Effects of alcohol on atrial fibrillation: myths and truths.

Alcohol is the most consumed drug worldwide. Both acute and chronic alcohol use have been associated with cardiac arrhythmias, in particular atrial fibrillation, or so-called 'holiday heart syndrome'. Epidemiological, clinical and experimental studies have attempted to elucidate the mechanisms involved in this association. However, because most of these studies have shown conflicting results, the connection between ethanol and atrial arrhythmias remains controversial. Historical, epidemiological and pharmacological aspects of alcohol, as well as recent concepts on atrial fibrillation are reviewed. We then examine the literature and provide a critical point of view on the still elusive association between alcohol and atrial fibrillation.

Characterization of the acute cardiac electrophysiologic effects of ethanol in dogs.

BACKGROUND: Alcohol has been related to atrial fibrillation (holiday heart syndrome), but its electrophysiologic actions remain unclear. METHODS: We evaluated the effects of alcohol in 23 anesthetized dogs at baseline and after 2 cumulative intravenous doses of ethanol: first dose 1.5 ml/kg (plasma level 200 mg/dl); second dose 1.0 ml/kg (279 mg/dl). In 13 closed-chest dogs (5 with intact autonomic nervous system, 5 under combined autonomic blockade and 3 sham controls), electrophysiologic evaluation and monophasic action potential (MAP) recordings were undertaken in the right atrium and ventricle. In 5 additional dogs, open-chest biatrial epicardial mapping with 8 bipoles on Bachmann's bundle was undertaken. In the remaining 5 dogs, 2D echocardiograms and ultrastructural analysis were performed. RESULTS: In closed-chest dogs with intact autonomic nervous system, ethanol had no effects on surface electrocardiogram and intracardiac variables. At a cycle length of 300 milliseconds, no effects were noted on atrial and ventricular refractoriness and on the right atrial MAP. These results were not altered by autonomic blockade. No changes occurred in sham controls. In open-chest dogs, ethanol did not affect inter-atrial conduction time, conduction velocity, and wavelength. Atrial arrhythmias were not induced in any dog, either at baseline or after ethanol. Histological and ultrastructural findings were normal but left ventricular (LV) ejection fraction decreased in treated dogs (77 vs. 73 vs. 66%; p = 0.04). CONCLUSION: Ethanol at medium and high doses depresses LV systolic function but has no effects on atrial electrophysiological parameters. These findings suggest that acute alcoholic intoxication does not directly promote atrial arrhythmias.

Ablaçäo por cateter de taquicardia de via de saída de ventrículo direito utilizando radiofrequência como fonte de energia / Catheter ablation of tachycardia of the outlet right ventricle using radiofrequency as power source

Two female patients, 54 and 38 years-old with refractory ventricular tachycardia were undertaken to electrophysiologic study for diagnosis and radiofrequency ablation of their arrhythmias. The tachycardias were only inducible with intravenous isoproterenol infusion. The site of the origin of ventricular tachycardia was localized in the right ventricular outflow tract in both cases. Radiofrequency current was delivered at 40V (40-60s) in each patient and was followed by complete abolition of ventricular arrhythmias

Mapeamento radioisotópico do foco arritmogênico em portadores de cardiopatia chagásica crônica e taquicardia ventricular sustentada / Radionuclide Angiography for Localization of the Site of Origin of Sustained Ventricular Tachycardia in Chronic Chagasic Cardiomyopathy

PURPOSE--To localize the site of the origin of sustained ventricular tachycardia in chronic chagasic cardiomyopathy patients refractory to antiarrhythmic therapy by radionuclide angiography techniques. METHODS--Five patients underwent radionuclide angiography by intravenous administration of 25mCi 99mTc. The images were obtained in sinus rhythm and during sustained ventricular tachycardia induced in the electrophysiologic laboratory for endocardial mapping. Amplitude and phase images were obtained resulting in a contraction wave synchronic to ventricular dispolarization. RESULTS--All patients had haemodynamic stability during the arrhythmia. One patient had incessant ventricular tachycardia. Mean ejection fraction was 0.38. In 4 patients the site of the origin of ventricular tachycardia was posterior and in one it was localized in the interventricular septum. There was identity in the site of the origin of ventricular tachycardia obtained by endocardial mapping or radionuclide angiography in all patients. The therapy was chemical ablation in 3 patients, surgical aneurysmectomy in one and pharmacologic therapy in the last patient. CONCLUSION--The site of the origin of ventricular tachycardia can be estimated by analyzing the contraction wave obtained by radionuclide angiography techniques in patients with hemodynamic stable sustained ventricular tachycardia.