Tuomas V Kenttä1, Bruce D Nearing2, Kimmo Porthan3, Jani T Tikkanen4, Matti Viitasalo3, Markku S Nieminen3, Veikko Salomaa5, Lasse Oikarinen3, Antti Jula5, Kimmo Kontula6, Chris Newton-Cheh7, Heikki V Huikuri8, Richard L Verrier9. 1. Medical Research Center Oulu, University of Oulu and University Hospital of Oulu, Oulu, Finland; Beth Israel Deaconess Medical Center, Boston, Massachusetts. 2. Beth Israel Deaconess Medical Center, Boston, Massachusetts; Harvard Medical School, Boston, Massachusetts. 3. Division of Cardiology, Heart and Lung Center, Helsinki University Central Hospital, Helsinki, Finland. 4. Medical Research Center Oulu, University of Oulu and University Hospital of Oulu, Oulu, Finland; Emergency Department, Haartman Hospital, Helsinki, Finland. 5. National Institute for Health and Welfare, Helsinki, Finland. 6. Department of Medicine, University of Helsinki, Helsinki, Finland. 7. Cardiovascular Research Center and Center for Human Genetic Research, Massachusetts General Hospital, Boston, Massachusetts; Program in Medical and Population Genetics, Broad Institute, Cambridge, Massachusetts. 8. Medical Research Center Oulu, University of Oulu and University Hospital of Oulu, Oulu, Finland. 9. Beth Israel Deaconess Medical Center, Boston, Massachusetts; Harvard Medical School, Boston, Massachusetts. Electronic address: rverrier@bidmc.harvard.edu.
Abstract
BACKGROUND: Heterogeneity of depolarization and repolarization underlies the development of lethal arrhythmias. OBJECTIVE: We investigated whether quantification of spatial depolarization and repolarization heterogeneity identifies individuals at risk for sudden cardiac death (SCD). METHODS: Spatial R-, J-, and T-wave heterogeneity (RWH, JWH, and TWH, respectively) was analyzed using automated second central moment analysis of standard digital 12-lead electrocardiograms in 5618 adults (2588, 46% men; mean ± SEM age 50.9 ± 0.2 years), who took part in the epidemiological Health 2000 Survey as representative of the entire Finnish adult population. RESULTS: During the follow-up period of 7.7 ± 0.2 years, a total of 72 SCDs occurred (1.3%), with an average yearly incidence rate of 0.17% per year. Increased RWH, JWH, and TWH in left precordial leads (V4-V6) were univariately associated with SCD (P < .001 for each). When adjusted with standard clinical risk markers, JWH and TWH remained independent predictors of SCD. Increased TWH (≥102 µV) was associated with a 1.7-fold adjusted relative risk for SCD (95% confidence interval [CI] 1.0-2.9; P = .048) and increased JWH (≥123 µV) with a 2.0-fold adjusted relative risk for SCD (95% CI 1.2-3.3; P = .006). When both TWH and JWH were above the threshold, the adjusted relative risk for SCD was 2.9-fold (95% CI 1.5-5.7; P = .002). When RWH (≥470 µV), JWH, and TWH were all above the threshold, the adjusted relative risk for SCD was 3.2-fold (95% CI 1.4-7.1; P = .009). CONCLUSION: Second central moment analysis of standard resting 12-lead electrocardiographic morphology provides an ultrarapid means for the automated measurement of spatial RWH, JWH, and TWH, enabling analysis of high subject volumes and screening for SCD risk in the general population.
BACKGROUND: Heterogeneity of depolarization and repolarization underlies the development of lethal arrhythmias. OBJECTIVE: We investigated whether quantification of spatial depolarization and repolarization heterogeneity identifies individuals at risk for sudden cardiac death (SCD). METHODS: Spatial R-, J-, and T-wave heterogeneity (RWH, JWH, and TWH, respectively) was analyzed using automated second central moment analysis of standard digital 12-lead electrocardiograms in 5618 adults (2588, 46% men; mean ± SEM age 50.9 ± 0.2 years), who took part in the epidemiological Health 2000 Survey as representative of the entire Finnish adult population. RESULTS: During the follow-up period of 7.7 ± 0.2 years, a total of 72 SCDs occurred (1.3%), with an average yearly incidence rate of 0.17% per year. Increased RWH, JWH, and TWH in left precordial leads (V4-V6) were univariately associated with SCD (P < .001 for each). When adjusted with standard clinical risk markers, JWH and TWH remained independent predictors of SCD. Increased TWH (≥102 µV) was associated with a 1.7-fold adjusted relative risk for SCD (95% confidence interval [CI] 1.0-2.9; P = .048) and increased JWH (≥123 µV) with a 2.0-fold adjusted relative risk for SCD (95% CI 1.2-3.3; P = .006). When both TWH and JWH were above the threshold, the adjusted relative risk for SCD was 2.9-fold (95% CI 1.5-5.7; P = .002). When RWH (≥470 µV), JWH, and TWH were all above the threshold, the adjusted relative risk for SCD was 3.2-fold (95% CI 1.4-7.1; P = .009). CONCLUSION: Second central moment analysis of standard resting 12-lead electrocardiographic morphology provides an ultrarapid means for the automated measurement of spatial RWH, JWH, and TWH, enabling analysis of high subject volumes and screening for SCD risk in the general population.
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Authors: Felipe R Monteiro; Ana B Rabelo Evangelista; Bruce D Nearing; Sofia A Medeiros; Fernanda Tessarolo Silva; Giovanna C Pedreira; Edward Ullman; Ernest V Gervino; Richard L Verrier Journal: Ann Noninvasive Electrocardiol Date: 2021-02-05 Impact factor: 1.468
Authors: Gordon M Burke; Bruna Araujo Silva; Alexandre A Marum; Alexandre L Bortolotto; Bruce D Nearing; Michael J Chen; Sarah Fostello; Jeffrey J Popma; Richard L Verrier; James D Chang Journal: Open Heart Date: 2021-10