Background: Cardiac infarction-induced necrosis is in long term considered as an electrical barrier that slows the pass by electrical conduction, forming the base of re-entry. However, this theoretic concept has never been demonstrated in the beating heart.
Methods: We produced a necrotic area in the left ventricle of rats with absolute ethanol, and the changes of ventricular excitation threshold (VET), ventricular conduction time (VCT) and effective refractory period (ERP) were measured with shortening the stimulation cycle length and varying the stimulation sites away from the lesion spot. The susceptibility to ventricular arrhythmias was assessed with arrhythmia scoring at different stimulation sites.
Results: We found that the VET was dramatically reduced after lesion induction. Interestingly, the VCT was shortened significantly along with a shortening of ERP, indicating a facilitation of excitation conduction. When the excitations were produced with progressive shortening of pacing interval, the VET and VCT further decreased. A higher arrhythmia score was recorded at the remote peripheral of the necrotic area compared to the boundary of the lesion by induction of ectopic stimulation.
Conclusion: Contrary to the conventional theory, we demonstrated that lesion production did not suppress but rather facilitate impulse induction and propagation in the ventricle, especially for the ectopic excitations. These electrical alterations facilitate ectopic beats induction and increase the susceptibility to ventricular arrhythmia after cardiac lesion, e.g. myocardial infarction.
