Influence of pattern of drinking on cardiovascular disease and cardiovascular risk factors-a review

• Published in: Addiction (Abingdon, England) England), 1999-05, Vol.94 (5), p.649-663
• Main Authors: Puddey, I. B., Rakic, V., Dimmitt, S. B., Beilin, L. J.
• Format: Article
• Language: English
• Subjects: Addictive behaviors; Adult and adolescent clinical studies; Alcohol; Alcohol consumption; Alcohol Drinking - adverse effects; Alcohol use; Alcoholism; Arteriosclerosis - etiology; Arteriosclerosis - prevention & control; Biological and medical sciences; Brain Ischemia - etiology; Cardiovascular disease; Cardiovascular diseases; Cardiovascular Diseases - blood; Cardiovascular Diseases - etiology; Cardiovascular Diseases - prevention & control; Cholesterol, HDL - blood; Effects; Health; Heart disease; Humans; Hypertension - etiology; Medical sciences; Psychology. Psychoanalysis. Psychiatry; Psychopathology. Psychiatry; Public health; Public policy; Relationship; Risk; Risk Factors
• ISSN: 0965-2140; 1360-0443
• DOI: 10.1046/j.1360-0443.1999.9456493.x

There is an established inverse relationship between the regular light consumption of alcohol (5‐10 g/day) and the incidence of coronary artery disease (CAD). This association has several biologically plausible mechanisms with dose‐dependent effects of alcohol to increase HDL cholesterol, lower plasma fibrinogen and inhibit platelet aggregation. However, such a protective effect against atheroma cannot be considered in isolation from known adverse effects on blood pressure and triglycerides or possible detrimental effects of episodic or binge drinking on several other cardiovascular end‐points and risk factors. In subjects with pre‐existing CAD, an alcoholic binge can increase both silent myocardial ischaemia and angina. During withdrawal following binge drinking, marked fluctuations in blood pressure together with heightened platelet activation and adverse changes in the balance of fibrinolytic factors, may offer an explanation for the reported association between episodic heavy drinking and ischaemic stroke. This has been seen particularly in young males and extends further to an increase in both subarachnoid haemorrhage and intracerebral haemorrhage after binge drinking. Intervention studies in man have shown acute increases in blood pressure in men who drink predominantly at weekends, compared to longer‐term pressor effects in regular daily drinkers. We have been unable, however, to reproduce the finding of unfavourable effects of binge drinking on the lipid profile that have been reported in animal studies and man. Binge drinking may also induce cerebrovascular spasm or cause both ventricular and supraventricular arrhythmias, especially atrial fibrillation. Alcohol‐induced arrhythmia has been postulated as the basis for alcohol‐related sudden coronary death in those subjects with pre‐existing CAD. Hence, further exploration of any protective association of alcohol against CAD needs to carefully consider the implications of pattern of drinking for the relationship. The modulating influences of co‐timing of drinking with meals, cigarette smoking or illicit drug use also need to be evaluated. Without such vital information, public health advice on alcohol and CAD will be limited in its scope and potentially flawed in its impact.