I was intrigued by the report of Morin et al in the June 15 issue of The American Journal of Cardiology on the differences in the frequency of T-wave inversion (TWI) in leads V ₁ to V ₃ between arrhythmogenic right ventricular cardiomyopathy (ARVC) and idiopathic ventricular tachycardia (VT), arising from the right ventricular outflow tract (RVOT). Certainly, it would constitute a diagnostic advancement to be sure that TWIs in leads V ₂ to V ₄ are helpful in distinguishing ARVC from RVOT, rightly making the transition from minor to major criterion in the diagnosis of the former. However, one is struck by the wide range of frequency of VT reported in the published research and cited by the investigators, in the RVOT (6% to 20%) and ARVC (36% to 96%). One wonders how reproducible are these TWIs in these 2 clinical entities. Along this line of thought, it would be helpful to evaluate whether what was found on the index electrocardiograms used in this study in the 79 patients with ARVC from the National Institutes of Health cohort and the 121 patients with RVOT from the Cornell University Medical Center registry is representative in other available electrocardiograms, of what was observed in these 2 populations long term. In other words, what is the reproducibility of the TWIs on the electrocardiograms in these 2 different databases? If we assume that the pattern described herein is truly representative of what was found in ≥2 electrocardiograms in the patients with these 2 different pathologies, another issue arises: is it possible that the difference in these 2 study populations is due to a difference in the frequency of VT or other ventricular ectopy, for example, premature ventricular contractions (PVCs) with left bundle branch block pattern seen in Figures 1 and 2 of the investigators’ report? TWIs have been observed in patients with transient VT, PVCs, and ventricular pacing (cardiac memory) and show a pattern of change in amplitude and duration, eventually disappearing, after the cessation of the inciting mechanism. Is it possible that in ARVC and/or RVOT, these TWIs, found not invariably, constitute manifestations of the cardiac memory phenomenon? There is no reason after all that ARVC and RVOT should be “immune” to the cardiac memory influences consequent to bouts of VT or time periods with frequent PVCs. Also, the polarity of the TWIs the investigators examined in their patients with ARVC and RVOT (negative in the right precordial leads) is exactly what one expects in the lingering for some time T-wave changes in the right precordial leads seen after the cessation of the inciting ventricular arrhythmia emanating from the right ventricle or right ventricular pacing (cardiac memory effect), which as per the classic report of Rosenbaum et al, “shows the same direction as the abnormal QRS forces,” that is, negative, or downward, as the S waves of the left bundle branch block–like appearances of the ventricular arrhythmia or pacing complexes. Consequently, one could envisage that the patients with ARVC and RVOT have different frequencies and durations of VT or PVCs, and thus the presence and depth of their TWIs are different. The investigators would make a real contribution by investigating (if data are available) the perceived frequency of VT and PVCs in these 200 patients via all of their available electrocardiograms, Holter monitors, “event recorders,” implantable cardioverter-defibrillator interrogations, and medical chart review. Information about the reproducibility of TWIs in ARVC and RVOT could confirm that there is a real differential after all between the frequency of TWIs in these 2 cardiac conditions and unequivocally establish TWIs in leads V ₂ to V ₄ as a major diagnostic criterion of ARVC.