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(Circulation. 2002;105:2574.)
© 2002 American Heart Association, Inc.

Editorial

Sudden Death Predictors

An Inflammatory Association

Peter M. Spooner, PhD; Douglas P. Zipes, MD

From the Division of Heart and Vascular Diseases (P.M.S.), National Heart, Lung, and Blood Institute, Bethesda, Md, and the Krannert Institute of Cardiology (D.P.Z.), Indiana University School of Medicine, Indianapolis.

Reprint requests to Douglas P. Zipes, MD, Indiana University School of Medicine, Krannert Institute of Cardiology, 1800 N Capitol Ave, Suite E475, Indianapolis, IN 46202. E-mail dzipes@iupui.edu

Key Words: Editorials • death, sudden • inflammation • protein, C-reactive

Sudden cardiac death (SCD), which is defined as an unexpected, usually arrhythmic death occurring in asymptomatic individuals shortly after the onset of symptoms, is responsible for more than half of the total cardiac mortality in developed countries throughout the world.¹ It frequently appears as the first and only manifestation of previously undetected coronary heart disease.² At least half these deaths occur outside a hospital setting and, according to recent Centers for Disease Control data, this proportion, as well as the overall prevalence in the United States, continues to increase.³

See p 2595

Pharmaceutical strategies to prevent SCD have been largely ineffective, and because device therapy is designed to rescue patients once an event has already occurred, primary SCD prevention has become one of today’s most critical public health challenges. Progress has been difficult, in part because although overall incidence in healthy adults is very low, it is precisely this group that continues to contribute the most to overall prevalence in the total population.⁴ Compared with identifying risk markers for secondary prevention, where the importance of clinical phenotypes such as low ejection fraction clearly has been established, work on reliable markers for primary SCD prevention has advanced much more slowly. Traditionally, approaches most often have been based on algorithms involving risk factors predictive of atherosclerotic and hypertensive coronary heart disease (CHD), yet these markers are often absent in a significantly large proportion of SCD victims. Although several population stratification approaches (like those based on the landmark Framingham Heart Study, which is . . . [Full Text of this Article]

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