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Circulation. 2002;106:2764-2766
doi: 10.1161/01.CIR.0000038983.96121.7F
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(Circulation. 2002;106:2764.)
© 2002 American Heart Association, Inc.


Editorial

NO Hope for Patients With Atrial Fibrillation

Michael Rubart, MD; Douglas P. Zipes, MD

From the Krannert Institute of Cardiology, Indianapolis, Ind.

Correspondence to Douglas P. Zipes, Krannert Institute of Cardiology, 1800 North Capitol Ave, Indianapolis, IN 46202. E-mail dzipes@iupui.edu


Key Words: Editorials • nitric oxide • atrium • fibrillation • thrombosis


An extract of the first 250 words of the full text is provided, because this article has no abstract.
 

Atrial fibrillation (AF), either in its paroxysmal or chronic form, is associated with an increased risk of systemic embolization. Currently, the only effective therapy to reduce this risk is long-term systemic anticoagulation. Such treatment comes at a considerable cost; approximately 3% of patients with nonvalvular AF receiving an oral anticoagulant experience major bleeding events that require hospital admission.1 Considering the often devastating sequelae of cerebral emboli and the potentially life-threatening side effects of chronic anticoagulation, it is alarming how little is known about the mechanisms linking AF to intraatrial thrombus formation. Although several randomized, prospective, nonvalvular AF trials have examined putative hemostatic markers of increased risk for thrombosis,2 knowledge of the etiology and pathophysiology of AF-induced thromboembolic complications has remained sketchy.

See p 2854

A new experimental study by Cai and co-workers3 published in this week’s issue of Circulation sets the stage for a better understanding of the mechanisms underlying thromboembolic events associated with AF. They discovered that 1 week of rapid pacing-induced AF in pigs is associated with a marked decrease in endothelial nitric oxide synthase (eNOS) expression, a reduction in production of nitric oxide (NO), and an increase in expression of plasminogen activator inhibitor 1 (PAI-1) in the left atrial endocardium. Because NO has antithrombotic properties, they concluded that loss of left atrial eNOS activity contributes to the thromboembolic events frequently associated with AF.

As innovative and thought provoking as this study is, and as plausible as this conclusion seems in light of the well established antithrombotic action . . . [Full Text of this Article]


Related Article:

Downregulation of Endocardial Nitric Oxide Synthase Expression and Nitric Oxide Production in Atrial Fibrillation: Potential Mechanisms for Atrial Thrombosis and Stroke
Hua Cai, Zongming Li, Andreas Goette, Fernando Mera, Clegg Honeycutt, Kristian Feterik, Josiah N. Wilcox, Samuel C. Dudley, Jr, David G. Harrison, and Jonathan J. Langberg
Circulation 2002 106: 2854-2858. [Abstract] [Full Text]



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