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(Circulation. 2007;116:1433.)
© 2007 American Heart Association, Inc.

Issue Highlights

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

	ATRIUM-SELECTIVE SODIUM CHANNEL BLOCK AS A STRATEGY FOR SUPPRESSION OF ATRIAL FIBRILLATION: DIFFERENCES IN SODIUM CHANNEL INACTIVATION BETWEEN ATRIA AND VENTRICLES AND THE ROLE OF RANOLAZINE, by Burashnikov et al.

 
Ventricular proarrhythmia is a major hurdle in drug development for therapy for atrial fibrillation. The cardiac sodium current that is a determinant of conduction and excitability in atrium and ventricles is a target for many antiarrhythmic drugs. Sodium-current blockers can suppress atrial fibrillation in some patients, but an adverse impact on mortality rate was observed with some agents administered after myocardial infarction. The recently approved antianginal drug ranolazine is a sodium-channel blocker without adverse mortality effects in human trials. Burashnikov and coworkers compared the electrophysiological effects of ranolazine in canine atrial and ventricular muscle. The drug’s interesting sodium channel–blocking effects and prolongation of action potential duration were greater in the atrium than in the ventricles. Ranolazine had efficacy against atrial fibrillation in tissue models. Selective blockade of atrial sodium channels appears to be a feasible target that warrants further exploration for treating atrial fibrillation without ventricular proarrhythmic effects. See p 1449.

	EFFECT OF DISTAL EMBOLIZATION ON MYOCARDIAL PERFUSION RESERVE AFTER PERCUTANEOUS CORONARY INTERVENTION: A QUANTITATIVE MAGNETIC RESONANCE PERFUSION STUDY, by Selvanayagam et al.

 
The high resolution of cardiac magnetic resonance imaging and the use of the delayed enhancement technique have suggested that after percutaneous coronary intervention (PCI), small new areas of necrosis may be seen in the vascular bed distal to the stented stenosis. In this issue of Circulation, Selvanayagam and colleagues assess changes in perfusion reserve after PCI and the effect of new local myocardial injury on perfusion reserve. They found that at 24 hours after the PCI procedure, perfusion reserve improves in normal myocardium. In segments with new distal injury, however, perfusion reserve is further impaired after PCI, . . . [Full Text of this Article]

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