Key result
Localized right precordial QRS prolongation on conventional ECG distinguished arrhythmogenic right ventricular dysplasia from idiopathic RVOT tachycardia with 93% sensitivity and 96% specificity.
Why the study?
Does localized right precordial QRS prolongation on conventional ECG accurately distinguish arrhythmogenic right ventricular dysplasia from idiopathic right ventricular outflow tract tachycardia?
Observational (n=67)
Does localized right precordial QRS prolongation on conventional ECG accurately distinguish arrhythmogenic right ventricular dysplasia from idiopathic right ventricular outflow tract tachycardia?
Localized right precordial QRS prolongation on a standard 12-lead ECG is a highly sensitive and specific marker for distinguishing arrhythmogenic right ventricular dysplasia from idiopathic RVOT tachycardia.
Answers are grounded in this paper and cite their sources.
May aid ECG differentiation of ARVD from RVOT tachycardia; leaves open prospective validation before clinical adoption.
Objective: Arrhythmogenic right ventricular dysplasia up to now is a rare cardiomyopathic entity with certain difficulties in clinical definition of diagnostic criteria. In 42 patients with major and minor criteria of arrhythmogenic right ventricular dysplasia and 25 patients with idiopathic ventricular arrhythmia, the role of conventional ECG in the diagnosis of arrhythmogenic right ventricular dysplasia was reevaluated. Methods: In standard 12‐lead ECG, QRS duration was measured in limb lead D1, and in V1‐V6. A ratio of the sum of right (V2+ V3) and left (V4+ V5) was calculated. T wave inversions, Epsilon wave, and mechanisms of advancing right bundle branch block were analyzed. Results: In 39 out of 42 patients (93%) with the diagnosis of arrhythmogenic right ventricular dysplasia, a ratio of right and left precordial QRS duration of >1.2, a maximum right precordial QRS duration of > 100 ms in 10 cases (26%) and >110 ms in 29 cases (74%) could be found. Incomplete right bundle branch block with right precordial T inversions was found in one case. The ECG in two patients revealed a precordial R/S transition in V1 or V2; in all other cases, R/S transition was localized in V3 or V4. R peak time was normal (< 0.04 s) in all cases, a “notching” or “slurring” of the S wave was striking in 16 cases. T wave inversions were found in 27 cases and definite Epsilon wave in only one case. Although incomplete right bundle branch block and certain preforms could also be disclosed in four patients with idiopathic right ventricular outflow tract (RVOT) tachycardia, localized right precordial QRS prolongation could be excluded in all but one of these cases. Localized right precordial QRS duration prolongation in one case was probably due to a rotation of the heart with a precordial R/S transition between V1 and V2. Conclusion: Localized right precordial QRS prolongation in a normal precordial R/S transition: (a) seems to be the most important aspect of arrhythmogenic right ventricular dysplasia at conventional ECG, with a sensitivity of 93% and a specificity of 96% in order to distinguish idiopathic RVOT tachycardia; (b) can appear with (64%) or without (36%) secondary T wave inversions; and (c) is due to a “parietal” block sparing the specialized conducting system.
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Peters et al. (1996) conducted an observational in Arrhythmogenic right ventricular dysplasia and idiopathic right ventricular outflow tract tachycardia (n=67). Conventional ECG (localized right precordial QRS prolongation) vs. Idiopathic ventricular arrhythmia / RVOT tachycardia was evaluated on Diagnostic accuracy of localized right precordial QRS prolongation for arrhythmogenic right ventricular dysplasia (Sensitivity 93%, Specificity 96%). Localized right precordial QRS prolongation on conventional ECG distinguished arrhythmogenic right ventricular dysplasia from idiopathic RVOT tachycardia with 93% sensitivity and 96% specificity.
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