title: Experimental myocardial infarction: XII. Dynamic changes in segmental mechanical behavior of infarcted and non-infarcted myocardium.
abstract: The mechanical behavior of ischemic myocardium was studied in anesthetized open chest dogs. In each animal, a small well localized myocardial infarction was produced by ligation of a single ventricular branch of the left circumflex coronary artery. Serial in situ measurements of segment length were made by mercury-in-Silastic gauges sutured directly to the left ventricular surface. After coronary ligation, systolic aneurysmal bulging of the ischemic segment was uniformly noted. This was quantified as follows: normalized segment length change in this region, expressed in muscle lengths (where muscle lengths = phasic segment length amplitude/end-diastolic segment length), immediately increased from 0.06 +/- 0.01 (standard error of the mean) to 0.10 +/- 0.02 muscle lengths (+67 percent, P less than 0.02). Over a 6 hour period, muscle lengths progressively declined to near control values, but retained an aneurysmal contour. End-diastolic segment length increased 5 percent above control values after coronary occlusion and remained fixed at this level for 6 hours. In contrast, noninfarcted myocardium exhibited no significant changes in muscle length or end-diastolic segment length. These studies demonstrate that the degree of systolic aneurysmal bulging in infarcted myocardium, although initially great, resolves within 6 hours but retains an aneurysmal contour. These findings are consistent with either partial return of contractility or diminished local compliance, but persistence of an aneurysmal shape favors the latter mechanism. The fixed increase in end-diastolic segment length suggests that "stress-relaxation" takes place in the infarcted region. It is possible that diminished compliance in zones of infarction, previously noted after several days, begins within a few hours after the onset of ischemia.
mesh_terms: D000818:Animals; D003187:Compliance; D003331:Coronary Vessels / Q000503:physiopathology; D006322:Heart Aneurysm / Q000209:etiology / Q000503:physiopathology; D006352:Heart Ventricles / Q000503:physiopathology*; D009200:Myocardial Contraction; D009203:Myocardial Infarction / Q000150:complications / Q000503:physiopathology*; D051381:Rats; D013997:Time Factors