ofleft ventricular systolic function. Thus, when the systolicblood pressure is high, e.g., 190 mm Hg, the ejection frac-tion is probably well preserved. A patient with a systolicblood pressure of 120 mm Hg at admission is likely introuble and too often that patient is treated the same as apatient with a higher systolic blood pressure. The systolicblood pressure is not only a good prognostic indicator, butwhen it is low, it indicates that maximal therapy from theoutset blockers, ACE inhibitors, aldosterone antago-nists, is warranted.

Dr. Roberts: How do you manage the blood pressure ina patient who was previously hypertensive and is admittedwith ADHF with a low systolic blood pressure?

Dr. Gheorghiade: That patient has a terrible prognosis.Trials have taught us that it is extremely important not tolower the blood pressure further. To do so can significantlydecrease the coronary perfusion pressure. It is extremelyimportant in such patients to improve cardiac function with-out decreasing coronary perfusion, because the myocardiumis likely ischemic and there is increased neurohormonalactivity that adds to the myocardial ischemia.

Dr. Roberts: Do you try at all to increase the bloodpressure?

Dr. Yancy: Even though marginal or low blood pressureis a risk of poor outcome, it is a terribly inappropriate targetfor therapy, because the only way to increase the bloodpressure is with vasoconstrictors and inotropes. Given thatblood pressure is a product of cardiac output and peripheralarterial resistance, increasing the cardiac output by reducingresistance using vasodilators and other strategies is a morephysiologic way to normalize and elevate the blood pres-sure. Fluctuations in blood pressure during ADHF mayincrease near-term event rates. Protecting the patient fromhypotension is probably a better therapeutic target thanactually raising the blood pressure.

Dr. Young: It is better for the HF patient to have a lowerblood pressure and a slower heart rate, as long as the patientis walking, talking, and urinating. What is most important isperfusion and organ function.

Dr. Friedewald: Does the initial blood glucose haveprognostic value?

Dr. Gheorghiade: In both OPTIMIZE and in ESCAPE,there was no short-term difference in outcomes betweenpatients with and without diabetes mellitus. These trials,however, only looked at short-term differences.

Dr. Yancy: What about hyponatremia and anemia?Dr. Young: The patients serum sodium level should be

normalized. Whether to treat anemia is highly controversial,

even though patients with anemia have worse short-termand long-term outcomes than those without anemia.

Dr. Roberts: How do you define anemia in these pa-tients?

Dr. Young: A hemoglobin 12 mg/dl.Dr. Roberts: How do you treat hyponatremia?Dr. Young: By a variety of measures, and all focusing

on limiting the amount of free water intake versus saltintake, and, if possible, lowering the doses of diuretics. In

anemic patients. thiazide-based diuretics also should beavoided.

Dr. Gheorghiade: In OPTIMIZE-HF, 25% of the pa-tients had hyponatremia. In ESCAPE, 25% of patientsalso had hyponatremia, both at admission and at dis-charge. Thus, hyponatremia is common, and it is notproperly treated. The most intriguing aspect of ESCAPEwas that, although patients with hyponatremia had thebest clinical and hemodynamic response to therapy, com-pared to patients with normal serum sodium levels, theirpost-discharge mortality was 3 times higher. Hyponatre-mia is an independent and major predictor of prognosis.Hyponatremia also indicates the presence of a unique

form of HF.Dr. Yancy: Hyponatremia also correlates with the extent

of neurohormonal activation in patients with ADHF. Iwould argue that treating hyponatremia has not been shownto be beneficial and, until we have done so, it is not neces-sarily a target of therapy.

Dr. Friedewald: Are results of tests for renal functionimproved by successful treatment of ADHF?

Dr. Yancy: That is not known.Dr. Friedewald: Which specific agents improve morbid-

ity and mortality in ADHF?Dr. Yancy: The therapeutic target in ADHF is primarily

hemodynamic, the same as in patients with chronic HF.

Currently, in patients with ADHF, the target of therapy isalso hemodynamic, but good results with this strategy havenot been seen.

Dr. Gheorghiade: Treatment of ADHF can be separatedinto 3 different phases: (1) early management for improvinghemodynamics; (2) in-hospital management for eliminatingresidual symptoms; and (3) predischarge management forimplementing life-saving therapies.

Dr. Young: The goal is to make the patient feel better, toprotect the patient from end-organ damage especially thecardiorenal syndromeand to set the stage for getting thepatient out of the hospital, which primarily requires decon-gestion.

Dr. Yancy: Given that ADHF is a heterogeneous diseaseprocess with multiple patient phenotypes, is lowering mor-tality an appropriate target? Will a single therapeutic strat-egy for a patient population this diverse lower mortality?

Dr. Young: ADHF cannot be viewed with the samemindset as patients with acute myocardial infarction,for example. Treatment of the latter is straight for-ward and much the same for all patients. Treating pa-tients with HF is far more complex. While I believe thatreduction in acute hospital mortality for ADHF is alaudable goal, that reduction is not going to be achievedwith any 1 specific intervention. Rather, it will require acombination of therapies related to the 3 goals I men-

tioned earlier and the 3 treatment phases Dr. Georghiadeoutlined.



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Dr. Gheorghiade: Improved survival is not the issue;rather, the issue is not increasing mortality with our treat-ment.

Dr. Yancy: I agree.Dr. Gheorghiade: One dilemma with ADHF is that

many therapies that improve hemodynamicssuch as do-butaminealso kill myocardial cells.

Dr. Yancy: I agree that seeking a single interventiontargeted towards lowering mortality is unrealistic. What ismore relevant is relieving symptoms and lowering morbid-ity while increasing mortality.

Dr. Gheorghiade: The HF guidelines are based more onopinion than facts, which we lack. The guidelines urgeimproving the pulmonary arterial wedge pressure with acombination of vasodilators and diuretics, but not excessivediuresis. We should not rely solely on diuretic therapy torelieve congestion.

Dr. Yancy: The guidelines do, however, emphasize de-congesting the patient.

Dr. Gheorghiade: By using combination therapy, not

single therapy.Dr. Young: The HF therapy is made more complex by

the need also to treat co-morbidities such as anemia, myo-cardial ischemia, hypertension, diabetes mellitus, and hy-perglycemia.

Dr. Yancy: Decongestion with diuretics is an appropri-ate first step. Is the second step the administration of high-bolus diuretic therapy, continuous diuretic infusion, or va-sodilators combined with standard diuretic therapy?

Dr. Young: I come back to the underlying co-morbid-ities. I would treat a patient admitted with ADHF andlong-standing hypertension and left ventricular systolicand diastolic dysfunction immediately with both vasodi-

lators and diuretics, relying more on the vasodilators tolower the left ventricular end-diastolic pressure ratherthan being aggressive with diuretics. Diuretic use haschanged with time. It is rare for me to see a patient whoneeds to be admitted to the hospital that I do not start ona continuous diuretic infusion. If a patient is sufficientlyvolume overloaded to be admitted to the hospital, guess-ing the doses of intermittent, pulsed diuretics is muchmore problematic than guessing the dose of continuousinfusion.

Dr. Gheorghiade: For some patients, diuretics are sec-ond-line therapy. Hypertensive patientseven those withreactive hypertensionare often older, and they may have

redistribution of body fluids rather than being total bodyfluid overloaded.

Dr. Friedewald: Do you not give these patients both avasodilator and a diuretic?

Dr. Gheorghiade: Yes. Most of the time, I use thecombination, but not always. There should not be any-thing routine. About 50% of these patients are hyperten-sive, and the goal in these patients is to reduce the bloodpressure, not reduce fluid overload. In other patients, thepulmonary arterial wedge pressure may be the only tar-get. In patients who are hypertensive, there are 2 targetsfor therapy: simultaneous reduction of both the bloodpressure and the pulmonary arterial wedge pressure.

Dr. Friedewald: Does everyone agree that patients withADHF should first be decongested?

Dr. Gheorghiade: Yes, but how to achieve that shouldbe determined by how the patient presents.

Dr. Young: How often do you not give diuretics topatients admitted with ADHF?

Dr. Gheorghiade: I usually use diuretics, but I do notrely solely on them, as happens too often.

Dr. Young: How often do you see acute pulmonary

edema with a normal total body volume?Dr. Gheorghiade: This occurs in about 5% of patients

with ADHF.Dr. Young: Do you give diuretics to those patients?Dr. Gheorghiade: No.Dr. Young: Most physicians do not think that way. Most

give all patients with pulmonary edema an intravenousbolus of diuretics.

Dr. Gheorghiade: The problem is mainly the quantity ofdiuretics given. According to ESCAPE, the deleterious ef-fects of diuretics were not so much related to the diuretic,but to the amount given.

Dr. Yancy: What is the role of inotropes?

Dr. Young: I use them only for patients in shock ornear-shock.

Dr. Gheorghiade: I use inotropes for patients in the lowcardiac output state. There is no other choice. Most physi-cians in the USA unfortunately use inotropes in patientswith normal cardiac output.

Dr. Friedewald: What is the role of vasodilatorsni-troprusside, nitroglycerin, and nesiritide?

Dr. Yancy: In patients with symptoms at rest in theabsence of hypotension, 1 of 3 vasodilators should be used:nitroprusside, nitroglycerin, or nesiritide. Nitroprusside hasan excellent profile, helping to normalize blood pressureand to relieve concomitant pulmonary congestion by reduc-

ing both preload and afterload. Nitroglycerin relieves pul-monary congestion in patients with ADHF by reducingpreload.

Dr. Gheorghiade: Nesiritide is an excellent choice bothfor hypertensive and normotensive patients. Unfortunately,nesiritide is too often used as rescue therapy in patients whodo not respond to other therapies. These patients are fre-quently hypotensive and have impaired renal function. Al-though nesiritide is an excellent drug for ADHF patientswith normal or elevated blood pressure, it is often used inpatients who are most likely to have adverse effects fromthis drug.

Dr. Roberts: How do you administer nitroglycerin for

ADHF?Dr. Yancy: Topically, intravenously or sublingually.Dr. Young: Nitrates are excellent drugs in ADHF when

used correctly. These patients must be carefully monitored,watching for tachyphylaxis, and titrating the drug over time.Vasodilators should not be used in the hypotensive patients.At presentation, patients with ADHF may be hypertensiveor normotensive or hypotensive, and each needs to be ad-dressed differently with respect to the vasodilator/diureticcombination. I make such decisions very early in the courseof ADHF.

Dr. Gheorghiade: Nitroprusside requires invasive mon-itoring, because it can rapidly lower the arterial blood pres-

sure to zero.Dr. Friedewald: What about oxygen?



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Dr. Yancy: Oxygen is the only pure pulmonary vasodi-lator we have. It will overcome any other influence, anddecongest the pulmonary circulation.

Dr. Friedewald: Lets discuss future therapies, startingwith aquaretic therapy.

Dr. Gheorghiade: Aquaretic therapy, or vasopressinantagonism, is safe, can be added to diuretic therapy, and

significantly reduces body weight, without adverse ef-fects on the heart rate, blood pressure, renal function, orserum potassium, and generally normalizes the serumsodium. Theoretically, it can be used with or without adiuretic.

Dr. Yancy: Acute administration of natriuretic pep-tides improves congestion and relieves dyspnea, butperhaps not more effectively than nitroglycerin. Natri-uretic peptides, however, may have adverse effects onrenal function and increased risk of death 30 days afteradministration. These questions are being resolved bya very large multicenter international trial in ADHFinvolving 7,000 patients. The planning stages are under-

way for this trial, called Acute Study of Clinical Effec-tiveness of Nesiritide in Decompensated Heart Failure(ASCEND-HF).

Dr. Friedewald: What about devices?Dr. Young: Mechanical removal of fluid has been

around a long time. Venoveno ultrafiltration devices toremove fluid are miniaturized, efficient, and easy to use.The UNLOAD trial and several other trials will give usgreater insight into their usefulness. I believe that me-chanical fluid removal devices are going to be a goodoption in the future.

Dr. Roberts: I understand that the average patient in theUSA with an acute coronary event has a body mass index of

about 29, which I suspect is the same as patients withADHF. How would significant weight loss affect the lon-gevity of ADHF patients?

Dr. Young: I believe it would be very effective.Dr. Gheorghiade: The problem is that chronic HF pa-

tients are malnourished, even including some who are over-weight.

Dr. Roberts: Malnourished from a protein standpoint?Dr. Gheorghiade: Yes. The heart requires a lot of pro-

tein to function properly. We are currently studying thepotential role of essential amino acid supplements and othertherapies to improve nutrition in HF patients.

Dr. Friedewald: How should future trials of ADHF be

conducted?Dr. Gheorghiade: Thus far, ADHF trials have involved

patients who are not stratified. There are different popula-tions of patients with ADHF, including those with variousblood pressures, serum sodium levels, geographical differ-ences (different continents), and each of these differentpatient types needs to be stratified for proper investigation.We are currently putting together a large trial that stratifiespatients admitted with acute HF into 2 groups: those treatedwith standard care, and those treated with maximal aggres-sion.

Dr. Friedewald: Is it difficult to find funding for suchtrials?

Dr. Young: It is a horrible problem. Support is mostlyfrom industry.

Dr. Friedewald: Lets discuss disease management.Dr. Yancy: Disease management in ADHF carries

some good news. There are indicators of quality that havebeen promulgated across all hospitals in this country.Using these indicators, we recently demonstrated thatcertain therapeutic strategies, such as the use of ACEinhibitors and blockers, appear to modify 60- to 90-day

outcomes. Such clinical trials have repetitively shownthat best practices make a difference in outcomes. Whena HF patient is hospitalized, an excellent opportunityarises to place that patient on the right drugs and into theright follow-up schemes.

Dr. Friedewald: How do you determine the optimaltime to discharge a patient with ADHF from the hospital?

Dr. Gheorghiade: This is a very important issue. Guide-lines do not tell us when patients are ready for discharge.Although congestion is the main reason for admission, 50%of these patients do not lose weight during hospitalization.When they go home, they go home with the same amount offluid, which has shifted from the lungs, where you can still

hear it with the stethoscope and see it on chest x-ray, toother portions of the body.

Dr. Yancy: I agree that we do not have a good barometerfor discharge.

Dr. Gheorghiade: There are things we could do better:watching the patient climb a flight of stairs, perform a BNP,and determine if a patient can lie fully reclined. These aresimple tasks, but they are not being done.

Dr. Yancy: I discharge the patient when the presentingsymptoms are gone, there is improvement in the back-ground medical therapy, and there is a well-defined plan ofcare for the future.

Dr. Gheorghiade: I rely on how patients feel. I perform

an orthopnea test to be certain that patients can lay flat for1 minute, and I ask them to climb 1 flight of stairs. If theypass these tests, and they have no signs of congestion, Idischarge them.

Dr. Young: I make certain the patient feels better com-pared to symptoms at admission, is ambulating, and isdecongested. I will send a patient home with a small amountof peripheral edema. It is more important to see improve-ment than total resolution. And a long-term treatment planis essential.

Dr. Roberts: Can we train more physicians to specializein treating patients with HF?

Dr. Yancy: As immediate past chair of the membership

committee of the Heart Failure Society of America, mycharge for 3 years was to try to find ways to get moreprofessionals involved in treatment of patients with HF.Although there are people who are interested in special-izing in HF, there is a disconnect between the way wetrain people and the way people are hired. Physicians aretypically hired according to what they can do procedur-ally, but we train people according to what they need toknow cognitively. This needs to be changed, and theHeart Failure Society of America is raising the awarenessof the value of the cognitive input of HF specialists. It isour hope that we can achieve certification of HF man-agement as a recognized subspecialty. Revenue and other

such resources, however, drive a lot of this sort of be-havior in our society, so if we can add value to the



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designation as a HF physician, more people will be in-terested in pursuing this subspecialty.

Dr. Young: A good HF clinician must have a goodunderstanding of renal pathophysiology, pulmonary patho-physiology, hemodynamics and heart transplantation. Thereare a lot of exciting aspects of this specialty. Reimburse-ment issues, however, hamper these efforts. Unless we cre-

ate more systems to deal with the reimbursement issues, HFspecialists will continue to struggle and inadequate numberswill enter the subspecialty.

Dr. Gheorghiade: The most important member of theHF team is the patient. The physician sees these patientsonce every 2 months, and the patients are with them-selves 24 hours a day, 7 days a week. So the patient is avery important component, because therapy for HF ischronic. When patients do not take their medicines and/orfail to do other proper things, outcomes are bad. Thepatient is the major part of the HF management team.

Dr. Friedewald: Thank you.

Needs Assessment: The need for this activity for cardi-ologists and other healthcare specialists in cardiovascularmedicine is based on the following premises:

1. Acute decompensated heart failure (ADHF) is a com-mon cause of morbidity and mortality.

2. ADHF is associated with many co-morbid conditions.3. ADHF is a complex, multidimensional condition de-

manding knowledge of cardiac, pulmonary, hemody-namic, and renal function.

4. Knowledge about ADHF is not as advanced as ourunderstanding of other cardiovascular conditions,such as chronic congestive heart failure and acute

myocardial infarction.

5. There is a need for more physicians to be trained intreating patients with ADHF.

Target Audience: This activity is designed for cardiol-ogists and all other health care specialists caring for patientswith acute and chronic coronary heart disease.

CME Credit: The A. Webb Roberts Center for Continu-

ing Medical Education of Baylor Health Care System, Dal-las, designates this educational activity for a maximum of 1

AMA PRA Category 1 Credit(s). Physicians should onlyclaim credit commensurate with the extent of their partici-pation in the activity.

The A. Webb Roberts Center for Continuing MedicalEducation for Baylor Health Care System, Dallas, is accred-ited by the Accreditation Council for Continuing MedicalEducation to provide continuing medical education forphysicians.

CME Instructions: After reading this article, go onlineat www.AJConline.org to register, complete a post-test with

a minimum score of 80%, complete an evaluation, and printa certificate.

Combination of Media: Print and InternetComputer Requirements: Windows 2000, Pentium 3 orgreater, 512 ram, 80 gigabytes storageEstimated Time to Complete: 1 hourRelease Date: June 2007Termination Date: June 2008

1. American Heart Association. Heart Disease and Stroke Statistics.Available at: http://circ.aha.journals.org/cgi/reprint/113/6/e85 .

2. American Cancer Society. Cancer Statistics 2005. Available at: http://int-caonline.amcancersoc.org/cgi/content/full/55 .

3. Executive Summary: HFSA 2006 Comprehensive Heart Failure Prac-

tice Guideline. J Cardiac Failure 2006;12:1038.

http://www.ajconline.org/http://www.ajconline.org/http://circ.aha.journals.org/cgi/reprint/113/6/e85http://circ.aha.journals.org/cgi/reprint/113/6/e85http://int.caonline.amcancersoc.org/cgi/content/full/55http://int.caonline.amcancersoc.org/cgi/content/full/55http://int.caonline.amcancersoc.org/cgi/content/full/55http://int.caonline.amcancersoc.org/cgi/content/full/55http://int.caonline.amcancersoc.org/cgi/content/full/55http://circ.aha.journals.org/cgi/reprint/113/6/e85http://www.ajconline.org/

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