Abstract
Despite a high incidence of non-sustained ventricular tachycardia in patients with transthyretin cardiac amyloidosis (TTR-CA), sudden tachyarrhythmic death is uncommon. Homogeneous myocardial deposition of amyloid fibrils may mitigate against sustained ventricular arrhythmias. In contrast, myocardial scar heterogeneity is an established predictor of sudden cardiac death in hypertrophic cardiomyopathy (HCM), as evidenced by increased myocardial dispersion of repolarization. Whether such indices of arrhythmogenesis are evident in TTR-CA has not been established.
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