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The precordial R' wave: A novel discriminator between cardiac sarcoidosis and arrhythmogenic right ventricular cardiomyopathy in patients presenting with ventricular tachycardia

JC. Hoogendoorn, J. Venlet, YNJ. Out, S. Man, S. Kumar, M. Sramko, DG. Dechering, I. Nakajima, KC. Siontis, M. Watanabe, Y. Nakamura, UB. Tedrow, F. Bogun, L. Eckardt, P. Peichl, WG. Stevenson, K. Zeppenfeld

. 2021 ; 18 (9) : 1539-1547. [pub] 20210503

Jazyk angličtina Země Spojené státy americké

Typ dokumentu časopisecké články, multicentrická studie, práce podpořená grantem

Perzistentní odkaz   https://www.medvik.cz/link/bmc22012244

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.

Citace poskytuje Crossref.org

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$a BACKGROUND: Cardiac sarcoidosis (CS) with right ventricular (RV) involvement can mimic arrhythmogenic right ventricular cardiomyopathy (ARVC). Histopathological differences may result in disease-specific RV activation patterns detectable on the 12-lead electrocardiogram. Dominant subepicardial scar in ARVC leads to delayed activation of areas with reduced voltages, translating into terminal activation delay and occasionally (epsilon) waves with a small amplitude. Conversely, patchy transmural RV scar in CS may lead to conduction block and therefore late activated areas with preserved voltages reflected as preserved R' waves. OBJECTIVE: The purpose of this study was to evaluate the distinct terminal activation patterns in precordial leads V1 through V3 as a discriminator between CS and ARVC. METHODS: Thirteen patients with CS affecting the RV and 23 patients with gene-positive ARVC referred for ventricular tachycardia ablation were retrospectively included in a multicenter approach. A non-ventricular-paced 12-lead surface electrocardiogram was analyzed for the presence and the surface area of the R' wave (any positive deflection from baseline after an S wave) in leads V1 through V3. RESULTS: An R' wave in leads V1 through V3 was present in all patients with CS compared to 11 (48%) patients with ARVC (P = .002). An algorithm including a PR interval of ≥220 ms, the presence of an R' wave, and the surface area of the maximum R' wave in leads V1 through V3 of ≥1.65 mm2 had 85% sensitivity and 96% specificity for diagnosing CS, validated in a second cohort (18 CS and 40 ARVC) with 83% sensitivity and 88% specificity. CONCLUSION: An easily applicable algorithm including PR prolongation and the surface area of the maximum R' wave in leads V1 through V3 of ≥1.65 mm2 distinguishes CS from ARVC. This QRS terminal activation in precordial leads V1 through V3 may reflect disease-specific scar patterns.
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$a Venlet, Jeroen $u Department of Cardiology, Willem Einthoven Center of Arrhythmia Research and Management, Leiden University Medical Center, Leiden, The Netherlands
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$a Out, Yannick N J $u Department of Cardiology, Willem Einthoven Center of Arrhythmia Research and Management, Leiden University Medical Center, Leiden, The Netherlands
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$a Man, Sumche $u Department of Cardiology, Willem Einthoven Center of Arrhythmia Research and Management, Leiden University Medical Center, Leiden, The Netherlands
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$a Kumar, Saurabh $u Department of Cardiology, Brigham and Women's Hospital, Boston, Massachusetts
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$a Sramko, Marek $u Department of Cardiology, Institute of Clinical and Experimental Medicine, Prague, The Czech Republic
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$a Dechering, Dirk G $u Department of Cardiology II (Electrophysiology), University Hospital Münster, Münster, Germany
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$a Nakajima, Ikutaro $u Department of Cardiology, Vanderbilt University Medical Center, Nashville, Tennessee
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$a Siontis, Konstantinos C $u Department of Cardiology, University of Michigan, Ann Arbor, Michigan; Department of Cardiovascular Medicine, Mayo Clinic, Rochester, Minnesota
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$a Watanabe, Masaya $u Department of Cardiology, Hokkaido University Hospital, Hokkaido, Japan
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$a Nakamura, Yoshinori $u Department of Cardiology, Willem Einthoven Center of Arrhythmia Research and Management, Leiden University Medical Center, Leiden, The Netherlands
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$a Tedrow, Usha B $u Department of Cardiology, Brigham and Women's Hospital, Boston, Massachusetts
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$a Bogun, Frank $u Department of Cardiology, University of Michigan, Ann Arbor, Michigan
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$a Eckardt, Lars $u Department of Cardiology II (Electrophysiology), University Hospital Münster, Münster, Germany
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$a Peichl, Petr $u Department of Cardiology, Institute of Clinical and Experimental Medicine, Prague, The Czech Republic
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$a Stevenson, William G $u Department of Cardiology, Vanderbilt University Medical Center, Nashville, Tennessee
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$a Zeppenfeld, Katja $u Department of Cardiology, Willem Einthoven Center of Arrhythmia Research and Management, Leiden University Medical Center, Leiden, The Netherlands. Electronic address: k.zeppenfeld@lumc.nl
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