Circulation. 1998;98:1699-1702
(Circulation. 1998;98:1699-1702.)
© 1998 American Heart Association, Inc.
Activation of Matrix Metalloproteinases in the Failing Human Heart
Breaking the Tie That Binds
Douglas L. Mann, MD;
; Francis G. Spinale, MD, PhD
From the Cardiology Section, Department of Medicine, Veterans
Administration Medical Center, Houston, Tex, Baylor College of Medicine
(D.L.M.) and the Division of Cardiothoracic Surgery, Medical University of
South Carolina, Charleston (F.G.S.).
Correspondence to Francis G. Spinale, MD, PhD, Room 418 CSB, Cardiothoracic Surgery, Medical University of South Carolina, 171 Ashley Ave, Charleston, SC.
Key Words: Editorials • metalloproteinases • heart failure • remodeling
The process of left
ventricular (LV) remodeling has been shown to be an
important predictor of morbidity and mortality in patients with heart
failure. Therefore, identifying the cascade of molecular and cellular
events that contribute to LV remodeling is likely to provide new and
novel targets for preventing disease progression in heart failure. In
this issue of Circulation, Li and
colleagues1 report that changes in the relative
abundance of tissue inhibitors of the metalloproteinases
(TIMPs) occur with the development of end-stage human heart failure,
thus raising the important possibility that alterations in the
extracellular matrix of the failing heart may contribute to disease
progression in heart failure. The purpose of this editorial was to
place the findings of the study by Li et al, as well as those of
recently published reports, in perspective with what we know about
myocardial extracellular remodeling in heart failure.
LV Remodeling in Heart Failure
The phenotype of dilated
cardiomyopathic disease in humans can be characterized
as a disproportionate increase in the ratio of LV
ventricular chamber radius to wall thickness, with no
increase in sarcomere length. The increased ratio of LV chamber radius
to wall thickness is accompanied by increased myocardial wall stress,
which can in turn promote further dilation and reduced pump function.
Taken together, these observations would suggest that significant
myocardial remodeling must occur within the LV free wall to allow for
the chamber dilation and wall thinning that occur during the
progression to severe LV dilation. Although the canonical view of LV
remodeling has held . . . [Full Text of this Article]
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