The precordial R' wave: A novel discriminator between cardiac sarcoidosis and arrhythmogenic right ventricular cardiomyopathy in patients presenting with ventricular tachycardia
Language English Country United States Media print-electronic
Document type Journal Article, Multicenter Study, Research Support, Non-U.S. Gov't
PubMed
33957319
DOI
10.1016/j.hrthm.2021.04.032
PII: S1547-5271(21)00411-2
Knihovny.cz E-resources
- Keywords
- Arrhythmogenic right ventricular cardiomyopathy, Cardiac sarcoidosis, Right bundle branch block, Twelve-lead surface electrocardiogram, Ventricular tachycardia,
- MeSH
- Arrhythmogenic Right Ventricular Dysplasia complications diagnosis physiopathology MeSH
- Diagnosis, Differential MeSH
- Adult MeSH
- Electrocardiography * MeSH
- Cardiomyopathies complications diagnosis physiopathology MeSH
- Tachycardia, Ventricular complications diagnosis physiopathology MeSH
- Middle Aged MeSH
- Humans MeSH
- Follow-Up Studies MeSH
- Retrospective Studies MeSH
- Sarcoidosis diagnosis physiopathology MeSH
- Check Tag
- Adult MeSH
- Middle Aged MeSH
- Humans MeSH
- Male MeSH
- Female MeSH
- Publication type
- Journal Article MeSH
- Multicenter Study MeSH
- Research Support, Non-U.S. Gov't MeSH
BACKGROUND: Cardiac sarcoidosis (CS) with right ventricular (RV) involvement can mimic arrhythmogenic right ventricular cardiomyopathy (ARVC). Histopathological differences may result in disease-specific RV activation patterns detectable on the 12-lead electrocardiogram. Dominant subepicardial scar in ARVC leads to delayed activation of areas with reduced voltages, translating into terminal activation delay and occasionally (epsilon) waves with a small amplitude. Conversely, patchy transmural RV scar in CS may lead to conduction block and therefore late activated areas with preserved voltages reflected as preserved R' waves. OBJECTIVE: The purpose of this study was to evaluate the distinct terminal activation patterns in precordial leads V1 through V3 as a discriminator between CS and ARVC. METHODS: Thirteen patients with CS affecting the RV and 23 patients with gene-positive ARVC referred for ventricular tachycardia ablation were retrospectively included in a multicenter approach. A non-ventricular-paced 12-lead surface electrocardiogram was analyzed for the presence and the surface area of the R' wave (any positive deflection from baseline after an S wave) in leads V1 through V3. RESULTS: An R' wave in leads V1 through V3 was present in all patients with CS compared to 11 (48%) patients with ARVC (P = .002). An algorithm including a PR interval of ≥220 ms, the presence of an R' wave, and the surface area of the maximum R' wave in leads V1 through V3 of ≥1.65 mm2 had 85% sensitivity and 96% specificity for diagnosing CS, validated in a second cohort (18 CS and 40 ARVC) with 83% sensitivity and 88% specificity. CONCLUSION: An easily applicable algorithm including PR prolongation and the surface area of the maximum R' wave in leads V1 through V3 of ≥1.65 mm2 distinguishes CS from ARVC. This QRS terminal activation in precordial leads V1 through V3 may reflect disease-specific scar patterns.
Department of Cardiology 2 University Hospital Münster Münster Germany
Department of Cardiology Brigham and Women's Hospital Boston Massachusetts
Department of Cardiology Hokkaido University Hospital Hokkaido Japan
Department of Cardiology Institute of Clinical and Experimental Medicine Prague The Czech Republic
Department of Cardiology University of Michigan Ann Arbor Michigan
Department of Cardiology Vanderbilt University Medical Center Nashville Tennessee
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