Electrophysiologic effects of cigarette smoking in patients with and without chronic beta-blocker therapy.
After refraining from smoking for at least 8 hours, 22 adult male habitual smokers underwent baseline electrophysiologic study including atrial and ventricular burst pacing and programmed premature stimulation with single extrastimuli. After smoking 2 of their usual brand of cigarettes in rapid succession, the electrophysiologic protocol was repeated. Nicotine, catecholamine and carbon monoxide concentrations all increased significantly. Smoking increased heart rate and improved atrioventricular conduction in the 13 patients receiving chronic beta-blocker therapy (mostly for angina pectoris); increases in heart rate and improvement in atrioventricular conduction were not different statistically from those seen in patients not receiving beta-blocker therapy, suggesting the possibility of a direct effect of nicotine or other components of tobacco smoke. Ventricular refractoriness was not altered and atrial and ventricular arrhythmias were not increased by smoking. Persistent sympathomimetic actions of cigarette smoking may explain in part the failure of beta-blocking drugs to reduce cardiac mortality risk in smokers after myocardial infarction.
D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use*; D000328:Adult; D000368:Aged; D001145:Arrhythmias, Cardiac / Q000097:blood / Q000188:drug therapy / Q000503:physiopathology*; D001283:Atrioventricular Node / Q000503:physiopathology; D006801:Humans; D008297:Male; D008875:Middle Aged; D012849:Sinoatrial Node / Q000503:physiopathology; D012907:Smoking / Q000097:blood / Q000503:physiopathology*
D000319:Adrenergic beta-Antagonists