Early and late global and regional left ventricular function after experimental transmural myocardial infarction: relationships of regional wall motion, wall thickening, and global performance.
Experimental myocardial infarction of the posterolateral wall of the left ventricle was produced in dogs by injecting 80 micron microspheres into the left circumflex coronary artery to determine changes in regional myocardial function after infarction, to examine how the changes in regional myocardial function relate to the changes in global left ventricular function, and to examine the relationship between regional wall motion and wall thickening after myocardial infarction. Serial measurements of global ventricular and regional myocardial function were made in six dogs before and during 20 days after infarction, with the use of M-mode echocardiography and chronic Swan-Ganz catheter implantation. One hour after infarction, stroke volume index had decreased 49% from baseline, percent fractional shortening had decreased 52%, lateral wall motion had decreased 80%, and lateral wall thickening had decreased 100%. By 6 days after infarction, stroke volume index had increased 41% from its low point, percent fractional shortening had increased 34%, and lateral wall motion had increased 100% toward but not to baseline. Lateral wall thickening did not return following infarction. Peak and end-systolic circumferential wall stresses and systemic arterial blood pressure remained stable. End-systolic diameter increased acutely (36%) after infarction and did not change during the 20-day time period, while end-diastolic diameter gradually increased, resulting in the increase in percent fractional shortening. In conclusion, after posterolateral wall infarction, wall motion can return without an improvement in regional myocardial function, presumably because the infarcted region stiffens, allowing it to be pulled inward.(ABSTRACT TRUNCATED AT 250 WORDS)
D000818:Animals; D001794:Blood Pressure; D002302:Cardiac Output; D004285:Dogs; D004562:Electrocardiography; D006321:Heart / Q000503:physiopathology*; D006352:Heart Ventricles / Q000503:physiopathology; D006439:Hemodynamics; D008297:Male; D009200:Myocardial Contraction; D009203:Myocardial Infarction / Q000473:pathology / Q000503:physiopathology*; D009206:Myocardium / Q000473:pathology*; D013318:Stroke Volume