We assessed the association between the incidence of coronary heart disease and alcohol consumption among hypertensive men enrolled in the Health "Professionals" Follow-Up Study. Moderate alcohol consumption (1 to 2 drinks per day) was associated with a lower risk of myocardial infarction, as in the general population, but was not associated with the risks of stroke, total mortality, or mortality from cardiovascular causes. These results show that men with hypertension who drink moderately may not need to change their drinking habits.
Hypertension, which affected approximately 65 million US adults in 1999,1 approximately doubles the risk of cardiovascular disease. This accounts for 30% of cardiovascular events.2 Moderate alcohol intake (1 to 2 drinks per day) is associated with a lower risk of cardiovascular disease and total mortality than is abstinence,3 but drinking more than 2 drinks per day (ie, 30 g alcohol/day) increases blood pressure and the risk of hypertension.4 There is disagreement regarding recommendations for alcohol consumption among patients with hypertension. A range of a maximum of 2 to 3 drinks per day to complete abstention has been proposed.5,6
To date, 3 studies have reported lower cardiovascular mortality with moderate alcohol consumption among hypertensive patients,7-9 but none has examined the incidence of myocardial infarction (MI). Because alcohol consumption was assessed after diagnosis of hypertension, these studies did not explore changes of alcohol consumption after the diagnosis of hypertension. To evaluate this issue, we assessed the relationship between alcohol consumption and cardiovascular events and mortality among hypertensive subjects enrolled in the Health Professionals Follow-Up Study.
Subjects and methods
In 1986, 51,529 US health professionals aged 40 to 75 years were enrolled in the Health Professionals Follow-Up Study when they responded to a mailed questionnaire regarding their medical and diet history. Every 2 years, a follow-up questionnaire was mailed to participants to collect data on any newly diagnosed illnesses and exposures. For the current study, we included 11,711 hypertensive men from the study who were either diagnosed with hypertension during the follow-up period or reported that they already had hypertension at the start of the study.
Men reported their alcohol consumption every 4 years on a food-frequency questionnaire that included questions about their intake of liquor, red wine, white wine, and beer. Portion size was denoted as a shot of liquor; 4-ounce glass of wine; or can, bottle, or glass of beer. We used Cox proportional hazards models to assess the association for categories of alcohol intake relative to abstainers with risk of fatal or nonfatal coronary heart disease occurring between 1986 and 2002. Other endpoints were stroke and total, cardiovascular, and alcohol-augmented mortality. We adjusted these analyses for lipid-lowering therapy, parental history of MI, aspirin use, hypercholesterolemia, diabetes, body mass index, smoking, age, leisure-time physical activity, energy intake, and energy-adjusted intake of saturated fat, dietary fiber, omega-3 fatty acids, potassium, sodium, magnesium, vitamin E, folate, and trans fatty acids. The influence of beverage type and drinking pattern was assessed in secondary analyses.
A total of 374 nonfatal and 279 fatal MIs occurred over a period of 16 years. As shown in Figure 1, there was generally a dose-dependent inverse relationship between alcohol intake and the risk of MI, both in age-adjusted, smoking-adjusted, and multivariate models. When dietary variables were excluded, the results were not significantly different. These results were similar for fatal and nonfatal endpoints (Figure 1).
Figure 1 Alcohol consumption and risk (95%
confidence interval) of total myocardial
infarction (MI), fatal coronary heart disease,
and nonfatal MI among 11 711 hypertensive men from the Health Professionals Follow-Up Study. Relative risks are adjusted for age, smoking, body mass index, physical activity, diabetes, hypercholesterolemia, family history of MI, aspirin use, lipid-lowering therapy, energy intake, and energy-adjusted quintiles of saturated fat, trans fatty acids, sodium, potassium, magnesium, folate, vitamin E, omega-3 fatty acids, and dietary fiber.
The risk of MI increased with an increase in the number of antihypertensive drugs taken (hazard ratio [HR] for each additional medication = 1.09; 95% confidence interval [CI], 0.97-1.21). However, the association for alcohol consumption remained the same when this factor was included in the analyses. The associations also remained the same after adjustment for use of individual antihypertensive drug classes.
Figure 2 shows the association between alcohol intake and the risk of total, cardiovascular, and coronary heart disease mortality. We did not observe significant associations between alcohol intake and total and cardiovascular mortality, although moderate alcohol intake tended to be associated with lower risk of cardiovascular mortality. When we limited the analysis to ischemic heart disease mortality, an inverse relationship similar to MI endpoints was shown. Mortality from causes usually associated with alcohol use was not associated with alcohol consumption in this population; a few cases (n = 142), however, were seen (data not shown). We also did not observe significant relationships or trends with risk of ischemic stroke, but an association with alcohol use cannot be excluded (data not shown). Liquor was the most common alcoholic beverage used by the participants, and it was also the beverage most strongly associated with lower risk (HR for total MI = 0.59 [95% CI, 0.43-0.80] for participants who drank 10.0-29.9 g liquor/day;  trend < .001).
Figure 2 Alcohol consumption and risks (95% confidence interval) of total and ischemic stroke and total, cardiovascular, and alcohol-augmented mortality among 11,711 hypertensive men from the Health Professionals Follow-Up Study. Relative risks are adjusted for age, smoking, body mass index, physical activity, diabetes, hypercholesterolemia, family history of myocardial infarction (MI), aspirin use, lipid-lowering therapy, energy intake and energy-adjusted quintiles of saturated fat, trans fatty acids, sodium, potassium, magnesium, folate, vitamin E, omega-3 fatty acids, and dietary fiber.
After participants were diagnosed with hypertension, alcohol intake decreased slightly, by 4.0 g/day (interquartile range, 1.9-2.1 g/day), and alcohol intake before and after diagnosis of hypertension was thus highly correlated (Spearman r = 0.83; < .001). Consequently, there was a similar relationship between the risk of MI and alcohol intake when we used prediagnosis and postdiagnosis intake levels (using prediagnosis alcohol intake, HRs for MI = 1.23 [95% CI, 0.86-1.75] for 0.1-9.9 g/day; 0.96 [95% CI, 0.64-1.44] for 10.0-29.9 g/day; and 0.57 [95% CI, 0.33-0.98] for = 30.0 g/day).
Among 11,711 hypertensive men, moderate alcohol intake correlated with a lower risk of fatal and nonfatal MI than abstaining, but did not correlate with risks of total and cardiovascular mortality. We could not accurately assess interactions between total and ischemic stroke and moderate alcohol intake because only a few cases of stroke occurred.
Two previous studies reported an association between alcohol intake and cardiovascular mortality among hypertensive men. A decreased risk of ischemic heart disease mortality among hypertensive men consuming > 21 units of alcohol per week was observed in one study,8 whereas another study showed a linear, inverse association between cardiovascular mortality and alcohol intake among 14,125 men with hypertension.7 However, these studies did not evaluate whether alcohol intake had changed after a diagnosis of hypertension and, if so, whether this affected the association with cardiovascular mortality. Although some men probably reduced their alcohol intake at the suggestion of their doctors once hypertension was diagnosed or because of medications they were taking, major changes in alcohol intake did not occur in our study once hypertension was diagnosed in this group of men. As a result, the lower risk of MI was not significantly different for alcohol intake levels reported before and after diagnosis of hypertension.
Although our study showed a lower risk of MI with moderate alcohol intake and other studies have shown a lower risk of cardiovascular mortality,7,8 there was no significant association between total or cardiovascular mortality and alcohol intake in our study. Only about one third of total mortality, however, was the result of cardiovascular causes. Because cardiovascular mortality is a composite endpoint of fatal MI and deaths from stroke and other cardiovascular diseases that are not as powerfully associated with alcohol intake as MI,10 this may have attenuated the association in our study. When we restricted analyses to ischemic heart disease mortality, we observed a similar lower risk with moderate alcohol consumption, as for MI endpoints.
A possible confounding factor in studies regarding cardiovascular disease and alcohol intake is that a lower risk of coronary heart disease may be the result of a higher risk of other, noncardiovascular-disease—related problems. Significant associations between alcohol intake and alcohol-augmented or cancer mortality were not found in our study, although analyses of alcohol-augmented or cancer mortality were restricted by the fact that there were few cases of these deaths. Therefore, the lower risk of MI shown in our study for heavier drinkers was most likely the result of higher mortality resulting from other causes.
Alcohol consumed from liquor, the most common beverage drunk by the men in our study, had the strongest inverse association with the risk of MI. This is contradictory to a study showing that moderate alcohol intake correlated with lower mortality only among hypertensive patients who drank wine.9 That study and our study are in line with the belief that the beverage most widely consumed by a certain population is most likely to be associated with a lower risk of cardiovascular disease in that population.11 This makes it probable that the risk reduction of MI results from ethanol itself. This lower risk with moderate alcohol consumption can be explained by an increase in high-density lipoprotein cholesterol,12 a decrease in inflammatory factors,13 improved insulin sensitivity,14 or a change in thrombogenic markers.12
As is the case in the general population, moderate alcohol intake among hypertensive men was associated with a lower risk of MI in our study. There was no significant correlation between alcohol intake and total or cardiovascular mortality. Although hypertensive patients should be evaluated individually, moderate drinkers may not need to change their drinking habits.