907-104 Endothelial Injury at a Transiently Occluded Coronary Artery Increases Myocardial Leukocyte Content and Necrosis. Effect of Aspirin

Coronary ligature with minimal intimal injury reproduces only in part acute coronary syndrome, in which reperfusion occurs through an extensively damaged artery. To analyze the influence of coronary endothelial injury (El) on PMN leukocyte accumulation and infarct size, 48 pigs were allocated to catheterization and endothelial denudation of the LAD or to no intervention immediately before a 48 min coronary occlusion and 6 h of reperfusion. Ninety min before they had received aspirin (ASA, 250 mg e.v.), or placebo (2 × 2 factorial design). Twelve animals presented reocclusion and were excluded for subsequent analysis, 2 of them receiving ASA and 10 not (p l 0.05). In the remaining pigs, blood flow (ml/[min.g]) in the area at risk was similar in those with than in those without EI. 30 min (2.2 ± 0.3 vs 2.3 ± 0.4) and 5 h (1.4 ± 0.2 vs 1.4 ± 0.2) after reflow. and was not modified by ASA. Infarct size (% of the area at risk, TIC reaction) was greater in pigs with EI. A significant interaction (p = 0.03) between El and ASA was detected, El being associated with larger infarcts in animals receiving placebo, but not in those receiving ASA: No EI (n = 18) EI (n = 18) p value Placebo (n = 18) 11 ± 4 36 ± 7 0.006 ASA (n = 18) 22 ± 6 20 ± 6 NS Myocardial content of PMNs (quantitative histology) in the area at risk was higher in animals with than in those without El (mean scores 4.9 ± 0.6 vs 3.0 ± 0.6, p = 0.04), and was not modified by ASA. In 12 additional experiments with 30 min coronary occlusion (no infarct), the content of Tc99 labeled PMNs in the area at risk was significantly increased in pigs with El (144 ± 23% of control myocardium), but not in those without (p = 003). Thus, El at the site of a transient coronary occlusion increases myocardial PMN content and necrosis. ASA reduces reocclusion rate and limits the deleterious effect of EI on infarct size in animals without reocclusion. This effect could be due to impared PMN-platelet cooperation, or to a direct effect of ASA on function of adhered PMNs.