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Articles in PresS, published online ahead of print September 26, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00511.2002
Submitted on June 27, 2002
Accepted on September 18, 2002
1 Department of Cardiothoracic Surgery, Medical University of South Carolinat, Charleston, South Carolina, USA
2 Departments of Pathology and Pharmacology, Cardiovascular Research Institute Maastrich (CARIM), University of Maastricht, Maastricht, Netherlands
3 Department of Cardiology, Medical University of South Carolina, Charleston, South Carolina, USA
* To whom correspondence should be addressed. E-mail: wilburnm{at}musc.edu.
Recent studies have directed the interests at modulating the heart failure process through inhibition of activated MMPs. We hypothesized that a loss of MMP inhibitory control by TIMP-1 deficiency alters the course of post-infarction remodeling and induced chronic myocardial infarction in wild-type and TIMP-1-/- mice. LV pressure-volume loops obtained from wild-type and TIMP-1-/- mice demonstrated that LV end-diastolic volumes (LVEDVWT vs TIMP-/-:52±4 vs 71±6µl) and LV end-diastolic pressures (LVEDPWT vs TIMP-/-: 9.0±1.2 vs 12.7±1.4mmHg) were significantly increased in the TIMP-1-/- mice 2 weeks post-MI. LV contractility was reduced to a similar degree in both the WT and TIMP-1-/- groups after MI, as indicated by a significant fall in preload recruitable stroke work. Ventricular weight and cross-sectional areas of LV myocytes were significantly increased in TIMP-1-/- 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 amplified adverse LV remodeling following MI in mice and emphasizes the importance of local endogenous control of cardiac MMP activity by TIMP-1.
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