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(Circulation. 2006;113:1817.)
© 2006 American Heart Association, Inc.

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

	A TAILORED APPROACH TO CATHETER ABLATION OF PAROXYSMAL ATRIAL FIBRILLATION, by Oral et al.

 
Paroxysmal atrial fibrillation is a complex arrhythmia initiated by rapid "triggering" foci and likely perpetuated by the triggers and abnormal conduction in regions outside the triggering sites. Although the location of this arrhythmogenic substrate varies among patients, a simple anatomic ablation approach encircling the pulmonary venous regions is often effective, but not always easy to achieve. Oral and colleagues evaluated a tailored approach to ablation, sequentially targeting areas identified as potentially arrhythmogenic on the basis of rapid electrical activity, seeking to achieve an electrophysiological end point of noninducibility of atrial fibrillation. The results are comparable to those of some studies utilizing purely anatomic approaches and show that a tailored approach can achieve efficacy without extensive anatomic ablation. Such an approach can avoid ablation in the high-risk area adjacent to the esophagus. The study illustrates the heterogeneity of this arrhythmia and supports continued evaluation of ablation strategies. See p 1824.

	ß2-ADRENERGIC RECEPTOR GENETIC VARIANTS AND RISK OF SUDDEN CARDIAC DEATH, by Sotoodehnia et al.

 
Sudden cardiac death is a major cause of death in developed countries and results in almost one half million deaths per year in the United States. Both experimental and clinical observations suggest that ß2 adrenergic receptors partially mediate sympathetic activation. Hence the ß2 adrenergic receptor gene (B2AR) represents an attractive candidate gene for susceptibility to sudden cardiac death. Sotoodehnia and colleagues examined the association of two polymorphisms in the B2AR gene (Gly16Arg and Gln27Glu) with sudden cardiac death in the community-based Cardiovascular Health Study. They report that Gln27 homozygotes had a 58% increased risk of sudden cardiac death (nominal P. . . [Full Text of this Article]