The precordial R-prime wave: a discriminator between cardiac sarcoidosis and ARVC

Cardiac sarcoidosis in the right ventricle may often mimic arrhythmogenic right ventricular cardiomyopathy (ARVC), but the histopathologic differences between the diseases result in different right ventricular activation patterns. A multicentre, retrospective study showed that cardiac sarcoidosis led to a larger precordial R-prime wave, which can be used to differentiate between the conditions [1].

Dr Jarieke Hoogendoorn (Leiden University Medical Centre, the Netherlands) presented the results of a multicentre, retrospective study aimed to discriminate between patients with cardiac sarcoidosis and ARVC using electrocardiogram (ECG) [1]. Cardiac sarcoidosis with right ventricular involvement may mimic ARVC. Thus, Dr Hoogendoorn and colleagues hypothesised that the histopathologic differences between the diseases would result in different specific right ventricular activation patterns detectable on ECG. In ARVC, scar tissue progresses from epicardium to endocardium and may lead to delayed activation of areas with reduced voltages with small amplitude on the ECG. In cardiac sarcoidosis, patchy transmural right ventricular scar tissue leads to conduction block and thus late activated areas with preserved voltages, reflected as preserved R-prime (R’)-waves in the right precordial leads.

This retrospective study included patients with cardiac sarcoidosis with right ventricular involvement (n=13) or gene-positive ARVC referred for ventricular tachycardia ablation (n=23). A non-ventricular-paced, 12-lead surface ECG prior to ablation was obtained and analysed using the Leiden ECG Analysis and Decomposition Software. Based on the hypothesis that conduction block in cardiac sarcoidosis leads to late activated areas with preserved voltages, the surface area of the R’-wave in V1-V3 was measured. An R’-wave was defined as any positive deflection from baseline after an S-wave.

An R’-wave in V1-V3 was present in all cardiac sarcoidosis patients compared with 11 (48%) of ARVC patients (P=0.002). The maximum R’-wave surface area in lead V1-V3 was 3.55 mm² in cardiac sarcoidosis (IQR 2.18-5.81) versus 0.00 mm² in ARVC (IQR 0.00-0.43; P<0.001). By ROC analysis, the maximum R’-wave surface area in lead V1-V3 was an excellent discriminator (AUC 0.980; 95% CI 0.945-1.000). A cut-off of ≥1.65 mm² had a sensitivity of 85% and specificity of 96% for diagnosing cardiac sarcoidosis. This was validated in a second cohort including 18 cardiac sarcoidosis and 40 ARVC patients, with 72% sensitivity and 88% specificity [1].

Dr Hoogendoorn concluded that transmural right ventricular scars in cardiac sarcoidosis lead to a localised conduction block and thus to a large R’-wave. An easily applicable algorithm including a terminal S-wave and surface area maximum R’-wave in V1-V3 was shown to be a good discriminator between cardiac sarcoidosis and ARVC. The QRS terminal activation in precordial leads V1-V3 may reflect disease specific scar patterns.

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   1. Hoogendorn J. The precordial R-prime wave: a novel discriminator between cardiac sarcoidosis and arrhythmogenic right ventricular cardiomyopathy in patients presenting with ventricular tachycardia. EHRA 2021 Congress, 23-25 April.

 

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Posted on 16 June 202123 June 2021