Association of alcohol consumption with morbidity and mortality in patients with cardiovascular disease: original data and meta-analysis of 48,423 men and women

Abstract

Background: Light-to-moderate alcohol consumption has been reported to be cardio-protective among apparently healthy individuals; however, it is unclear whether this association is also present in those with disease. To examine the association between alcohol consumption and prognosis in individuals with pre-existing cardiovascular disease (CVD), we conducted a series of meta-analyses of new findings from three large-scale cohorts and existing published studies.

Methods: We assessed alcohol consumption in relation to all-cause mortality, cardiovascular mortality, and subsequent cardiovascular events via de novo analyses of 14,386 patients with a previous myocardial infarction, angina, or stroke in the UK Biobank Study (median follow-up 8.7 years, interquartile range [IQR] 8.0-9.5), involving 1640 deaths and 2950 subsequent events, and 2802 patients and 1257 deaths in 15 waves of the Health Survey for England 1994-2008 and three waves of the Scottish Health Survey 1995, 1998, and 2003 (median follow-up 9.5 years, IQR 5.7-13.0). This was augmented with findings from 12 published studies identified through a systematic review, providing data on 31,235 patients, 5095 deaths, and 1414 subsequent events. To determine the best-fitting dose-response association between alcohol and each outcome in the combined sample of 48,423 patients, models were constructed using fractional polynomial regression, adjusting at least for age, sex, and smoking status.

Results: Alcohol consumption was associated with all assessed outcomes in a J-shaped manner relative to current non-drinkers, with a risk reduction that peaked at 7 g/day (relative risk 0.79, 95% confidence interval 0.73-0.85) for all-cause mortality, 8 g/day (0.73, 0.64-0.83) for cardiovascular mortality and 6 g/day (0.50, 0.26-0.96) for cardiovascular events, and remained significant up to 62, 50, and 15 g/day, respectively. No statistically significant elevated risks were found at higher levels of drinking. In the few studies that excluded former drinkers from the non-drinking reference group, reductions in risk among light-to-moderate drinkers were attenuated.

Conclusions: For secondary prevention of CVD, current drinkers may not need to stop drinking. However, they should be informed that the lowest risk of mortality and having another cardiovascular event is likely to be associated with lower levels of drinking, that is up to approximately 105g (or equivalent to 13 UK units, with one unit equal to half a pint of beer/lager/cider, half a glass of wine, or one measure of spirits) a week.

Keywords: Alcohol; Cardiovascular disease; Meta-analysis; Mortality; Secondary prevention.

Fig. 1

Association of drinking categories with all-cause mortality, cardiovascular mortality, and cardiovascular events by study cohorts. Hazard ratios are adjusted for age, sex, smoking status, diabetes, hypertension, socioeconomic position or education, body mass index, and regular use of cholesterol-lowering medications, antihypertensive medications, antiplatelet agents, digoxin, and warfarin. CI indicates confidence interval; HR, hazard ratio; HSE, the Health Survey for England; SHeSs, the Scottish Health Survey

Fig. 2

Overall dose-response relationship between alcohol consumption and risk of mortality and subsequent cardiovascular events, using maximally-adjusted estimates. Best-fitting second-degree fractional polynomial models (with 95% CIs) are shown in solid curves with each data point overlaid as circles. Circle size indicates the weighting of each data point and is inversely proportional to the variance of the log-transformed relative risk