Interactions between alcohol and cardiovascular medications

Alcohol Health & Research World, Summer, 1990 by Barbara A. Thomas, Timothy J. Regan

Warfarin

Occasional or moderate drinking is unlikely to affect significantly the anticoagulant action of warfarin. Continuous heavy alcohol consumption is a different story. Saunders and Williams (1984) cited a case of a patient who was treated with warfarin and who developed a severe hemorrhagic tendency after a 5-day bout of heavy drinking. Chronic alcohol abuse may impair drug metabolism in the liver or synthesis of clotting factor precursors in the liver (Shinn and Shrewsbury 1988), with the result that the effects of warfarin intensify. Although Kater and colleagues (1969) found that warfarin was removed more rapidly from the blood of a group of alcoholics, they also noted that prothrombin time, an indicator of impaired coagulation, did not increase. This suggests that the mechanism underlying the warfarin-alcohol interaction is enhanced hepatic metabolism.

Pelkonen and Sotaniemi (1982) studied the warfarin-alcohol interaction at the cellular and biocehmical levels. They found normal or elevated levels of the enzymes responsible for metabolizing warfarin in healthy liver tissue taken from alcoholic patients. In contrast, they found decreased levels of these enzymes in apparently diseased liver tissue taken from alcoholic patients. These findings suggest that alcohol's effect on metabolism of warfarin may be influenced by the presence of liver disease in alcoholics.

Aspirin

Aspirin blocks the synthesis of thromboxane [A.sub.2], a factor required for induction of the clotting process. The effect is cumulative, because aspirin permanently inactivates the enzyme involved in the synthesis; however, the effect is short lived, because platelets have a lifespan of only 7-10 days (Majerus et al. 1990). Alcohol enhances the anticlotting effect of aspirin, leading to prolongation of bleeding time (Shinn and Shrewsbury 1988). Using in vitro studies, Jakubowski and colleagues (1988) found that alcohol mildly inhibited production of thromboxane [A.sub.2]; in the presence of aspirin, alcohol's inhibition of platelet aggregation was found to be dose-dependent.

CONCLUSIONS

Alcohol clearly interacts with many cardiovascular medications. Many of the interactions are mild, so that physicians may feel justified in overlooking them. However, in light of the evidence of alcohol's contributions to the etiology of high blood pressure, cardiac arrhythmias, cardiomyopathy, and stroke, physicians would probably best serve patients by recommending strict limitation of alcohol intake. Because of the range of effects that alcohol has on drug metabolism, cardiovascular patients taking medications should be made aware of possible effects of concurrent alcohol use.

Because alcohol use is prevalent in our society, because it is sometimes concealed, and because inadvertent exposure to alcohol is fairly common, physicians should consider alcohol's interactions with medications when trying to understand a patient's idiosyncratic responses to cardiovascular medications. Physicians should be especially aware of the fact that drug metabolism may be modified significantly in heavy drinkers and former alcoholics, even in the absence of liver disease. Finally, special care should be taken when managing cardiovascular emergencies in persons who have consumed alcohol.