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Articles in PresS, published online ahead of print February 21, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00561.2001
Submitted on June 27, 2001
Accepted on February 15, 2002
1 Cardiovascular Medicine, The Cleveland Clinic Foundation, Cleveland, OH, USA
2 Biomedical Engineering, Case Western Reserve University, Cleveland, OH, USA; Cardiovascular Medicine, The Cleveland Clinic Foundation, Cleveland, OH, USA
* To whom correspondence should be addressed. E-mail: chengy{at}ccf.org.
Little is known about the mechanisms of vulnerability and defibrillation under ischemic conditions. We investigated these mechanisms in 18 Langendorff-perfused rabbit hearts during 75% reduced-flow ischemia. Electrical activity was optically mapped from the anterior-epicardium during right ventricular shocks applied at various phases of cardiac cycle while an excitation-contraction de-coupler 2,3-butanedione monoxime (BDM, 15 mM) was used to suppress motion artifact caused by contraction of the heart. During ischemia, vulnerable window width increased (30-90% of action potential duration (APD) in control to -10-100% of APD in ischemia). Moreover, arrhythmias severity increased along with the reduction of APD (176 ± 9 ms in control, 129 ± 26 ms in ischemia, p<0.01) and increased dispersion of repolarization (45 ± 17 ms in control, 73 ± 28 ms in ischemia, p<0.01). Shock-induced virtual electrode polarization was preserved. Depolarizing (contrary to hyperpolarizing) response time-constants increased. Virtual electrode-induced wavefronts of excitation had much more tortuous pathways leading to wavefront fractionation. Defibrillation failure at all shock strengths was observed in 4 hearts. Optical mapping revealed that the shock extinguished arrhythmia, however, the arrhythmia self-originated after an isoelectric window of 339 ± 189 msec. Conclusions: In most cases, virtual electrode-induced phase singularity (VEIPS) was responsible for shock-induced arrhythmogenesis during acute global ischemia. Enhancement of arrhythmogenesis was associated with an increased dispersion of repolarization and altered de-excitation. In 4 hearts, arrhythmogenesis could not be explained by VEIPS.
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