Abstract 2351: Transient Type II Ventricular Fibrillation During Global Ischemia in the in-situ Human Heart
Introduction. Experimental studies in animal hearts have shown that ventricular fibrillation (VF) may be sustained by different mechanisms. Type I VF is characterised by steep restitution and multiple wavelets, whereas type II VF is characterised by flat restitution, reduced excitability, and a smaller number of wavelets. In this study we tested the hypothesis that there is a transition from type I to type II VF in the ischemic human heart.
Methods. We recorded epicardial electrical activity in 10 patients aged 30 to 79 (mean 63 years; 8 male) having cardiac surgery with cardiopulmonary bypass for coronary artery disease (CAD, n=5) or valve replacement (VD, n=5). VF was induced by burst pacing. After 30 s, ischemia was induced by aortic cross clamp for 2.5 min, with cross clamp release and subsequent reperfusion for 30 s. Epicardial activity was sampled at 1 kHz using a sock with 256 unipolar contact electrodes. Electrograms were processed as described previously (Nash et al., Circulation 2006) to extract dominant frequency (DF), wavefronts, and phase singularities (PS).
Results. In four patients (3 with CAD) there was a switch to organised epicardial activity consistent with type II VF, and lasting between 10 and 60 s. During these periods the activity on the epicardium was coherent, the number of epicardial phase singularities fell below 90% of the overall mean value, the number of wavefronts decreased, and DF was uniformly distributed across the epicardium. In each case the period of organised activity was transient, with a return to more disorganised epicardial activity. In the remaining six patients there was no period of activity consistent with type II VF.
Conclusion. The progression from type I to type II VF during ischemia in the human heart is transient and reversible, and is modulated by other factors in addition to global ischemia.