Effects of alcohol intake on atrial arrhythmias and P-wave dispersion.

Alcohol has acute and chronic cardiovascular effects. Acutely, it depresses cardiac function and alters regional blood flow. In addition, there is an association between alcohol use and rhythm disturbances, particularly supraventricular tachyarrhythmias even in apparently healthy people. The induction of rhythm disturbances by acute alcohol consumption, especially supraventricular tachyarrhythmias, is known for longer time, generating the term “holiday heart syndrome” (1). Although arrhythmogenic effects of alcohol have been demonstrated even in individuals with no evident heart disease, they are more common in patients with underlying heart disease. Not only chronic alcohol abuse, even a single heavy consumption typically at weekends or in holiday seasons might be associated with temporary arrhythmogenic disorders. Also, it may occur in individuals who usually drink little alcohol. The most common rhythm disorder after alcohol intake is atrial fibrillation (AF), which usually converts to normal sinus rhythm within 24 hours. Although recurrences occur, the clinical course is benign and specific antiarrhythmic therapy is usually not warranted. In a previous study that assessed supraventricular tachyarrhythmias related factors, alcohol consumption was not associated with the induction of supraventricular tachyarrhythmias other than AF (2). Nevertheless, atrial flutter has occasionally been noted. In an animal model study, an ethanol infusion facilitates a variety of atrial arrhythmias related to the ethanol concentration (3). In this study, the higher concentration required for atrial flutter, exceeding that usually seen in humans, may help to explain the rarity of atrial flutter in clinical alcohol intoxication. Although the role of alcohol appears particularly conspicuous in idiopathic AF, the potential mechanisms of its arrhythmogenic effects have not been definitively determined. Increased adrenergic activity, electrolyte abnormalities, impaired vagal heart rate control, changed conduction and refractory times, and myocardial damage have been suggested (4,5). Subclinical heart muscle injury from alcohol use may be instrumental in producing patchy delays in conduction. The data in a previous study suggest that intracoronary ethanol administration at human abuse levels of blood alcohol concentrations produces histological and electrophysiologic injury in the canine heart (6). Intramural lesions observed varied from focal acute myofibrillar degeneration and necrosis to severe local scarring. The electrophysiologic changes provide a substrate sufficient for the induction and maintenance of arrhythmia. These changes were a decreasing in resting membrane potential, action potential amplitude and phase “0” upstroke, and prolongation in refractoriness without a prolongation of action potential duration. Additionally, alcohol intake may lead to prolongation of conduction (7). Increased adrenergic activity, magnesium depletion, and hypokaliemia are often seen after heavy drinking, and these factors may be responsible for arrhythmias (5). Acute intake of moderate amounts of alcohol causes a significant decrease in heart rate variability owing to diminished vagal modulation of the heart rate (8,9). Diminution of vagal stimulus leads to sympathetic predominance. Persons with a liability to alcohol-induced AF may be characterized by an increase in beta-adrenoreceptor density during ethanol intake, which could be associated with greater responsiveness to the adrenergic stimuli. Therefore, decreased vagal activity and increased adrenergic stimuli may be etiological factors for alcohol-induced AF (10). There is no study that assesses predictors of AF after alcohol intake. As known, P-wave dispersion, which is defined as maximum P-wave duration minus minimum P-wave duration, on surface electrocardiogram is a noninvasive marker of inhomogeneous and discontinuous propagation of sinus impulses through the atrial wall, which are believed to be the main electrophysiological cause of AF (11). P-wave dispersion is an easy to obtain and a useful parameter for assessing AF occurrence risk in various patients groups (11-16). In the study of Uyarel et al (17), published in this issue of The Anatolian Journal of Cardiology, it has been demonstrated that acute alcohol intake is associated with increased PD. However, in the study of Uyarel et al (17), only acute effect of alcohol consumption on PD has been evaluated. Clinical significance of this effect has not been evaluated. It should be assessed whether increased PD due to alcohol is associated with increased risk of AF. Moreover, the level of PD that predicts AF occurrence risk after alcohol intake and its diagnostic accuracy may be determined. Actually, a conflicting issue in PD assessment is that there are several cut of points of PD to predict AF occurrence in different group of patients. The PD value that separates patients from control subjects is 40 msec (11) and 36 msec (12) in idiopathic paroxysmal AF, 52 msec in hypertrophic cardiomyopathy (13), and 25 msec in acute myocardial infarction (14).