Effect of ethanol drinking, hangover, and exercise on adrenergic activity and heart rate variability in patients with a history of alcohol-induced atrial fibrillation.
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.
Mäki
T
T
Department of Clinical Chemistry, Helsinki University Central Hospital, Finland.
Toivonen
L
L
Koskinen
P
P
Näveri
H
H
Härkönen
M
M
Leinonen
H
H
D000318:Adrenergic beta-Agonists / Q000494:pharmacology; D000328:Adult; D000428:Alcohol Drinking / Q000097:blood / Q000503:physiopathology*; D001281:Atrial Fibrillation / Q000097:blood / Q000139:chemically induced / Q000503:physiopathology*; D002395:Catecholamines / Q000097:blood; D000242:Cyclic AMP / Q000096:biosynthesis / Q000097:blood; D015716:Electrocardiography, Ambulatory; D000431:Ethanol / Q000009:adverse effects* / Q000097:blood; D015444:Exercise; D005080:Exercise Test; D006339:Heart Rate / Q000502:physiology*; D006801:Humans; D007545:Isoproterenol / Q000494:pharmacology; D019344:Lactic Acid / Q000097:blood; D008214:Lymphocytes / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D011863:Radioimmunoassay; D011943:Receptors, Adrenergic, beta / Q000097:blood*; D013375:Substance Withdrawal Syndrome / Q000097:blood / Q000503:physiopathology*
D000318:Adrenergic beta-Agonists; D002395:Catecholamines; D011943:Receptors, Adrenergic, beta; D019344:Lactic Acid; D000431:Ethanol; D000242:Cyclic AMP; D007545:Isoproterenol