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Am J Physiol Heart Circ Physiol 276: H873-H880, 1999;
0363-6135/99 $5.00
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Vol. 276, Issue 3, H873-H880, March 1999

Effects of AT1 receptor blockade after myocardial infarct on myocardial fibrosis, stiffness, and contractility

Hoang M. Thai, Hohai T. Van, Mohamed A. Gaballa, Steven Goldman, and Thomas E. Raya

Department of Internal Medicine, Veterans Affairs Medical Center and Sarver Heart Center, University of Arizona, Tucson, Arizona 85723

Angiotensin II type 1 (AT1) receptor blockade attenuates myocardial fibrosis after myocardial infarction (MI). However, whether inhibition of fibrosis by AT1 receptor blockade influences myocardial stiffness and contractility is unknown. We measured left ventricular (LV) hemodynamics, papillary muscle function, and myocardial stiffness and fibrosis in rats randomized to losartan or placebo 1 day after MI and treated subsequently for 8 wk. Losartan decreased LV and right ventricular weights as well as mean aortic and LV systolic pressures in sham and MI rats. LV end-diastolic pressure increased after MI and was decreased with losartan. Maximal developed tension and peak rate of tension rise and decline were decreased in MI vs. sham rats. Interstitial fibrosis developed after MI and was prevented in losartan-treated MI rats. The development of abnormal myocardial stiffness after MI was prevented by losartan. After MI, AT1 receptor blockade prevents an abnormal increase in myocardial collagen content. This effect was associated with a normalization of passive myocardial stiffness.

heart failure; fibrosis; angiotensin II; stress-strain


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