06 May 2014 In Cardiovascular System

Alcohol has complex effects on the cardiovascular system. The purpose of this article is to review physio-pathological effects of alcohol on cardiovascular and related systems and to describe its role in hypertension and cardiovascular disease. The relationship between alcohol and hypertension is well known, and a reduction in the alcohol intake is widely recommended in the management of hypertension. Moreover, alcohol has both pressor and depressor actions. The latter actions are clear in Oriental subjects, especially in those who show alcohol flush because of the genetic variation in aldehyde dehydrogenase activity. Repeated alcohol intake in the evening causes an elevation in daytime and a reduction in nighttime blood pressure (BP), with little change in the average 24-h BP in Japanese men. Thus, the hypertensive effect of alcohol seems to be overestimated by the measurement of casual BP during the day. Heavy alcohol intake seems to increase the risk of several cardiovascular diseases, such as hemorrhagic stroke, arrhythmia and heart failure. On the other hand, alcohol may act to prevent atherosclerosis and to decrease the risk of ischemic heart disease, mainly by increasing HDL cholesterol and inhibiting thrombus formation. A J- or U-shaped relationship has been observed between the level of alcohol intake and risk of cardiovascular mortality and total mortality. It is reasonable to reduce the alcohol intake to less than 30 ml per day for men and 15 ml per day for women in the management of hypertension. As a small amount of alcohol seems to be beneficial, abstinence from alcohol is not recommended to prevent cardiovascular disease.

06 May 2014 In Cardiovascular System

BACKGROUND: Moderate alcohol intake is associated with lower risk of coronary heart disease (CHD), but the association with sudden cardiac death (SCD) is less clear. In men, heavy alcohol consumption may increase risk of SCD, whereas light-to-moderate alcohol intake may lower risk. There are no parallel data among women.

OBJECTIVE: The purpose of this study was to assess the association between alcohol intake and risk of SCD among women and to investigate how this risk compared to other forms of CHD.

METHODS: We conducted a prospective cohort study among 85,067 women from the Nurses' Health Study who were free of chronic disease at baseline. Alcohol intake was assessed every 4 years through questionnaires. Primary endpoints included SCD, fatal CHD, and nonfatal myocardial infarction.

RESULTS: We found a U-shaped association between alcohol intake and risk of SCD, with the lowest risk among women who drank 5.0-14.9 g/day of alcohol (P for quadratic trend = 0.02). Compared to abstainers, the multivariate relative risk (95% confidence interval) for SCD was 0.79 (0.55-1.14) for former drinkers, 0.77 (0.57-1.06) for 0.1-4.9 g/day, 0.64 (0.43-0.95) for 5.0-14.9 g/day, 0.68 (0.38-1.23) for 15.0-29.9 g/day, and 1.15 (0.70-1.87) for >/=30.0 g/day. In contrast, the relationship of alcohol intake and nonfatal and fatal CHD was more linear (P for linear trend <.001).

CONCLUSION: In this cohort of women, the relationship between light-to-moderate alcohol intake and SCD is U-shaped, with a nadir at 5.0-14.9 g/day. Low levels of alcohol intake do not raise the risk of SCD and may lower risk in women.

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