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TRANSLATIONAL PHYSIOLOGY

Stretch-induced ventricular arrhythmias during acute ischemia and reperfusion

¹Living State Physics Group, Department of Physics and Astronomy, Vanderbilt University, and ²Division of Cardiology, Department of Internal Medicine, Vanderbilt University School of Medicine, Nashville, Tennesse 37232

Submitted 14 December 2001 ; accepted in final form 22 January 2004

Mechanical stretch has been demonstrated to have electrophysiological effects on cardiac muscle, including alteration of the probability of excitation, alteration of the action potential waveform, and stretch-induced arrhythmia (SIA). We demonstrate that regional ventricular ischemia due to coronary artery occlusion increases arrhythmogenic effects of transient diastolic stretch, whereas globally ischemic hearts showed no such increase. We tested our hypothesis that, during phase Ia ischemia, regionally ischemic hearts may be more susceptible to triggered arrhythmogenesis due to transient diastolic stretch. During the first 20 min of regional ischemia, the probability of eliciting a ventricular SIA (P_SIA) by transient diastolic stretch increased significantly. However, after 30 min, P_SIA decreased to a value comparable with baseline measurements, as expected during phase Ib, where most ventricular arrhythmias are of reentrant mechanisms. We also suggest that mechanoelectrical coupling may contribute to the nonreentrant mechanisms underlying reperfusion-induced arrhythmia. When coronary artery occlusion was relieved after 30 min of ischemia, we observed an increase in P_SIA and the maintenance of this elevated level throughout 20 min of reperfusion. We conclude that mechanoelectrical coupling may underlie triggered arrhythmogenesis during phase 1a ischemia and reperfusion.

ventricular; Langendorf; myocardial infarction; mechanoelectric signaling

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