Pacing in proximity to scar during cardiac resynchronization therapy increases local dispersion of repolarization and susceptibility to ventricular arrhythmogenesis.

Background: Cardiac resynchronization therapy (CRT) increases the risk of ventricular tachycardia (VT) in patients with ischemic cardiomyopathy (ICM) when the left ventricular (LV) epicardial lead is implanted in proximity to scar.

Objective: The purpose of this study was to determine the mechanisms underpinning this risk by investigating the effects of pacing on local electrophysiology (EP) in relation to scar that provides a substrate for VT in ICM patients undergoing CRT.

Methods: Imaging data from ICM patients (n = 24) undergoing CRT were used to create patient-specific LV anatomic computational models including scar morphology. Simulations of LV epicardial pacing at 0.2-4.5 cm from the scar were performed using EP models of chronic infarct and heart failure (HF). Dispersion of repolarization and the vulnerable window were computed as surrogates for VT risk.

Results: Simulations predict that pacing in proximity to scar (0.2 cm) compared to more distant pacing to a scar (4.5 cm) significantly (P <.01) increased dispersion of repolarization in the vicinity of the scar and widened (P <.01) the vulnerable window, increasing the likelihood of unidirectional block. Moreover, slow conduction during HF further increased dispersion (∼194%). Analysis of variance and post hoc tests show significantly (P <.01) reduced repolarization dispersion when pacing ≥3.5 cm from the scar compared to pacing at 0.2 cm.

Conclusion: Increased dispersion of repolarization in the vicinity of the scar and widening of the vulnerable window when pacing in proximity to scar provides a mechanistic explanation for VT induction in ICM-CRT with lead placement proximal to scar. Pacing 3.5 cm or more from scar may avoid increasing VT risk in ICM-CRT patients.