Losartan treatment for 8 weeks after myocardial infarction in rats prevented the abnormal increase in myocardial collagen content and normalized passive myocardial stiffness.
RCT
randomized
Does losartan prevent myocardial fibrosis and abnormal stiffness in rats after myocardial infarction?
AT1 receptor blockade with losartan after myocardial infarction in rats prevents abnormal increases in myocardial collagen content and normalizes passive myocardial stiffness.
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.
Thai et al. (Mon,) conducted a rct in myocardial infarction. losartan vs. placebo was evaluated on LV hemodynamics, papillary muscle function, and myocardial stiffness and fibrosis. Losartan treatment for 8 weeks after myocardial infarction in rats prevented the abnormal increase in myocardial collagen content and normalized passive myocardial stiffness.