(Circulation. 2002;106:1180.)
© 2002 American Heart Association, Inc.
From the Department of Pharmacology, College of Physicians & Surgeons of Columbia University, New York, NY.
Correspondence to Michael R. Rosen, MD, Department of Pharmacology, College of Physicians & Surgeons of Columbia University, 630 West 168th St, PH7West-321, New York, NY 10032.
Key Words: Editorials antiarrhythmia agents drugs hypertrophy
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
In an era that finds us continually bombarded with numbers and images about threats, both real and imagined, a threat as old as the Bible that continues its dangerous course is that of cardiac arrhythmia.
See p 1288
The year of Wenckebachs observation,2 1914, was the same year in which George Ralph Mines3 published his initial experiments on reentry, observations on "circulating excitations in heart muscles and their possible relation to tachycardia and fibrillation" that were seminal to the field. That year was little more than a decade after Einthovens description of the ECG,4,5 which rapidly became and has since remained the primary tool facilitating both our understanding and our diagnosis of arrhythmias during these 100 years since its invention.
The decades after the first therapeutic application of quinidine saw the testing and addition to arrhythmia therapy of drugs such as procaine,
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M. R. Rosen Blunderbuss to Mickey Mouse: The Evolution of Antiarrhythmic Targets Circulation, September 3, 2002; 106(10): 1180 - 1182. [Full Text] [PDF] |
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