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(Circulation. 2008;117:711-713.)
© 2008 American Heart Association, Inc.

Clinical Summaries

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

	Cell Therapy for Modification of the Myocardial Electrophysiological Substrate

 
Cardiac arrhythmias account for significant worldwide morbidity and mortality. Preventive antiarrhythmic therapies are aimed at modifying the abnormal electrophysiological substrate by either focal injury (surgery or radiofrequency catheter ablation) or pharmacological therapy. Antiarrhythmic drug therapy has been hampered by often low efficacy, global cardiac and systemic actions that often lead to poorly tolerated systemic side effects, and most important, life-threatening proarrhythmic effects. In this study, we present a novel combined cell and gene therapy approach for the modification of the myocardial electrophysiological substrate. Using fibroblast cell grafts genetically engineered to express specific potassium ionic channels, we aimed to perform a targeted modification of local cardiac electrophysiological properties. Detailed in vitro, in vivo, and computer modeling studies demonstrated the feasibility of this approach by showing that the engineered cells could couple with host cardiac cells and that this modified their electrophysiological properties. The cell grafts modulated important properties that are of interest for future antiarrhythmic strategies. These include prolongation of the local refractory period by a mechanism that does not involve action potential prolongation (potentially reducing the proarrhythmic risk associated with many antiarrhythmic agents that prolong the QT interval) and reduction in local automaticity (decreasing the spontaneous firing rate). See p 720.

	Angiotensin II Receptor Blockade Reduces Tachycardia-Induced Atrial Adhesion Molecule Expression

 
Vascular thrombi develop in the presence of reduced blood velocities, when the activity of the clotting system is increased, and in the presence of endothelial alterations (Virchow’s triad). Virchow’s triad also applies to atrial thrombus formation during atrial fibrillation (AF). It is well known that AF causes loss . . . [Full Text of this Article]