Article

Over the last 2 decades, observational evidence largely supports an association
between light to moderate alcohol consumption (up to 1 drink per day in women and
up to 2 drinks per day in men) and a lower risk of cardiovascular disease (CVD),
largely driven by a reduction in coronary heart disease. Most studies suggest a
nadir in risk in the light to moderate range of alcohol intake, which is then
countered by an increase in cardiomyopathy, sudden death, and hemorrhagic stroke
at higher drinking levels that offsets potential benefits. The mechanisms of
cardioprotective effects of alcohol are complex and there are multiple pathways
by which moderate alcohol consumption reduces the risk of CVD. Recent evidence
continues to emerge on the physiologic and genetic mechanisms through which
alcohol may reduce the risk of developing CVD. Ongoing debate also lingers
whether there are important differences in cardiovascular effects according to
alcoholic beverage type (beer vs red wine vs liquor). Another emerging area of
interest is the role of alcohol consumption on the development of intermediate
cardiovascular endpoints such as hypertension and diabetes that lead to the
development of CVD as well as other important cardiovascular sequelae. Alcohol
consumption has also been shown to impact the risk of other CVD endpoints
including congestive heart failure, alcoholic cardiomyopathy, atrial
fibrillation, and peripheral artery disease. Overall, alcohol still carries
significant public health implications given its plausible benefits on CVD along
with its well-documented adverse effects, warranting continued caution and a
discussion with one's primary care provider regarding intake.

Langue : ANGLAIS