In rats 3 weeks post-myocardial infarction, maximal extent of cell shortening at high extracellular calcium was significantly less in MI myocytes compared to sham (16% vs. 22%).
Depressed LV function in post-MI hearts is driven by both cellular abnormalities in calcium handling and global structural changes.
Absolute Event Rate: 16% vs 22%
The inotropic responsiveness of isolated perfused rat hearts and single left ventricular (LV) myocytes to extracellular Ca2+ (Ca2+o) was examined 3 wk after ligation of left main coronary artery. Myocytes isolated from myocardial infarcted (MI) hearts were 10% longer. At Ca2+o of 1.1 mM, cell shortening as well as intracellular Ca2+ concentration dynamics were similar between MI and sham LV myocytes. At Ca2+o of 4.9 mM, maximal extent of cell shortening was significantly less in MI myocytes (16 +/- 1 vs. 22 +/- 1%), and peak intracellular Ca2+ concentration was also substantially lower. Thus, under conditions of high Ca2+o, decreased sarcolemmal Ca2+ influx and Ca2+ release during excitation-contraction may contribute to systolic dysfunction in MI hearts. Perfused working hearts and isovolumic heart preparations with infarcted LV displayed depressed maximal systolic pressure and decreased sensitivity to the inotropic effects of Ca2+o. Our data also indicate that, in addition to possible abnormalities in the contractile response of single myocytes, global factors such as loss of functional myocardium, altered chamber geometry, tissue fibrosis, and/or subendocardial ischemia contributed to depressed LV function in post-MI hearts perfused at physiological Ca2+o.
Cheung et al. (Sat,) conducted a other in Myocardial infarction. Myocardial infarction (ligation of left main coronary artery) vs. Sham was evaluated on Maximal extent of cell shortening at [Ca2+]o of 4.9 mM. In rats 3 weeks post-myocardial infarction, maximal extent of cell shortening at high extracellular calcium was significantly less in MI myocytes compared to sham (16% vs. 22%).