ST SEGMENT ELEVATION AT THE SURFACE OF A HEALED TRANSMURAL MYOCARDIAL-INFARCTION IN PIGS - CONDITIONS FOR PASSIVE TRANSMISSION FROM THE ISCHEMIC PERIINFARCTION ZONE

Background Ischemia of the myocardium surviving an infarction induces ST segment elevation in infarct-related ECG leads. In cases with no vi able tissue, ischemia adjacent to the infarction could induce a simila r ECG pattern if there is ST segment potential transmission through th e necrotic scar. We analyzed whether acute ischemia adjacent to a heal ed infarction with no viable tissue may induce ST segment elevation on the surface of the necrotic scar. Methods and Results Epicardial ST s egment changes elicited during 30 minutes of acute reocclusion of the left anterior descending (LAD) coronary artery 2 cm above the first di agonal branch were analyzed by 32-channel mapping in 18 chloralose-ane sthetized open-chest pigs with 1-month-old anterior infarctions induce d by permanent ligature below the first diagonal branch (group 1). The effect of a previous infarction on the magnitude of ischemic ST segme nt changes was assessed by similar mapping in 21 control pigs submitte d to a LAD ligature 2 cm above the first diagonal branch (group 2, n=1 1) or just below this branch (group 3, n=10). Myocardial perfusion aft er coronary ligature was estimated in 7 pigs with chronic infarction a nd in 3 control pigs by mapping of myocardial technetium-99m-methoxyis obutyl isonitrile (Tc-99m-MIBI) activity in transmural samples underly ing each epicardial electrode. The width of cell layers surviving the infarction was measured and their viability after 60 minutes of corona ry reocclusion was assessed by intracellular glycogen staining. Reoccl usion of the LAD induced parallel ST segment elevation at the periinfa rction zone and at the necrotic scar, although in the latter region th e changes were less marked (maximal ST segment, 8.4+/-3.0 mV versus 2. 7+/-1.8 mV, ANOVA, P<.001). ST seg ment elevation inside the scar was greater at the margins (3.9+/-1.8 mV) than at sites 20 mm toward the c enter (2.8+/-1.7 mV, P=.003). The necrotic area was virtually devoid o f surviving cells except for a 0.22+/-0.04-mm-wide subendocardial band that continued to show a positive intracellular glycogen reaction aft er the second LAD ligature. Acute ischemia adjacent to the infarction (group 1) induced lower ST segment elevation than acute ischemia at a comparable cardiac region in noninfarcted pigs (group 2) (ANOVA, P=.02 ), despite the fact that these areas developed similar underperfusion after coronary occlusion (percent MIBI activity of that in normal myoc ardium, 7+/-8 versus 7+/-6, P=NS). ST segment changes in group 2 pigs were comparable to those induced in group 3 pigs with a 2-cm-lower cor onary occlusion. Conclusions Acute ischemia adjacent to a chronic infa rction induces ST segment elevation at the surface of the scar despite the virtual absence of viable tissue within the infarction. Data sugg est a passive ST segment potential transmission through the infarction . Moreover, ischemia adjacent to a chronic infarction induces lower ST segment elevation than ischemia not adjacent to a necrosis. The mecha nisms accounting for these regional differences are probably independe nt of collateral myocardial perfusion and ischemia extension.