Dependence of ventricular fibrillation propensity on coronary blood flow without myocardial ischemia.

Abstract Ventricular fibrillation threshold (VFT) changes have been linked to coronary blood flow (CBF) in the context of CBF reduction and subsequent myocardial hypoxia. To clarify the effect of CBF on VFT in the absence of myocardial hypoxia, 18 open-chest pentobarbital-anesthelized dogs with uniformly controlled heart rate, cardiac output, and mean systemic arterial pressure (SAP¯) were studied as follows: CBF, coronary sinus O 2 content (CcsO 2 ), and thereby myocardial O 2 consumption were continuously monitored. Baseline VFT determined by the single stimulus scanning technique was 33.0 ± 3.9 mA. Initial values of CBF index (I) and VFT (n = 18) were positively correlated (VFT mA = 0.8 ± 0.245 · CBFI ml/min · 100g −1 LV; r=0.60, p −1 LV were then induced by changing in random order,SAP¯ (n = 10), left coronary perfusion pressure (n = 7), and arterial O 2 content (n = 10) with VFT determined at each step; CcsO 2 remained above 5.5 vol% while CBFI and VFT changes were positively correlated, and mean weighted slope of VFT mA = 16.6 ± 0.103 · CBFI ml/min · 100g −1 LV (F = 0.82, p 2 content did not appear to affect VFT independently. It is concluded that even in the absence of myocardial hypoxia, CBF itself is a major determinant of VFT and thereby of innate arrhythmogenic propensity.