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Departments of 1 Pathology and 3 Pharmacology, Cardiovascular Research Institute Maastricht, University of Maastricht, 6200 MD Maastricht, The Netherlands; and Departments of 2 Cardiothoracic Surgery and 4 Cardiology, Medical University of South Carolina, Charleston, South Carolina 29425
Recent studies have been directed at
modulating the heart failure process through inhibition of activated
matrix metalloproteinases (MMPs). We hypothesized that a loss of MMP
inhibitory control by tissue inhibitor of MMP (TIMP)-1 deficiency
alters the course of postinfarction chamber remodeling and induced
chronic myocardial infarction (MI) in wild-type (WT) and
TIMP-1
/ mice. Left ventricular (LV) pressure-volume
loops obtained from WT and TIMP-1/ mice demonstrated
that LV end-diastolic volume [52 ± 4 (WT) vs. 71 ± 6 (TIMP-1/) µl] and LV end-diastolic pressure
[9.0 ± 1.2 (WT) vs. 12.7 ± 1.4 (TIMP-1/)
mmHg] were significantly increased in the TIMP-1/ mice
2 wk after MI. LV contractility was reduced to a similar degree in the
WT and TIMP-1/ groups after MI, as indicated by a
significant fall in the LV end-systolic pressure-volume relationship.
Ventricular weight and cross-sectional areas of LV myocytes were
significantly increased in TIMP-1/ mice, indicating
that the hypertrophic response was more pronounced. The observed
significant loss of fibrillar collagen in the TIMP-1/
controls may have been an important contributory factor for the observed LV alterations in the TIMP-1/ mice after MI.
These findings demonstrate that TIMP-1 deficiency amplifies adverse LV
remodeling after MI in mice and emphasizes the importance of local
endogenous control of cardiac MMP activity by TIMP-1.
myocardial remodeling; pressure-volume loops
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