We appreciate the comments of Dr. Madias, who questions whether the observed difference in precordial T-wave inversion between patients with arrhythmogenic right ventricular cardiomyopathy (ARVC) and right ventricular outflow tract tachycardia is related to cardiac memory. We agree that this is a pertinent point.
As discussed in our report, the prevailing theory for the cause of T-wave inversion in ARVC is progressive fibrofatty replacement of the right ventricular myocardium. According to this hypothesis, as right ventricular disease progresses, the extent of precordial T-wave inversion increases. T-wave inversion has been shown to correlate with the severity of right ventricular involvement and/or enlargement. Of note, all patients in our ARVC registry had been recently diagnosed. However, we agree that the link between later stage disease and T-wave inversion could indeed be caused by a higher burden of ventricular premature contractions. An alternative hypothesis would be that patients with ARVC are more susceptible to the effects of cardiac memory, causing more pronounced T-wave inversion in response to a similar arrhythmic burden.
Our study examined baseline 12-lead sinus rhythm electrocardiograms, without consideration of (or recording of) the frequency of ectopy immediately preceding the tracings. Not every patient in the registries underwent the same workup (e.g., Holter monitoring or even serial electrocardiography at defined intervals). Despite these limitations, we are investigating the potential association of precordial T-wave inversion and ventricular ectopy burden. We also plan to investigate the long-term reproducibility of T-wave inversions in these patients.