Abstract 1056: Inhomogeneous Structure of Ventricular Walls Contributes to Stretch-Induced Arrhythmias
Mechanical induction of cardiac rhythm disturbances has been reported with increasing frequency. In commotio cordis, stretch-induced focal excitation develops into ventricular fibrillation. We assessed the hypothesis that, in the inhomogeneously structured ventricular walls, mechanical stresses produce the inhomogeneous strain distribution, and initiate focal excitation. To examine the role of ventricular structure in stretch-induced arrhythmogenicity, we applied transient stretch pulses (5%–25%) to arterially perfused rabbit right ventricular myocardial sheet (n = 8). The strain distribution and excitation propagation were measured by our original optical mapping system, which enabled us to map action potentials even in moving objects. The 3-D morphology of preparations was examined by the laser displacement meter. The large stretch (15% < ) induced the whole excitation of preparation, whereas the medium stretch (10%–15%) induced focal excitation. The focus of excitation located in the thinner area of preparation where the local strain was large (Fig. 1⇓, 2⇓). Using a computer simulation, we confirmed whether the structure of ventricular walls can initiate the focal excitation. The computer simulation was performed by using a finite element model, where the 3-D morphology was incorporated. The model successfully reproduced the process (Fig. 2⇓). In conclusion, Inhomogeneous structure of ventricular walls contributes to stretch-induced focal excitation and resultant fatal arrhythmias.