Evaluation and Management of a Patient With Congestive Heart Failure*

clinical problems in cardiopulmonary disease Evaluation and Management of a Patient With Congestive Heart Failure* Mary Norine Walsh, MD; and Morton E. Tavel, MD, FCCP

(CHEST 2003; 124:728 –731) Key words: congestive dilated cardiomyopathy; heart failure Abbreviations: ACE ⫽ angiotensin-converting enzyme; BNP ⫽ B-type natriuretic peptide; CAD ⫽ coronary artery disease; CHF ⫽ congestive heart failure; NYHA ⫽ New York Heart Association

Case Presentation 44-year-old woman initially presented to her A primary physician in April 1998 with a cough and

dyspnea that had persisted for about 1 month. A chest roentgenogram demonstrated clear lungs but a “globular” cardiac configuration. She was given therapy with amoxicillin combined with clavulanate potassium (Augmentin; GlaxoSmithKline; Research Triangle Park, NC) for 1 week with apparent diminution of the severity of the dyspnea. After feeling fairly well for 1 month, she began experiencing cough, dyspnea, chest pressure, and extreme fatigue. The dyspnea resulted from minimal activity and was associated with orthopnea. The patient’s medical history was unrevealing. Specifically, there was no evidence of prior coronary artery disease (CAD), hypertension, heavy alcohol intake, or recent pregnancy. She then was referred to a cardiologist and was found to have a BP of 100/70 mm Hg, sinus tachycardia at 120 beats/min, and no evidence of jugular venous distension or peripheral edema. A cardiac examination disclosed an apical impulse displaced 2-cm lateral to the midclavicular line, a prominent third heart sound, and a grade 2/6 apical systolic

*From the Congestive Heart Failure Program (Dr. Walsh), St. Vincent Hospital (Dr. Tavel), Indianapolis, IN. Manuscript received December 10, 2002; revision accepted December 11, 2002. Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (e-mail: [email protected]). Correspondence to: Morton E. Tavel, MD, FCCP, Clinical Problems in Cardiopulmonary Disease, 8333 Naab Rd, Suite 200, Indianapolis, IN 46260-1983; e-mail: [email protected] 728

murmur of mitral regurgitation. A chest roentgenogram again demonstrated cardiomegaly with clear lung fields. An echocardiogram disclosed a moderately dilated left ventricle with normal wall thickness and severe global hypokinesis (estimated ejection fraction, 20 to 25%), which is indicative of generalized dilated cardiomyopathy. The left atrium was mildly dilated, and the right heart chambers were normal in size and motion. The patient then was admitted to the hospital and received therapy with digoxin, diuretics, and a lowdose angiotensin-converting enzyme (ACE) inhibitor. Her symptoms gradually improved. Questions for the Consultant 1. What further information, if any, do you require to establish a firm diagnosis? 2. Under what circumstances would cardiac catheterization combined with coronary cineangiography be necessary? 3. What role could noninvasive tests play in establishing the presence or absence of significant CAD? Which tests could be used, and could they obviate the need for an invasive study? 4. Assuming that no significant coronary disease is present, how would you proceed with medical management? How would this differ from the management of the patient found to have severe obstructive multivessel coronary disease? 5. Should this individual be given anticoagulant agents, and if so, which one? 6. Under what circumstances should this patient be considered for cardiac transplantation? Comments by Consultant Mary Norine Walsh, MD What Further Information, If Any, Do You Require To Establish a Firm Diagnosis? The constellation of the patient’s symptoms and the findings from a physical examination, chest raClinical Problems in Cardiopulmonary Disease

diograph, and echocardiogram clearly establish a diagnosis of congestive heart failure (CHF). The patient currently has orthopnea and extreme fatigue, thus New York Heart Association (NYHA) class IV symptoms. An echocardiogram with Doppler flow imaging is the best initial assessment of left ventricular function in patients with symptoms of heart failure because it allows for the concomitant evaluation of valvular function.1 Radionuclide or angiographic ventriculography, however, may also be used to distinguish between those patients with symptoms of CHF and preserved or normal left ventricular function, as opposed to those with abnormal systolic function, as demonstrated by this patient. This is an important distinction to make from the standpoint of prognosis as well as treatment. The performance of a 12-lead ECG is essential in the evaluation of a patient with CHF. Evidence of myocardial infarction or conduction abnormalities such as left bundle-branch block and other abnormalities serve to heighten the suspicion of left ventricular systolic dysfunction. An ECG at the time of this patient’s initial presentation to her primary care physician might have led to an earlier diagnosis of CHF rather than to treatment for an upper respiratory infection. An ECG evaluation also is needed to rule out arrhythmias that can worsen symptoms of CHF or predict potential complications such as sudden cardiac death. Since atrial tachyarrhythmias such as atrial fibrillation with uncontrolled ventricular response may be the sole cause of CHF and left ventricular dysfunction, the early identification of this arrhythmia is crucial.2 A newer tool being used in the diagnosis and assessment of CHF is the measurement of blood levels of B-type natriuretic peptide (BNP). BNP is a peptide that is secreted by the left ventricle in response to stretch and can be used to differentiate dyspnea due to CHF from that caused by COPD, obesity, or other chronic illnesses.3 The patient presented, however, has fairly classic signs and symptoms of CHF, so a BNP level would predictably be elevated and would add little to the diagnosis. On the other hand, a BNP level at the time of this patient’s initial presentation would likely have allowed for an earlier diagnosis. Although this patient was initially presumed to have an upper respiratory infection, the description of the cardiac silhouette as globular suggests cardiomyopathy with CHF as the cause of her symptoms. In some patients, though, a history of a febrile illness that precedes the development of CHF symptoms can suggest an infectious (ie, viral) etiology of cardiomyopathy. A detailed family history is needed to rule out familial cardiomyopathy. A CBC count, www.chestjournal.org

urinalysis, metabolic panel (ie, electrolytes, BUN, and creatinine levels, and liver function tests), and an assessment of thyroid function should be performed in all patients with newly diagnosed CHF. Under What Circumstances Would Cardiac Catheterization Combined With Coronary Cineangiography Be Necessary? The echocardiogram performed in this patient demonstrated global hypokinesis, which does not exclude CAD as an underlying etiology but does make it unlikely. For CAD to cause such a severe reduction in left ventricular function as is present in this patient, multivessel disease would almost certainly be present, and the echocardiogram would likely demonstrate segmental wall motion abnormalities. Cardiac catheterization to evaluate for CAD should be considered in patients who have noninvasive evidence of this condition (eg, ECG or echocardiographic signs) and for patients with anginal chest pain or multiple coronary risk factors (eg, hypertension, diabetes, dyslipidemia, tobacco use, or family history). What Role Could Noninvasive Tests Play in Establishing the Presence or Absence of CAD? Which Tests Could Be Used and Could They Obviate the Need for Invasive Study? The role of rest/stress nuclear myocardial perfusion imaging has not been well-characterized in patients with CHF, although studies of such patients are ongoing. In the low-risk patient (ie, one with no risk factors for CAD, no chest pain, and no echocardiographic evidence of CAD), a myocardial perfusion scan that demonstrates no evidence of ischemia or scarring may obviate the need for cardiac catheterization. A similarly normal finding on a stress echocardiographic study also would be reassuring. The results of an electron beam CT scan demonstrating no coronary calcium would rule out CAD as the sole cause of cardiomyopathy. Of course, for the patient with known CAD, the performance of perfusion imaging with thallium, utilizing positron emission tomography or single photon emission tomography with F-fluorodeoxyglucose as the tracer agent, is important. Graduated dobutamine infusion in conjunction with echocardiographic imaging also can differentiate the viable myocardium from the irreversibly scarred myocardium and can guide the physician in making recommendations regarding revascularization. CHEST / 124 / 2 / AUGUST, 2003

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Assuming That No Significant Coronary Disease Is Present, How Would You Proceed With Medical Management? How Would This Differ From Management of the Patient Found To Have Severe, Obstructive, Multivessel CAD? The patient already has received therapy with an ACE inhibitor, and the initiation of therapy with a ␤-blocker agent as soon as the patient is euvolemic is equally important. Thereafter, titration to maximally tolerated doses of both the ACE inhibitor and the ␤-blocker should be accomplished. Patients who are hypertensive may tolerate the maximum doses of both the ACE inhibitor and the ␤-blocker (eg, 50 mg tid captopril and 50 mg bid carvedilol). On the other hand, a patient with symptomatic hypotension may not tolerate these higher doses. The titration of these medications requires that the patient have close follow-up as an outpatient, and that she carefully monitor her weight and notify her physician of any abrupt changes. Spironolactone has been demonstrated to benefit patients with recent or current severe heart failure.4 Because of the risk of hyperkalemia, spironolactone should be used cautiously, and only for patients with normal renal function and potassium concentrations. It is generally thought that the benefits of ACE inhibitors for patients with CHF represent a class effect, so the selection of an ACE inhibitor for an individual may be primarily influenced by cost considerations. If a patient is unable to tolerate ACE inhibitors (ie, due to cough), an angiotensin receptor-blocking agent should be substituted. To date, angiotensin receptor-blocking agents have not been demonstrated to be superior to ACE inhibitors, and they are indicated as a second-line choice for the ACE-intolerant patient. Robust clinical trials have demonstrated the benefits of therapy with various ␤-blockers in the CHF population. Bisoprolol, long-acting metoprolol, and carvedilol have all been shown to improve survival and to decrease hospitalizations for heart failure. In the instance of severe CHF (ie, NYHA class IV), only carvedilol thus far has been demonstrated to improve survival and is also well-tolerated. Although several small trials have demonstrated differences among patient responses to these agents, a large, randomized direct comparison trial demonstrating the superiority of one over another has not yet been completed. For a patient with CHF, left ventricular dysfunction, and severe obstructive CAD, the same approach to the initial medical management should be taken. The consideration of surgical revascularization, however, should be undertaken soon after the patient presents, especially if the patient has chest 730

pain or objective evidence of ischemia. The assessment of myocardial viability using the noninvasive techniques described above is important, particularly since the patient’s risk of surgery is usually quite high. If extensive myocardial scarring were found with little evidence of viability, surgical or mechanical revascularization would be inadvisable. Should the Individual Be Given Anticoagulants, and If So, Which One? Antiplatelet agents such as aspirin are recommended for the prevention of myocardial infarction and death in patients with CHF and underlying CAD. Anticoagulation therapy with warfarin is essential for patients with atrial fibrillation or a previous thromboembolic event. Warfarin anticoagulation is prescribed by some physicians for patients with CHF and a dilated left ventricle in the absence of these two conditions, but the evidence for doing so has not been demonstrated in controlled trials.5,6 One could consider warfarin anticoagulation therapy for this patient, maintaining the international normalized ratio between 2.0 and 3.0, early in the course of her illness. The need for continued anticoagulation therapy should then be reevaluated, depending on her response to the overall therapy. Under What Circumstances Should This Patient Be Considered for Cardiac Transplantation? Numerous large, randomized, controlled trials have demonstrated the benefits of the medical therapies outlined for this patient.1 With the optimal titration of the ACE inhibitor and ␤-blocker, one should expect her symptoms to improve and, over time, especially if she does not have CAD, her left ventricular function to improve. If the expected improvement does not occur and her symptoms worsen, other therapies, including transplantation should be considered. If her ECG findings demonstrate a marked intraventricular conduction delay, cardiac resynchronization with a biventricular pacing device may be beneficial.7 Should transplantation prove to be the only viable option, evaluation for any concomitant diseases that would preclude transplantation (eg, cancer and severe renal dysfunction) should be undertaken. The decision regarding listing the patient for cardiac transplantation can be facilitated by an assessment of a patient’s exercise-induced maximal oxygen uptake. A peak oxygen uptake of ⬍ 14 mL/kg/min (or ⬍ 50% of predicted normal values) or the need for continuous therapy with IV inotropic agents generally identifies the need for transplantation.8,9 The placement of an implantable left ventricular assist device is sometimes needed as a “bridge” to cardiac transClinical Problems in Cardiopulmonary Disease

plantation for a patient who requires a greater degree of hemodynamic support.10

ejection fraction had increased to 48%, and she reported almost no exertional limitation (ie, NYHA class I).

Follow-up Information The patient underwent right and left heart catheterization with the following results: right atrial mean pressure, 10 mm Hg; right ventricular pressure, 60/15 mm Hg; pulmonary arterial pressure, 60/30 mm Hg (mean, 30 mm Hg); pulmonary arterial mean wedge pressure, 32 mm Hg; left ventricular pressure, 120/30 mm Hg; cardiac output, 4.0 L/min (index value, 2.3 L/min/m2); and pulmonary vascular resistance, 2.0 Wood units. Coronary cineangiography disclosed healthy coronary arteries. Left ventriculography showed dilatation of the chamber with severe global hypokinesis (estimated ejection fraction, 10%). A dobutamine infusion was begun IV, and therapy with diuretics was continued. An evaluation for cardiac transplantation was begun. The patient was gradually weaned from dobutamine, and therapy was then discontinued. Therapy with lowdose carvedilol (ie, 3.125 mg bid) was started orally, and she was discharged from the hospital (hospital admission weight, 171 lbs; hospital discharge weight, 160 lbs) receiving therapy with digoxin (0.125 mg qd), potassium chloride (10 mEq qd), furosemide (20 mg bid), lisinopril (5 mg qd), warfarin (5 mg qd), carvedilol (3.125 mg bid), and spironolactone (25 mg qd). The dose of carvedilol was gradually increased to 25 mg bid over several weeks, and by 6 months after hospital discharge the patient reported a marked decrease in dyspnea and fatigue. A radionuclide ventriculogram showed her to have a left ventricular ejection fraction of 35%. The warfarin therapy then was stopped. A full year later, the

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References 1 Hunt SA, Baker DW, Chin MH, et al. ACC/AHA guidelines for the evaluation and management of chronic heart failure in the adult: executive summary; a report of the American College of Cardiology/American Heart Association task force on practice guidelines (Committee to revise the 1995 guidelines for the evaluation and management of heart failure). J Am Coll Cardiol 2001; 38:2101–2113 2 Shinbane JS, Wood MA, Jensen DN, et al. Tachycardiainduced cardiomyopathy: a review of animal models and clinical studies. J Am Coll Cardiol 1997; 29:709 –715 3 Maisel AS, Krishnaswamy P, Nowak RM, et al. Rapid measurement of B-type natriuretic peptide in the emergency diagnosis of heart failure. N Engl J Med 2002; 347:161–167 4 Pitt B, Zannad F, Remme WJ et al. The effect of spironolactone on morbidity and mortality in patients with severe heart failure: Randomized Aldactone Evaluation Study investigators. N Engl J Med 1999; 341:709 –717 5 Falk RH. A plea for a clinical trial of anticoagulation in dilated cardiomyopathy. Am J Cardiol 1990; 65:914 –915 6 Al Khadra AS, Salem DN, Rand WM, et al. Warfarin anticoagulation and survival: a cohort analysis from the Studies of Left Ventricular Dysfunction. J Am Coll Cardiol 1998; 31:749 –753 7 Abraham WT, Fisher WG, Smith AL, et al. Cardiac resynchronization in chronic heart failure. N Engl J Med 2002; 346:1845–1853 8 Mancini DM, Eisen H, Kussmaul W, et al. Value of peak exercise oxygen consumption for optimal timing of cardiac transplantation in ambulatory patients with heart failure. Circulation 1991; 83:778 –786 9 Miller LW. Listing criteria for cardiac transplantation: results of an American Society of Transplant Physicians–National Institutes of Health conference. Transplantation 1998; 66: 947–951 10 Goldstein DJ, Oz MC, Rose EA. Implantable left ventricular assist devices. N Engl J Med 1998; 339:1522–1533

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