Excessive alcohol intake is known to promote the development of hypertension. However, some studies have found a J-shaped curve when alcohol consumption is compared with blood pressure [1]. Furthermore, several studies have reported a lower incidence of coronary heart disease in light-to-moderate drinkers than in those who abstain, possibly because of increased levels of high-density lipoprotein cholesterol [2]. Therefore, the overall benefits and risks brought about by alcohol intake should be carefully assessed before hypertensive patients are advised about alcohol intake. The ultimate purpose of antihypertensive therapy is to inhibit target-organ injuries and cardiovascular diseases. This should be considered when the optimal alcohol intake for a hypertensive patient is being evaluated; however, little work has been done to determine the relation between alcohol intake and development of hypertensive organ injuries.

We investigated the influence of alcohol intake on cardiac hypertrophy in 302 untreated hypertensive patients who were selected from 4557 men who entered the health-check program of our institute from 1990 to 1994. Hypertension was defined as blood pressure exceeding 140/90 mm Hg after 15 minutes of supine rest. According to the daily alcohol consumption obtained by a self-administered questionnaire, the patients were classified into four categories: nondrinker (0 to 10 mL of ethanol per day), light drinker (11 to 29 mL/d), moderate drinker (30 to 58 mL/d) and heavy drinker ( 59 mL/d). A 12-lead resting electrocardiogram was recorded, and signs of left ventricular hypertrophy were evaluated using the revised Minnesota code [3]. Although blood pressure levels were similar among the groups, electrocardiographic findings of left ventricular hypertrophy were increased in moderate and heavy drinkers but not in light drinkers (Table 1) (P < 0.01). Serum -glutamyl transpeptidase and triglyceride levels were increased in moderate and heavy drinkers, which suggests that alcohol intake was reported reliably. Serum levels of high-density lipoprotein cholesterol were increased even among light drinkers compared with nondrinkers, but no change was seen in total cholesterol levels.

These findings suggest that habitual consumption of ethanol in excess of 29 mL/d facilitates the development of left ventricular hypertrophy in hypertensive patients, even when blood pressure is not elevated. Hypertensive patients who are light drinkers seem to receive the greatest benefit in terms of the prevention of organ injuries and reduction of risks for cardiovascular disease. Thus, our investigation shows that excessive alcohol intake is associated with an increased occurrence of left ventricular hypertrophy that is independent of blood pressure in hypertensive patients. In addition to alcohol-induced myocardial damage, the mechanism of this increased cardiac hypertrophy in moderate drinkers may involve the effects of long-term alcohol consumption on whole-day blood pressure variation and humoral factors such as angiotensin II and catecholamines, which are known to stimulate cardiomyocyte hypertrophy [4, 5].