Lack of effect of aspirin on myocardial infarct size in the dog

Pretreatment with platelet-inhibitory doses of aspirin (3 mg/kg body weight) has been shown to augment epicardial collateral flow by more than 50 percent (p <0.05) 4 hours after ligation of the left anterior descending coronary artery in dogs. To determine whether this favorable influence of aspirin is sufficient to decrease the amount of infarcted tissue, either intravenous aspirin, 3 mg/kg (n = 17), or saline solution (n = 17) was administered to dogs 10 minutes before occlusion of the left anterior descending coronary artery. Administration of saline solution or aspirin was repeated every 24 hours. By 72 hours, 5 dogs in each treatment group had died. Survivors were killed at 72 hours. The portion of the left ventricle at risk of infarction was delineated by perfusion of the aortic root with Evans blue and simultaneous perfusion of the distal left anterior descending coronary artery with saline solution under equal physiologic pressures. Slices of the stained heart were incubated with triphenyl-tetrazolium to identify gross infarct (with histologic confirmation). Total mass of left ventricle, myocardium at risk, and infarct size were measured in each dog. A direct relation was found between the mass at risk and the mass infarcted (r = 0.84, p <0.001). Aspirin-treated dogs did not differ from control dogs in percent ventricle at risk (mean ± standard error 7 ± 2 versus 40 ± 2), percent infarct weight/left ventricle (29 ± 3 versus 31 ± 2) or percent infarct weight/weight of ventricle at risk (78 ± 4 versus 77 ± 3). Thus, despite aspirin's ability to inhibit platelet aggregation and to increase epicardial collateral flow by more than 50 percent, aspirin treatment failed to reduce infarct size in this dog model.