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(Circulation. 2000;101:738.)
© 2000 American Heart Association, Inc.

Editorial

Distinguishing Mechanisms From Markers of Cardiac Contractile Dysfunction

More Than 1 Way to Skin the Cat of Heart Failure

C. William Balke, MD; Yibin Wang, PhD

From the Departments of Medicine (C.W.B.) and Physiology (C.W.B., Y.W.), University of Maryland School of Medicine, Baltimore.

Key Words: Editorials • contractility • genes • mechanics • heart failure

The incidence of death from cardiac hypertrophy and heart failure has increased steadily over the past 25 years despite the overall decline in mortality from heart disease during the same period. As of 1990, heart failure was responsible for more than 400 000 deaths per year and was the most common discharge diagnosis in the Medicare population.¹ Overall, patients with heart failure have a 5-year mortality rate of 50%. Patients with New York Heart Association class III and IV heart failure have a 2-year mortality approaching 50% despite nearly optimal treatment with ACE inhibitors, diuretics, and digoxin.² Therefore, it is fair to say that the prevalence of heart failure has reached epidemic proportions in this country and in most industrialized western societies. Clearly, a better understanding of the primary mechanisms that underlie the contractile abnormalities of the failing heart is needed to develop new therapeutic strategies for the treatment of existing heart failure and more effective guidelines for the prevention of heart failure.

After nearly 3 decades of intensive investigation, the precise mechanisms that underlie the contractile abnormalities of cardiac hypertrophy and heart failure remain elusive. The distinction between true mechanisms and mere markers of disease has been particularly difficult in heart failure, because the complex cascade of physiological, neurohumoral, and biochemical abnormalities undoubtedly represents the complex interaction of a multitude of environmental and genetic factors. Obviously, making this distinction has far-reaching therapeutic implications. Fresh insights regarding the cellular and molecular bases of heart failure have come from very recent . . . [Full Text of this Article]