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 Liggett, S. B. Search for Related Content PubMed PubMed Citation Articles by Liggett, S. B. Pubmed/NCBI databases Medline Plus Health Information Cardiac Arrest Related Collections Congestive Arrythmias-basic studies Arrhythmias, clinical electrophysiology, drugs Related Article

(Circulation. 2006;113:1818-1820.)
© 2006 American Heart Association, Inc.

Editorial

ß₂-Adrenergic Receptor Polymorphisms and Sudden Cardiac Death

A Signal to Follow

Stephen B. Liggett, MD

From the Cardiopulmonary Genomics Program, University of Maryland School of Medicine, Baltimore.

Correspondence to Stephen B. Liggett, MD, Cardiopulmonary Genomics Program, University of Maryland School of Medicine, 20 Penn St, HSF-II, Room S-114, Baltimore, MD 21201. E-mail sligg001@umaryland.edu

Key Words: Editorials • genetics • polymorphisms • receptors, adrenergic, beta

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

Sudden cardiac death (SCD) is defined as an unexpected death from a cardiac cause generally within 1 hour of the onset of symptoms. The great majority of SCD cases are due to ventricular fibrillation and subsequent hemodynamic collapse. Eighty percent of SCD is attributable to ischemic heart disease, with much of the remainder caused by cardiomyopathies/heart failure and intrinsic conduction system abnormalities.¹ These predisposing conditions place patients at risk for SCD, and a trigger for the fatal arrhythmias may come from an imbalance of the parasympathetic and sympathetic nervous systems,^2–5 the latter being mediated by cardiac ß₁- and ß₂-adrenergic receptors (ß₁AR, ß₂AR). Indeed, treatment with ß-blockers of patients with heart failure and those who have suffered a myocardial infarction significantly reduces ventricular tachyarrhythmias and SCD. Typically, the pathophysiology of SCD is considered in terms of the underlying disease. However, there is evidence for genetic variability of the ß₁AR and ß₂AR genes that has functional consequence in transfected cells, endogenously expressing cells, and transgenic mice.^6,7 Familial clustering of certain pathological arrhythmias and the unexplained variability in susceptibility among unrelated individuals to fatal arrhythmias raise the possibility of common polymorphisms such as those of the ß₁AR or ß₂AR being genetic risk factors for SCD.

Article p 1842

In this issue of Circulation, Sotoodehnia et al⁸ examined polymorphisms of the ß₂AR and potential associations with SCD. The study used individuals in the Cardiovascular Health Study (CHS), amounting to 4441 European Americans and 808 . . . [Full Text of this Article]

Related Article:

ß2-Adrenergic Receptor Genetic Variants and Risk of Sudden Cardiac Death

Nona Sotoodehnia, David S. Siscovick, Matteo Vatta, Bruce M. Psaty, Russell P. Tracy, Jeffrey A. Towbin, Rozenn N. Lemaitre, Thomas D. Rea, J. Peter Durda, Joel M. Chang, Thomas S. Lumley, Lewis H. Kuller, Gregory L. Burke, and Susan R. Heckbert
Circulation 2006 113: 1842-1848. [Abstract] [Full Text]