Gender does not influence acute myocardial infarction in adult dogs

Mechanisms responsible for the well-documented "protection" against myocardial ischemia and infarction in young women and subsequent loss of protection after menopause remain speculative. One possibility is that gender-related variables (such as endogenous hormone levels or regular loss of stored iron) alter the susceptibility of the heart to ischemia: if so, then premenopausal women when compared with men may manifest endogenous protection against acute myocardial ischemic injury. Using the canine model we therefore sought to determine whether gender influences acute myocardial ischemia and infarction. Retrospective analysis was performed on data compiled from 60 mature adult dogs subjected to 1 hour of coronary artery occlusion and ≥4 hours of reperfusion. We first compared the incidence of lethal ventricular fibrillation in the male and female cohorts and then for survivors compared collateral blood flow during coronary occlusion (by injection of radioactive microspheres), infarct size (assessed by tetrazolium staining and expressed as a percentage of the myocardium at risk), and regional wall motion (by somomicrometry) in the infarct-related area. The incidence of lethal ventricular fibrillation was 23% in the male dogs and 19% in the female dogs ( p = 0.70, difference not significant). For survivors, the area at risk of infarction was comparable in males and females (23 ± 2% and 22% ± 1% of the total left ventricular weight), and the groups were equally ischemic during coronary occlusion, with collateral blood flow to the ischemic subendocardium averaging 0.05 ± 0.02 and 0.07 ± 0.01 ml/min/g tissue. There was no difference in infarct size between the two cohorts: area of necrosis was 17% ± 6% and 18% ± 3% of the myocardium at risk in the males and females, respectively. In addition, the groups were equally dyskinetic during occlusion and equally hypokinetic after reperfusion. We conclude that gender does not influence acute myocardial ischemia and infarction in the canine model.