Site of the Arrhythmogenic Focus and Cardiac Vulnerability to Ventricular Fibrillation

Abstract

The aim of this study was to test the hypothesis that a subendocardial arrhythmogenic focus makes the heart more susceptible to VF due to electrical interaction with the Purkinje network. Monofocal ventricular tachycardia (mVT) was created by injecting 5-microg aconitine into the left ventricular subepicardium (EPI-mVT, n = 8) or subendocardium (ENDO-mVT, n = 13) in anesthetized dogs. Despite the similar cycle length of mVT, the incidence of VF was significantly different between EPI-mVT and ENDO-mVT (100 [8/8] vs 46% [6/13], P <0.05). VF was invariably preceded by hemodynamic deterioration. Three-dimensional cardiac mapping (n = 10, 221 +/- 11 recording sites) revealed that VF was triggered solely by focal firing unrelated to the primary arrhythmogenic focus in both mVT models. No interaction between the primary focus and adjacent endocardial tissue was indicated. These results suggest that the proximity of the arrhythmogenic focus to the Purkinje network has little role in cardiac vulnerability to VF, and that progression of mVT to VF is largely caused by sporadic focal firing regardless of the site of the arrhythmogenic focus in the present animal model.

Focal and Reentrant Mechanisms of Torsades de Pointes: EAD, Reentry, or Chimera?

“…In a preliminary experiment of our previous study, 9) we assessed the propagation of activation from focal origin created by injecting aconitine which is known to induce focal firing via triggered activity due to early and delayed afterdepolarizations. In the presence of monofocal aconitineinduced VT, additional ventricular pacing at a variable rate around that of aconitine-induced VT easily developed twisting QRS morphology.…”