Nonischemic heart failure: epidemiology, pathophysiology, and progression of disease.
The prevalence of nonischemic heart failure including idiopathic dilative cardiomyopathy is not well known. It may vary considerably in different population sub-groups and geographic areas. In ambulatory and hospitalized patients with clinically manifest heart failure primary cardiomyopathy is diagnosed in 2-15%, while in recent large scale therapeutic trials the proportion of patients with nonischemic heart failure ranged from 18% to 53%. There is a relation between sex, age and etiology of chronic heart failure, nonischemic cardiomyopathy being more frequent in women and in younger individuals. In contrast to ischemic heart failure, where the severity usually correlates with the extent of coronary artery lesions, the pathophysiology of cardiomyopathy is less clear. Genetic factors, myocarditis from infectious agents, auto-immune mechanisms, cytokine activation, hormonal and metabolic influences can play a role. The functional consequences of myocardial damage in nonischemic heart failure is a global instead of localized abnormality of ventricular contractility. There is epidemiological evidence that in general the prognosis of nonischemic heart failure is better than in ischemic heart failure. The mortality of patients with ischemic heart failure was usually higher in the placebo groups of recent heart failure trials than in patients with nonischemic etiology. Furthermore, therapeutic responses to angiotensin-converting enzyme (ACE) inhibitors, beta-blockers, amlodipine and amiodarone were also different in some studies. The outcome of nonischemic heart failure is better even in transplant candidates with the most advanced stages of heart failure, they survive longer and respond better to intensified drug regimens than patients with similar clinical severity of ischemic heart failure. Thus, an early and precise diagnosis of the etiology of heart failure should be encouraged not only in clinical trials but also in every day patient management. As more therapeutic options are developed, individualized drug selection for patients with various etiologies of heart failure may become possible.
Follath
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Medicine A, Department of Medicine, University Hospital Zurich, Switzerland.
D000818:Animals; D002303:Cardiac Output, Low / Q000188:drug therapy / Q000453:epidemiology / Q000503:physiopathology / Q000628:therapy*; D018450:Disease Progression; D006801:Humans