Myocardial infarction significantly reduced active stiffness of the left ventricle only after complete scarring and thinning had occurred.
Does myocardial infarction alter the active stiffness of the intact left ventricle in dogs?
A functional defect in the overall active stiffness of the ventricle may contribute to the pathogenesis of congestive heart failure due to ventricular aneurysm following complete scarring of a myocardial infarction.
Three methods were employed to measure the overall active stiffness of the intact left ventricle in anesthetized dogs. In two of these, isovolumic contractions of the ventricle were examined, and in the third the response to a minor increase in afterload was analyzed. The average modulus of active stiffness of the normal left ventricle by all three methods was found to be lower than that reported for the cat papillary muscle (57-76%). Myocardial infarction studied 1 hour and 2 to 3 weeks following ligation of the anterior descending coronary artery did not alter active stiffness of the left ventricle. When sufficient time had elapsed, however, for complete scarring and thinning of the infarction to occur, active stiffness was significantly reduced. It is suggested that a functional defect of the overall active stiffness (series elasticity) of the ventricle may be operative in the pathogenesis of congestive failure due to ventricular aneurysm.
Forwand et al. (Tue,) conducted a other in Myocardial infarction. Myocardial infarction (coronary ligation) vs. Normal left ventricle was evaluated on Overall active stiffness of the intact left ventricle. Myocardial infarction significantly reduced active stiffness of the left ventricle only after complete scarring and thinning had occurred.