Unfavorable left ventricular remodeling due to experience of chronic sleep restriction after myocardial infarction: The role of matrix metalloproteinases & oxidative stress

Disturbed sleep or sleep loss due to vocational or lifestyle changes following MI is a common problem that may affect many physiological processes involved in left ventricle (LV) remodeling. Herein, we pro-posed that experience of sleep disruption and/or restriction after myocardial infarction (MI) may aggra-vate cardiac extracellular matrix remodeling and induce apoptosis in the cardiomyocytes. MI was induced in adult male rats by permanent ligation of the left anterior descending coronary artery. Twenty-four hours after surgery, some animals experienced chronic sleep restriction (CSR) for 6 days. Serum levels of CK-MB, PAB, and TNF-alpha were evaluated at days 1, 8, and 21 postsurgery. Twenty-one days after surgery, hemodynamic parameters and expression of MMP-2, MMP-9, TIMP-1, and TNF-alpha, as well as myocardial fibrosis and apoptosis in the noninfarcted area of the LV were assessed. Our results showed a clear de-crease in serum concentrations of CK-MB, PAB and TNF-alpha at day 21 postsurgery in the MI group as compared to MI + SR animals in which these markers remained at high levels. CSR following MI deteri-orated LV hemodynamic indexes and also impaired the balance between MMPs and TIMP-1. Further, it yielded an increase in oxidant and inflammatory state which caused deleterious fibrotic and apoptotic effects on cardiomycytes. Our data suggest post-MI sleep loss may cause adverse LV remodeling due to increased inflammatory reactions as well as oxidative burden and/or anti-oxidative insufficiency that in turn impede the balance between MMPs and their inhibitors.(c) 2022 Elsevier Inc. All rights reserved.