Alcohol and Coronary Spasm

Alcohol is known to sometimes cause coronary spasm, the mechanism of which is still unknown. The authors monitored changes in plasma levels of prostanoids (thromboxane [TX B ₂], 6-keto prostaglandin F_1α [PGF_1α]), catecholamines (CA), serotonin (5-HT), cyclic nucleotides (cyclic adenosine monophosphate—cAMP, cyclic guanosine monophosphate— cGMP), and platelet aggregation after alcohol ingestion (Japanese rice wine 400 mL) in 8 patients with alcohol-induced variant angina and 8 healthy men as controls. Coronary spasm was confirmed to have been induced in 4 patients nine hours after alcohol challenge (VA[+]), when their plasma ethanol levels had already returned to a null level. Neither CA nor 5-HT levels showed any change after alcohol ingestion either in patients or controls, though controls showed high levels of CA during alcohol ingestion. TX B2 in VA (+) patients increased gradually after alcohol ingestion to reach up to a statistically signifi cantly high level just before attack, as compared with those of controls and VA(-) patients, who, on the contrary, did not show such changes. The levels of 6-keto PGF_1α, however, which were significantly lower in patients than in controls before the test, exhibited a gradual increase in VA (+) patients in parallel with the increase in TX B₂.

No significant changes in cAMP levels between either controls or patients were present.

On the contrary, cGMP levels had a gradual decrease in patients after alcohol ingestion. Especially six hours after alcohol ingestion, cGMP levels in VA (+) patients decreased so much as to make a statistically significant difference, as compared with the level in controls.

Platelet aggregability in controls showed a decrease after alcohol ingestion, in spite of no change or even increase in patients.

These data suggest that low levels of PGF_1α and the decrease of cGMP levels from alcohol ingestion play important roles in the mechanism of coronary spasm induced by alcohol ingestion.