Right Ventricular Function: A Stepchild in the Management of Congestive Heart Failure (2004)

In this issue of Congestive Heart Failure, Beck-da-Silva et al.1 present the results of a 4-month trial testing the effects of β-blocker therapy (bisoprolol) on right ventricular function. Of the 30 patients in the study, 12 had ischemic cardiomyopathy and 16 had nonischemic cardiomyopathy. The authors report a significant (7.1%) improvement in right ventricular ejection fraction from a depressed baseline of 30.7% (p=0.001) with a similar increase in left ventricular ejection fraction, confirming the observations of Quaife et al.2in a subset of patients from a large, double-blind study of carvedilol in left ventricular heart failure. From a conceptual viewpoint, Beck-da-Silva and colleagues make a small contribution by showing improvement in right ventricular function with a second β blocker; however, their emphasis on the role of right ventricular function in heart failure is extremely important. Right ventricular function has long been clinical cardiology's figurative stepchild. Early cardiologists were extremely busy worrying about left-sided valvular disease and the emerging epidemic of myocardial infarction. Later generations of cardiologists concentrated on the epidemic of coronary artery disease and its sequelae: unstable angina, myocardial infarction, sudden death, and the progression to left ventricular failure. New cardiologists are taught that a hallmark of coronary artery disease is a depression of left ventricular function with preservation of right ventricular function, with the result that our training programs have produced left-sided heart doctors. Success in treating ischemic heart disease, combined with an aging patient population, has contributed to the epidemic increase in congestive heart failure. Since the demonstration of increased survival with hydralazine and nitrates, significant progress has been made in the treatment of left ventricular failure. The optimization of medical therapy, including angiotensin-converting enzyme inhibitors, aldosterone antagonists, and β blockers, has resulted in symptomatic improvement for patients, a slowing of the progression of the disease, and an increase in survival—the ultimate goals in the management of this disease. Even under the best circumstances of medical therapy, the Randomized Aldactone Evaluation Study (RALES)3 demonstrated a mortality rate of approximately 35% at 2 years in patients maintained on diuretics, angiotensin-converting enzyme inhibitors, and spironolactone. The weakness of this study was its timing: only 11% of its patients were taking β blockers. With the advances has come a new awareness that the progression of the disease can be slowed but it cannot be stopped. There is a progressive increase in left ventricular end diastolic pressure with subsequent increases in pulmonary artery pressure and right ventricular afterload. This results in a slow, progressive decrease in right ventricular ejection fraction. The problem is compounded in patients with a primary cardiomyopathy who demonstrate biventricular dysfunction with the same pathophysiologic sequence except with the primary cardiomyopathies. By and large, the right ventricle is involved as much as the left ventricle and there is a more rapid progression of right ventricular dysfunction. This progression of right ventricular dysfunction has significant sequelae for those involved in the treatment and management of advanced heart failure. Pulmonary hypertension and increases in right ventricular afterload are a relative contraindication to cardiac transplantation. In the emerging era of left ventricular assist devices, acute right heart failure due to underlying decreased right ventricular function is one of the largest contributors to the postoperative mortality rate. The problem of sudden death in patients with congestive heart failure is likely contributed to by progressive right ventricular dysfunction. The contributions of β blockers and aldosterone antagonists to reductions in sudden death may be due, in part, to an improvement in right ventricular function. There is a growing population of patients with left ventricular dysfunction who, because of advances in technology and pharmacology, are surviving for a longer period of time. But progression of the underlying disease process continues, with sequelae such as pulmonary hypertension and right ventricular failure. Di Salvo et al.4 demonstrated that right ventricular ejection fractions <35% at rest and exercise are potent predictors of survival in advanced heart failure, and de Groote et al.5 concluded that right ventricular ejection fraction is an independent predictor of survival in patients with moderate congestive heart failure. This work needs to be expanded and the heart failure community will have to take the lead. Our ability to accurately access right ventricular function and diagnose right ventricular dysfunction is limited. Seeking improvements in our ability to understand and diagnose right ventricular dysfunction should receive more importance and a firmer understanding of the coupling of right ventricular function to left ventricular function should be achieved. Questions about the contribution of right ventricular function to the progression of heart failure will not go away. This topic should be aggressively approached and firmly appreciated by everyone involved in the attempt to curtail the epidemic progression of congestive heart failure.