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OBJECTIVE: Epidemiologic studies have shown that individuals who consume low-moderate doses of alcohol have a lower risk of developing cardiovascular disease compared to abstainers. However, the effect of alcohol on ischemic myocardium is still unclear. We developed a clinically relevant animal model of chronic myocardial ischemia to investigate the effects of moderate alcohol consumption on ischemic myocardium.
Design: Swine model of chronic myocardial ischemia and alcohol consumption.

Setting: Basic science laboratory.

PATIENTS/PARTICIPANTS: Fourteen Yorkshire swine.

INTERVENTION:
Diet: Animals were supplemented with 90mL 50% ethanol (ETOH n=7) or 80g sucrose daily (SUC n=7) to normalize caloric intake between groups.
Surgical: All animals underwent placement of an ameroid constrictor to the left circumflex artery to induce chronic myocardial ischemia. After seven weeks, the animals were sacrificed, and the chronically ischemic myocardium was harvested.

MAIN OUTCOME MEASURE: Tissues were analyzed for protein expression and stained for apoptosis quantification.
RESULTS: Alcohol down-regulated pro-apoptotic proteins FOX03, BAD and caspase 9. Alcohol also attenuated MTOR signaling by increasing expression of AMPK and Deptor (see table). There was also a significant reduction in apoptotic cells in the ETOH group compared to SUC (see figure).
CONCLUSION: Alcohol consumption down regulates apoptosis and promotes cell survival in ischemic myocardium. Ethanol also modulates MTOR signaling, which regulates senescence and apoptosis. Perhaps MTOR and apoptosis regulation is another mechanism by which moderate ethanol consumption is cardioprotective.