作者: Nicholas S. Peters , James Coromilas , Nicholas J. Severs , Andrew L. Wit
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摘要: Background Slow, nonuniform conduction caused by abnormal gap-junctional coupling of infarct-related myocardium is thought to be a component the arrhythmogenic substrate. The hypothesis that changes in distribution epicardial border zone (EBZ) healing canine infarcts define locations reentrant ventricular tachycardia (VT) circuits was tested correlating activation maps surviving subepicardial myocardial layer with immunolocalization principal protein, connexin43 (Cx43). Methods and Results EBZ overlying 4-day-old anterior three dogs inducible VT noninducible mapped high-resolution electrode array systematically examined standard histology confocal Cx43. thickness significantly less hearts (538±257 μm) than without (840±132 μm; P<.05) VT. At interface underlying necrotic cells, showed marked disrup...