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Am J Physiol Heart Circ Physiol (July 11, 2002). doi:10.1152/ajpheart.00965.2001
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Articles in PresS, published online ahead of print July 11, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00965.2001
Submitted on November 5, 2001
Accepted on July 8, 2002

Transmural reentry triggered by epicardial stimulation during acute ischemia in canine ventricular muscle

Jiashin Wu1* and Douglas P. Zipes1

1 Medicine, Indiana University School of Medicine, Indianapolis, Indiana, USA

* To whom correspondence should be addressed. E-mail: jiaswu{at}iupui.edu.

Ischemia depresses tissue excitability more rapidly in the ventricular epicardium than in endocardium. We hypothezed that this would provide the substrate for transmural reentry originating in the epicardium. We mapped transmural conduction in isolated and perfused wedges taken from canine left ventricles during global ischemia, while pacing alternately between the epicardium and endocardium. Ischemia reduced conduction velocity more in the epicardium than in endocardium. We observed that the epicardial-initiated activation penetrated the ventricular wall transmurally while failing to conduct laterally along the epicardium, then conducted laterally along the endocardium and midmyocardium and reentered the epicardium, in 9 of 16 wedges during epicardial stimulation after 600±182 seconds of ischemia. Endocardial stimulation, applied immediately before or after the epicardial stimulation, initiated activation that spread quickly along the endocardium, then transmurally to the epicardium without reentry in 6 of the above 9 wedges. The transmural asymmetric conduction was not observed in 4 separate wedges after the endocardium was removed. Therefore, ischemia-induced transmural gradient of excitability provided the substrate for reentry during epicardial stimulation.




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