Mäki T, Toivonen L, Koskinen P, Näveri H, Härkönen M, Leinonen H
Department of Clinical Chemistry, Helsinki University Central Hospital, Finland.
Am J Cardiol. 1998 Aug 1;82(3):317-22. doi: 10.1016/s0002-9149(98)00299-9.
To elucidate the mechanism of alcohol-induced atrial fibrillation (AF) we studied the heart rate variability and parameters of the adrenergic system during alcohol intake, hangover, and exercise in 6 men (mean age 43 years) prone to alcohol-induced AF, together with 6 age-matched controls. The ambulatory (15 hour) electrocardiogram was recorded and blood samples were taken for lymphocytic beta adrenoceptor, plasma catecholamine, and cyclic adenosine monophosphate (cAMP) measurements before and after alcohol intake (blood alcohol 1.5 per thousand), during hangover, and after a standardized bicycle exercise test. The beta-adrenoceptor density in lymphocytes was unchanged in the control group after alcohol intake or during hangover. Each of the AF patients had an increase in beta-adrenoceptor density after ethanol drinking (mean increase 29%, p <0.05). The hangover or exercise beta-receptor values did not differ from those in corresponding controls. Plasma adrenaline concentration tended to decrease and noradrenaline to increase after drinking and during hangover in both groups. Plasma cAMP levels were lower in patients after drinking than in controls (p <0.05). The exercise values of the adrenergic parameters were very similar in AF patients whether or not preceded by alcohol. Analysis of ambulatory electrocardiography showed a very low rate of ectopic beats in both AF patients and controls. Analysis of heart rate variability revealed a tendency toward an increase in sympathetic/parasympathetic component ratio (low-frequency/high-frequency ratio) in AF patients, but not in controls, after ethanol drinking. In conclusion, no signs of arrhythmogenic cardiac disease were detected in patients with AF to explain the tendency toward AF. Increases in beta-adrenoceptor density and low-frequency/high-frequency ratio during ethanol intoxication in patients with AF suggest an exaggerated sympathetic reaction.
为阐明酒精性心房颤动（AF）的机制，我们研究了6名易患酒精性AF的男性（平均年龄43岁）在饮酒、宿醉和运动期间的心率变异性及肾上腺素能系统参数，同时设置了6名年龄匹配的对照者。记录动态（15小时）心电图，并在饮酒前、饮酒后（血酒精浓度1.5‰）、宿醉期间以及标准化自行车运动试验后采集血样，检测淋巴细胞β肾上腺素受体、血浆儿茶酚胺和环磷酸腺苷（cAMP）。对照组饮酒后或宿醉期间淋巴细胞中的β肾上腺素受体密度未发生变化。每位AF患者饮酒后β肾上腺素受体密度均升高（平均升高29%，p<0.05）。宿醉或运动后的β受体值与相应对照组无差异。两组饮酒后及宿醉期间血浆肾上腺素浓度均有下降趋势，去甲肾上腺素浓度则升高。饮酒后患者血浆cAMP水平低于对照组（p<0.05）。无论是否饮酒，AF患者运动后的肾上腺素能参数值非常相似。动态心电图分析显示，AF患者和对照组的异位搏动发生率均很低。心率变异性分析显示，饮酒后AF患者交感神经/副交感神经成分比（低频/高频比）有升高趋势，而对照组无此现象。总之，未在AF患者中检测到致心律失常性心脏病迹象以解释其发生AF的倾向。AF患者在酒精中毒期间β肾上腺素受体密度增加及低频/高频比升高提示交感反应过度。
