Abstract 13144: Epsilon Waves on Electrocardiograms in Pulmonary Hypertensive Patients With and Without Right Ventricular Hypertrophy or Fibrosis: Comparison With Arrhythmogenic Right Ventricular Cardiomyopathy

Abstract

Introduction: Epsilon waves on V1-3 leads are one of the specific ECG findings in patients with arrhythmogenic right ventricular (RV) cardiomyopathy (ARVC) that suggest the presence of RV conduction delay. Hypothesis: In patients with pulmonary hypertension (PH) due to RV pressure load, RV hypertrophy and fibrosis are frequently observed that may lead to RV conduction delay and epsilon waves. Methods: We retrospectively analyzed 43 PH patients (33 females, 55 ± 15 years, 31 chronic thromboembolic PH, seven idiopathic pulmonary arterial hypertension), with proven PH by right heart catheterization. On CT, RV fibrosis was defined as a contrast defect in the early phase and a conversely abnormal enhancement in the late phase. We also retrospectively analyzed 17 patients (11 males, 57 ± 17 years) with suspected ARVC who underwent cardiac CT. Of these, nine met 2010 ARVC task force criteria on cardiac CT. Results: All 9 ARVC patients (100%) had epsilon waves on ECG. In PH patients, 32 and 9 patients had RV hypertrophy and fibrosis, respectively. Of these, 4 patients had both. Among 32 PH patients with RV hypertrophy, 2 had complete right bundle branch block (RBBB) and 8 had incomplete RBBB. Of 22 PH patients with RV hypertrophy but without any RBBB, two (9%, P < 0.01, compared with ARVC) had waves with abnormal small upward spikes after the QRS wave. These were more marked in lead II and aVF leads than in V1 and 2 leads, and were not typical epsilon waves, suggesting RV conduction delay shown in ARVC. Fourteen patients had a negative T wave in V1-3 leads (5 had only a V1 lead, one had only V1 and 2 leads, four had only V1-3 leads, and four only had V1-4 leads, respectively). Of nine PH patients with RV hypertrophy, one had complete RBBB and one had incomplete RBBB. Of seven PH patients with RV fibrosis but without any RBBB, none (0%, P < 0.01, compared with ARVC) had epsilon waves in V1-3 leads; all seven had a negative T wave in V1-3 leads (three only had a V1 lead, one had only V1 and 2 leads, two had only V1-3 leads, and one had V1-4 leads). Conclusions: In PH patients with an organized RV myocardial change, such as RV hypertrophy and/or fibrosis, the frequency of epsilon waves was significantly less than those in ARVC. Epsilon waves seem not only to be caused by an organized RV myocardium but also by other factors.