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1 Department of Cardiovascular Medicine, Cleveland Clinic Foundation, Cleveland 44195; and 2 Department of Biomedical Engineering, Case Western Reserve University, Cleveland, Ohio 44106
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 the cardiac cycle while
the excitation-contraction decoupler 2,3-butanedione monoxime (BDM; 15 mM) was used to suppress motion artifacts caused by contraction of the
heart. During ischemia, vulnerable window width increased
[from 30-90% of the action potential duration (APD) in the
control to 
10 to 100% of the APD in ischemia]. Moreover,
arrhythmia severity increased along with the reduction of APD (176 ± 9 ms in control and 129 ± 26 ms in ischemia,
P < 0.01) and increased dispersion of repolarization
(45 ± 17 ms in control and 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 four hearts. Optical mapping revealed that the shock
extinguished the arrhythmia; however, the arrhythmia self-originated
after an isoelectric window of 339 ± 189 ms. In conclusion, 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 deexcitation. In
four hearts, arrhythmogenesis could not be explained by VEIPS.
cardiac vulnerability; defibrillation; voltage-sensitive dye; optical mapping
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