JACC. Clinical electrophysiology · 2026
Genotype and Family History as Risk Markers of Sudden Cardiac Death in Hypertrophic Cardiomyopathy.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Sakhnini Ali, Montazeri Mahdi, Chow Cindy, Silver Josh, Signorile Marisa, Chan Raymond, Gollob Michael H, Runeckles Kyle, Steve Fan Chun-Po, Rowin Ethan, Maron Martin, Rakowski Harry, Adler Arnon
Аннотация
BACKGROUND: There are limited data on genotype as a risk marker of sudden cardiac death (SCD) in hypertrophic cardiomyopathy (HCM). It remains unknown whether family history of SCD (FHxSCD) is a risk marker of SCD independently of genotype.
OBJECTIVES: The goal of this study was to assess the association of genotype and FHxSCD with SCD outcomes in HCM and investigate methods for incorporation of genotype into SCD risk stratification models.
METHODS: This historical cohort study used registries of 2 HCM referral centers. Association of FHxSCD and genotype with SCD was assessed by multivariable hazard regression analysis.
RESULTS: Of 3,258 patients, 896 (27.5%) were genotype-positive, and 332 (10.2%) had FHxSCD. During 4.9 years' median follow-up, 114 patients reached the SCD outcome. On multivariable analysis, the hazard ratios for SCD were 1.83 (95% CI: 1.161-2.9; P = 0.01) for FHxSCD and 1.52 (95% CI: 1.01-2.31; P = 0.047) for being genotype-positive. Among patients with FHxSCD but no other risk markers, the risk of SCD events was 6.4% at 5 years (95% CI: 2.7%-14.9%) in genotype-positive patients and 2.6% (95% CI: 0.6%-10.0%) in genotype-negative patients.
CONCLUSIONS: FHxSCD remained independently associated with SCD in adult patients with HCM even after adjusting for genotype. Among patients with FHxSCD but no other risk markers, genotype-positive patients were at high risk of SCD but genotype-negative patients were not. These data suggest that ICD insertion is not indicated for most genotype-negative patients with FHxSCD unless other risk markers are present.
OBJECTIVES: The goal of this study was to assess the association of genotype and FHxSCD with SCD outcomes in HCM and investigate methods for incorporation of genotype into SCD risk stratification models.
METHODS: This historical cohort study used registries of 2 HCM referral centers. Association of FHxSCD and genotype with SCD was assessed by multivariable hazard regression analysis.
RESULTS: Of 3,258 patients, 896 (27.5%) were genotype-positive, and 332 (10.2%) had FHxSCD. During 4.9 years' median follow-up, 114 patients reached the SCD outcome. On multivariable analysis, the hazard ratios for SCD were 1.83 (95% CI: 1.161-2.9; P = 0.01) for FHxSCD and 1.52 (95% CI: 1.01-2.31; P = 0.047) for being genotype-positive. Among patients with FHxSCD but no other risk markers, the risk of SCD events was 6.4% at 5 years (95% CI: 2.7%-14.9%) in genotype-positive patients and 2.6% (95% CI: 0.6%-10.0%) in genotype-negative patients.
CONCLUSIONS: FHxSCD remained independently associated with SCD in adult patients with HCM even after adjusting for genotype. Among patients with FHxSCD but no other risk markers, genotype-positive patients were at high risk of SCD but genotype-negative patients were not. These data suggest that ICD insertion is not indicated for most genotype-negative patients with FHxSCD unless other risk markers are present.