FUNCTIONAL-CHARACTERIZATION OF LEFT-VENTRICULAR SEGMENTAL RESPONSES DURING THE INITIAL 24-H AND 1-WK AFTER EXPERIMENTAL CANINE MYOCARDIAL-INFARCTION

Characterization of the temporal evolution of resting segmental function and inotropic reserve after coronary occlusion may be important in evaluating attempts to salvage ischemic but non-necrotic myocardium. Accordingly, we chronically implanted up to six pairs of pulse-transient piezoelectric crystals in the left ventricular myocardium of dogs to measure segmental wall thickness. Segments were separated into groups according to the loss of net systolic thickening (NET) at 5 min postocclusion of the left anterior descending coronary artery in awake, unsedated dogs. Group 1 included segments with NET values of 67-100+ (percent control); group 2 between 67 and 0; and group 3<0 (paradoxical motion). 5 min after coronary occlusion, group 1 NET was 92±5% (SEM) although significant decreases occurred in NET in group 2 (36±4%) and group 3 segments (-33±5%). Between 5 min and 24 h after coronary occlusion, no further significant changes occurred in NET in groups 1, 2 and 3 crystals. Some segments underwent further functional deterioration between 24 h and 1 wk after left anterior descending coronary artery occlusion, although no overall change occurred in segments with mild to moderate ischemic dysfunction. Segments with NET <0 at 24 h, on the other hand, exhibited a reduction in aneurysmal bulging between 24 h and 1 wk from =41±10 to -23±11% (n=12, P=0.02). Inotropic reserve was assessed with postextrasystolic potentiation (PESP) in 14 dogs, and with infusions of dopamine (11 dogs), and isoproterenol (13 dogs). PESP was the most potent intervention and produced a significant augmentation in NET in group 2 crystals at 1, 2, 4, 6, 8, and 24 h after coronary occlusion but only at 1 and 2 h in NET in group 3 crystals. Thus, following experimental coronary occlusion, the evolution of ischemic segmental dysfunction is dynamic and variable. A significant degree of inotropic reserve, as assessed by PESP, dopamine, and isoproterenol, exists in segments with moderate ischemic dysfunction for 24 h but for only 2 h after coronary occlusion in those segments with the most severe ischemic dysfuncton. In addition, at least some segmental sites with mild to moderate ischemic dysfunction at 24 h deteriorate further between 24 h and 1 wk after experimental coronary occlusion.