Reviews |
From the Division of Cardiology (D.A.K.), Department of Medicine, Johns Hopkins School of Medicine, Baltimore, Md; and the Institute for Cardiovascular Research (W.J.P., J.G.F.B.), Vrije Universiteit Amsterdam, Amsterdam, the Netherlands.
Correspondence to David A. Kass, Johns Hopkins Medical Institutions, Medicine, Cardiology, 500 Halstead, Baltimore, MD 21224. E-mail dkass{at}jhmi.edu
This Review is part of a thematic series on Unanswered Questions in Heart Failure, which includes the following articles:
Is Depressed Contractility Centrally Involved in Heart Failure?
What is the Role of B-Adrenergic Signaling in Heart Failure?
What Mechanisms Underlie Diastolic Dysfunction in Heart Failure?
What Causes Sudden Death in Heart Failure?
Is Abnormal Cell Growth and Hypertrophy the Cause of Heart Failure?
Does Energy Starvation Cause Heart Failure
Steven Houser Guest Editor
Abnormalities of diastolic function are common to virtually all forms of cardiac failure. However, their underlying mechanisms, precise role in the generation and phenotypic expression of heart failure, and value as specific therapeutic targets remain poorly understood. A growing proportion of heart failure patients, particularly among the elderly, have apparently preserved systolic function, and this is fueling interest for better understanding and treating diastolic abnormalities. Much of the attention in clinical and experimental studies has focused on relaxation and filling abnormalities of the heart, whereas chamber stiffness has been less well studied, particularly in humans. Nonetheless, new insights from basic and clinical research are helping define the regulators of diastolic dysfunction and illuminate novel targets for treatment. This review puts these developments into perspective with the major aim of highlighting current knowledge gaps and controversies.
Key Words: myocardium dilated cardiomyopathy heart failure hypertrophy compliance diastole relaxation
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