(Circulation. 1997;95:562-564.)
© 1997 American Heart Association, Inc.
Articles |
the Krannert Institute of Cardiology, Department of Medicine, Indiana University School of Medicine, and the Roudebush Veterans Administration Medical Center, Indianapolis, Ind.
Correspondence to Douglas P. Zipes, MD, Krannert Institute of Cardiology, 1111 W 10th St, Indianapolis, IN 46202-4800.
Key Words: Editorials fibrillation arrhythmia atrium cardiomyopathy
| Introduction |
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Atrial fibrillation affects a larger population than ventricular tachyarrhythmias, with a prevalence of
0.5% in patients 50 to 59 years old, incrementing to 8.8% in patients in their 80s. Indeed, Framingham data indicate that the age-adjusted prevalence, particularly in men, has increased substantially over the last 30 years.1 Atrial fibrillation usually accompanies disorders such as rheumatic and coronary heart disease, heart failure, mitral valve prolapse, hypertension, cardiomyopathies, hyperthyroidism, and the postoperative state but can occur in the absence of any recognized abnormality (lone atrial fibrillation) in at least 10% of cases. Although it may not carry the inherent lethality of a ventricular tachyarrhythmia, it does have a mortality twice that of control subjects,1 and the palpitations, hemodynamic consequences, side effects of drugs, and, most importantly, brain involvement due to thromboembolic complications make atrial fibrillation a formidable problem. It is a frontier to be challenged, as clinicians wrestle with its three most important clinical issues: control of the ventricular rate, maintenance of sinus rhythm, and prevention of thromboembolism.
Recently, we have begun to understand some of the electrophysiological issues surrounding atrial fibrillation, and in the context of this editorial,
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