This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Rosen, M. R. Search for Related Content PubMed PubMed Citation Articles by Rosen, M. R. Related Collections Cardiovascular Pharmacology Arrhythmias, clinical electrophysiology, drugs

(Circulation. 1999;100:1942-1944.)
© 1999 American Heart Association, Inc.

Editorial

Leaky Dikes and Fibrillating Swine

Michael R. Rosen, MD

From the Departments of Pharmacology and Pediatrics, Columbia University, College of Physicians and Surgeons, New York.

Correspondence to Michael R. Rosen, MD, Department of Pharmacology, Columbia University, College of Physicians and Surgeons, 630 West 168th St, Box 40 PH7 W-318, New York, NY 10032.

Key Words: Editorials • antiarrhythmic agents • atrial fibrillation • serotonin

Interest in developing new antiarrhythmic drugs has vacillated between recession and eclipse since the CAST trial.¹ This mind-set has been reinforced by additional studies of drugs (eg, SWORD² ) and of drugs versus devices (eg, AVID³ ). A recent editorial⁴ and related publications^{5 6} focus on redefining the role of antiarrhythmic drugs, stressing a largely adjunctive strategy in which drugs are an accompaniment of nonpharmacological therapies for ventricular arrhythmias. It is suggested that first-line drug therapy be reserved for arrhythmias like atrial fibrillation.⁴

Is the future for pharmacological therapy of cardiac arrhythmias as bleak as it appears to be? Perhaps so, if we continue to define and develop antiarrhythmic drugs in a traditional sense as blockers of ion channels (Na, K, and Ca²⁺) and/or adrenergic receptors. In this setting, we may expect continued refinement of decades-old thinking, perhaps more selective, more effective, and safer drugs, but hardly the stuff of which breakthroughs are made. Recent publications⁷ have stressed the need for alternatives to ion channel blocking drugs in the prevention and therapy of cardiac arrhythmias. These needs have arisen because 1) although often effective, ion channel blocking agents have not yet achieved sufficient target selectivity or sufficient safety to provide optimal intra- and interpatient treatment over extended periods of time, 2) the ability to prolong life and improve quality of life when these drugs are administered alone has been marginal, and 3) the recognition, through molecular and biophysical technology, of increasing arrays of potential molecular targets has not yet identified . . . [Full Text of this Article]