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Chronic Heart Rate Reduction Facilitates Cardiomyocyte Survival After Myocardial Infarction
Author(s) -
Zhang RongLin,
Christensen Lance P.,
Tomanek Robert J.
Publication year - 2010
Publication title -
the anatomical record: advances in integrative anatomy and evolutionary biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.678
H-Index - 62
eISSN - 1932-8494
pISSN - 1932-8486
DOI - 10.1002/ar.21081
Subject(s) - ivabradine , atenolol , cardiology , medicine , ejection fraction , endocardium , myocardial infarction , infarction , heart failure , perfusion , heart rate , blood pressure
Chronic heart rate reduction (HRR) therapy following myocardial infarction, using either the pure HRR agent ivabradine or the β‐blocker atenolol, has been shown to preserve maximal coronary perfusion, via reduction of perivascular collagen and a decrease in renin‐angiotensin system activation. In addition ivabradine, but not atenolol, treatment attenuated the decline in ejection fraction and decreased left ventricular wall stress. In this study, we tested the hypothesis that cell survival within the infarct region was enhanced by these two pharmacological agents. Four weeks after ligating the left anterior descending coronary artery, the percentage of the LV that contained the infarct was similar in the untreated (MI) rats and those chronically treated with ivabradine (MI + IVA) or atenolol (MI + ATEN). However, the mean thickness (mm) of the ventricular wall containing the scar was significantly greater in the MI + IVA, 1.54 ( P ≤ 0.01) and the MI + ATEN 1.32, compared to 1.1 in the MI group, due to a 2‐fold greater area of surviving cardiomyocytes ( P ≤ 0.01) in the treated rats compared to the untreated group. Regions of cell survival were usually in the subepicardium, with cardiomyocytes surrounding veins or venules. However, some hearts displayed surviving cells along the endocardium. These data suggest that HRR by either ivabradine or atenolol facilitates a more favorable O2 microenvironment via improved venous flow and decreased O2 demand. We conclude that chronic HRR by these agents may serve to limit infarct expansion and wall thinning and may serve to reduce the potential for ventricular rupture. Anat Rec, 2010. © 2010 Wiley‐Liss, Inc.