American journal of preventive cardiology · 2026
Small, dense LDL-C as a predictor of cardiovascular risk and benefit of alirocumab in patients with recent acute coronary syndrome receiving optimized statin treatment.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Schwartz Gregory G, Szarek Michael, Cobbaert Christa M, Ruhaak L Renee, Schwertfeger Markus, Bhatt Deepak L, Bittner Vera A, Goodman Shaun G, Harrington Robert A, Stevanovic Irena, Tavori Hagai, Reijnders Esther, Romijn Fred, van Neer Nicolaas J M, White Harvey D, Jukema J W, Steg P Gabriel
Аннотация
INTRODUCTION: Small, dense low-density lipoprotein (sdLDL) particles are considered a highly atherogenic subfraction of LDL. Automated biochemical measurement of sdLDL cholesterol (sdLDL-C) has good fidelity to gold-standard measurements. We evaluated relationships of sdLDL-C and LDL-C to risk of major adverse cardiovascular events (MACE) and treatment benefit of the PCSK9-directed monoclonal antibody alirocumab in patients with recent acute coronary syndrome (ACS) and elevated atherogenic lipoproteins despite optimized statin treatment.
METHODS: Analyses comprised 11,837 participants in the ODYSSEY OUTCOMES trial randomized to receive alirocumab or placebo. sdLDL-C was measured using the Denka method; baseline LDL-C was calculated with the Friedewald formula. In the placebo group (n = 5920), cubic splines depicted relationships of sdLDL-C, LDL-C, and their ratio to risk of MACE (cardiovascular death, non-fatal myocardial infarction, ischemic stroke, hospitalization for unstable angina, and ischemia-driven coronary revascularization). Treatment hazard ratio (HR) was calculated across sdLDL-C and LDL-C ranges.
RESULTS: Over 2.8 years median follow-up, risk of MACE in the placebo group increased with higher baseline sdLDL-C or LDL-C with nearly superimposable splines and without variation according to sdLDL-C/LDL-C. Findings were similar in patients with greater or lesser degrees of insulin resistance. Alirocumab reduced risk of MACE (HR 0.87, 95% CI 0.79, 0.95). Treatment HR did not vary significantly across the range of LDL-C or sdLDL-C.
CONCLUSION: In patients with recent ACS on optimized statin treatment, sdLDL-C and LDL-C similarly predict risk of MACE and benefit of alirocumab treatment. Measurement of sdLDL-C does not appear to provide additional prognostic or predictive information in this population.
METHODS: Analyses comprised 11,837 participants in the ODYSSEY OUTCOMES trial randomized to receive alirocumab or placebo. sdLDL-C was measured using the Denka method; baseline LDL-C was calculated with the Friedewald formula. In the placebo group (n = 5920), cubic splines depicted relationships of sdLDL-C, LDL-C, and their ratio to risk of MACE (cardiovascular death, non-fatal myocardial infarction, ischemic stroke, hospitalization for unstable angina, and ischemia-driven coronary revascularization). Treatment hazard ratio (HR) was calculated across sdLDL-C and LDL-C ranges.
RESULTS: Over 2.8 years median follow-up, risk of MACE in the placebo group increased with higher baseline sdLDL-C or LDL-C with nearly superimposable splines and without variation according to sdLDL-C/LDL-C. Findings were similar in patients with greater or lesser degrees of insulin resistance. Alirocumab reduced risk of MACE (HR 0.87, 95% CI 0.79, 0.95). Treatment HR did not vary significantly across the range of LDL-C or sdLDL-C.
CONCLUSION: In patients with recent ACS on optimized statin treatment, sdLDL-C and LDL-C similarly predict risk of MACE and benefit of alirocumab treatment. Measurement of sdLDL-C does not appear to provide additional prognostic or predictive information in this population.