(Circulation. 1997;96:4065-4082.)
© 1997 American Heart Association, Inc.
Articles |
Extracellular Matrix Remodeling in Heart Failure
A Role for De Novo Angiotensin II Generation
From the Division of Cardiology, Department of Internal Medicine, University of Missouri Health Sciences Center, Columbia.
Correspondence to Karl T. Weber, MD, Division of Cardiology, MA432 Medical Sciences Building, University of Missouri Health Sciences Center, Columbia, MO 65212.
Key Words: angiotensin • collagen • diastole • heart failure • remodeling
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Introduction |
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Heart failure is a major health problem worldwide. In the United States, it represents the number one hospital discharge diagnosis among elderly persons each year. It appears most commonly in patients with previous MI.1,2 The chronically failing heart of ischemic origin is characterized by iterations in tissue structure, particularly fibrous tissue formation, that appear in infarcted and noninfarcted myocardium of both right and left ventricles.3,4 In other words, fibrosis appears at the site of MI as well as remote from it. Fibrosis remote from the infarct site is considered "the major cause of ventricular remodeling" in ischemic cardiomyopathy.4 Such an adverse accumulation of extracellular matrix initially raises myocardial stiffness; its continued accumulation further increases stiffness and impairs contractile behavior.5–10 Elucidating cellular and molecular mechanisms responsible for accumulation of extracellular matrix is essential to designing cardioprotective and reparative strategies that could prevent or regress fibrosis, respectively, after infarction.11,12
ACE inhibition has proved effective in reducing mortal and morbid
events, improving symptomatic status, and attenuating the
progressive nature of cardiac failure in symptomatic
patients with ventricular diastolic and/or
systolic dysfunction in whom activation of the circulating RAAS
is present.1,13,14 ACE
inhibitor–mediated reductions in circulating Ang II and
aldosterone no doubt contribute to this salutary response.
This would include an attenuation of well-recognized endocrine
properties of these hormones, such as altered sodium homeostasis and
vascular tonicity, and their adverse influence on matrix structure of
atria and ventricles.15–20 Collectively, these
adverse responses to RAAS effector hormones contribute to the
progressive nature of chronic cardiac
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