Alcohol and arrhythmias

PHILADELPHIA, PENNSYLVANIA. Alcohol is probably the oldest mood-altering substance known to man. The earliest writings regarding alcohol use can be found in 6000-year-old Mesopotamian clay tablets. Warnings against alcohol abuse go back almost 4,000 years and can be found in ancient scriptures including the Koran and the Old and New Testaments. The observation that alcohol abuse can be detrimental to the heart was first reported in the medical literature in the 19th Century. More recently, medical literature has extolled the benefits of moderate alcohol consumption and linked it to reductions in heart attacks, strokes, and sudden cardiac death (SCD). It is believed that alcohol benefits the cardiovascular system by increasing high-density lipoprotein (HDL), increasing fibrinolysis, and enhancing endothelial function. It is also thought that alcohol reduces blood viscosity and decreases fibrinogen concentration and platelet aggregation and coagulation.

Unfortunately, alcohol can also precipitate arrhythmias as first discovered in 1959. In 1978 Dr. Philip Ettinger coined the term “holiday heart” defined as an acute cardiac arrhythmia, mostly atrial fibrillation (AF), associated with heavy drinking in a person without clinical evidence of heart disease. Dr. Ettinger observed a seasonal peak in the incidence of alcohol-induced arrhythmia at the end of the year and New Year’s Day. Other researchers have reported that bouts of alcohol-related AF occur most frequently in the early hours of the morning or upon arising from an alcoholic binge.

Finnish researchers found that 15 to 30% of idiopathic AF may be alcohol-related, while researchers involved in the Framingham study concluded that consumption of more than 3 alcoholic drinks (36 grams/day) increased the risk of AF by 34% after adjusting for potential confounders. More recently, researchers at Brigham and Women’s Hospital reported that women who consumed two or more alcoholic drinks a day had a 60% increased risk of AF.

Alcohol consumption has also been implicated in ventricular arrhythmias and SCD. However, the relationship is more complicated than that with AF. It now appears that individuals with a low alcohol intake (2 – 6 drinks a week) have a lower risk of ventricular tachycardia and SCD than do those who never or rarely consume alcohol or those with a high intake (3 – 5 drinks a day) and binge drinking. A study involving one million individuals observed a J-shaped relationship between alcohol intake and total mortality. Ventricular arrhythmias and SCD are both associated with prolongation of the QT interval and alcohol has been found to prolong the QT interval.

Alcohol withdrawal is associated with a rebound beta-adrenergic hypersensitivity and elevated catecholamine levels both of which can precipitate arrhythmias if accompanied by low levels of magnesium and potassium. Acute alcohol intoxication and withdrawal are both associated with the development of magnesium and potassium deficiencies (hypomagnesemia and hypokalemia). It is also noted that magnesium deficiency is closely tied to potassium deficiency and can result in refractory hypokalemia.

The authors conclude that there is a strong correlation between alcohol abuse and AF, particularly among younger men. Alcohol consumption is also positively correlated with ventricular tachycardia and SCD in heavy drinkers. Nevertheless, moderate alcohol consumption produces desirable health benefits, which are lost as the amount consumed increases or a pattern of binge drinking develops.

George, A and Figueredo, M. Alcohol and arrhythmias: a comprehensive review. Journal of Cardiovascular Medicine, Vol. 11, No. 4, 2010, pp. 221-28

Editor’s comment: Our early LAF surveys showed that alcohol consumption was the trigger for 6% of first ever AF episodes and triggered 22% of subsequent episodes.