Changes in Follow‐Up ECG and Signal‐Averaged ECG in Patients with Arrhythmogenic Right Ventricular Cardiomyopathy

Abstract

Follow-up ECGs and SAECGs showed changes in 39% of patients with ARVC. Larger studies with a longer follow-up period are needed to investigate the clinical implications of changes in follow-up ECG and SAECG.

Late potentials and their correlation with ventricular structure in patients with ventricular arrhythmias

“…Unfortunately, no absolute consistency between these electrocardiographic markers of myocardial damage has been demonstrated. In fact, the presence of an epsilon wave may not always correlate with positive LP and diagnostic findings on the ECG may develop over time and independently of right ventricular size in ARVC patients . On a normal 12‐lead ECG, a low noise level will make the identification of epsilon waves easier; similarly, the sensitivity for LP will be increased on an SAECG .…”

Right ventricular scar‐related ventricular tachycardia in nonischemic cardiomyopathy: Electrophysiological characteristics, mapping, and ablation of underlying heart disease

“…This observation suggests that RCUS patients may have more extensive electrical abnormalities relative to structural abnormalities at the time of VT ablation. Further, detailed analysis of ECG patterns showed a lower incidence of abnormalities such as localized QRS prolongation, fragmented QRS, parietal block, negative T waves, and T‐wave inversion in the inferior leads, which are associated with more severe phenotype of ARVC/D or with increased risk of arrhythmic events …”

“…The following parameters were compared: mean QRS duration, presence of complete right, left, or incomplete bundle branch block. In the absence of bundle branch block on the ECG, the following published parameters, associated with ARVC/D, were compared between the three groups: localized QRS prolongation (> 110 milliseconds) right precordial leads; fragmented QRS (defined as deflections at the beginning of the QRS complex, on top of the R wave, or in the nadir of the S wave in either one or more right precordial lead or in more than one lead including all remaining standard ECG leads); parietal block (defined as QRS duration [QRS d ] in leads V 1 through V 3 that exceeds the QRS d in lead V 6 by ≥ 25 milliseconds); QRS d ratio (a ratio of the QRS d in leads V 1 +V 2 +V 3 /V 4 +V 5 +V 6 ≥ 1.2); R/S ratio in V 2 < 1; prolonged QRS d in the inferior leads (II, III or avF of ≥ 100 milliseconds, longer than in other limb leads); left or right axis deviation (frontal plane axis of < − 30 ° or > 90 °, respectively); low QRS amplitude in the limb leads (≤0.5 mV); delayed S‐wave upstroke in the right precordial leads (> 60 milliseconds from nadir of S wave to baseline in leads V 1 ‐V 3 ); poor R‐wave progression; T‐wave inversion in the inferior leads (II, III, avF); negative T waves (≥1 mm in depth in ≥2 adjacent leads); QRS dispersion (difference between the maximum and minimum QRS d values occurring in any of the precordial leads) . All ECG measurements were performed blinded to clinical and procedural characteristics.…”

Cell Junctions in the Specialized Conduction System of the Heart

“…ARVC is a prime example of a cardiac disease associated with mutations/defects in desmosomal cell-cell junction components leading to defects in cardiac conduction, which include specific defects in the His-Purkinje system (Zusterzeel et al, 2013, Quarta et al, 2011, Bae et al, 2013, Bao et al, 2013, Cox et al, 2011) (Table 2). The electrophysiological criteria for diagnosing ARVC include epsilon waves, late potentials, prolonged terminal activation duration, ventricular tachycardia, and extrasystoles (Marcus et al, 2010).…”