American heart journal · 2008
Quantitative troponin elevation does not provide incremental prognostic value beyond comprehensive risk stratification in patients with non-ST-segment elevation acute coronary syndromes.
Оценочное исследованиеСтатьяМногоцентровое исследованиеПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
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.
Lim Ki-Dong, Yan Andrew T, Casanova Amparo, Yan Raymond T, Mendelsohn Aurora, Jolly Sanjit, Fitchett David H, Langer Anatoly, Goodman Shaun G, Canadian ACS Registry II Investigators
Аннотация
BACKGROUND: The aim of this study was to evaluate whether quantitative cardiac troponin (cTn) assessment can improve risk stratification in a spectrum of patients with non-ST-segment elevation (NSTE) acute coronary syndrome (ACS) using the validated Global Registry of Acute Cardiac Events (GRACE) risk model.
METHODS: The Canadian ACS Registry II is a prospective, multicenter study that enrolled patients admitted to hospital with a suspected NSTE ACS within 24 hours of symptom onset. Of the total 2297 patients, those with elevated cTn (n = 1013) were further stratified into tertiles of cTn ranges. Our primary end point was death and our secondary end point was a composite of death or/and recurrent myocardial infarction at 1-year follow-up.
RESULTS: Multivariable analysis adjusting for validated predictors of death confirmed the independent prognostic value of any abnormal cTn (vs normal) for death (adjusted odds ratio 2.28, 95% CI 1.49-3.49, P < .001) and for the composite outcome (adjusted odds ratio 2.18, 95% CI 1.61-2.95, P < .001) at 1 year. With quantitative assessment, the gradient of mortality risk with increasing cTn level was not evident after adjusting for other prognosticators. Quantitative (compared to qualitative) assessment of cTn level did not improve either the GRACE risk model discrimination for 1-year death.
CONCLUSIONS: Any cTn elevation is associated with higher rate of death at 1 year, but its quantitative assessment did not prove as important as its mere presence as an independent long-term prognosticator in a nonclinical trial, "real-world" NSTE ACS population.
METHODS: The Canadian ACS Registry II is a prospective, multicenter study that enrolled patients admitted to hospital with a suspected NSTE ACS within 24 hours of symptom onset. Of the total 2297 patients, those with elevated cTn (n = 1013) were further stratified into tertiles of cTn ranges. Our primary end point was death and our secondary end point was a composite of death or/and recurrent myocardial infarction at 1-year follow-up.
RESULTS: Multivariable analysis adjusting for validated predictors of death confirmed the independent prognostic value of any abnormal cTn (vs normal) for death (adjusted odds ratio 2.28, 95% CI 1.49-3.49, P < .001) and for the composite outcome (adjusted odds ratio 2.18, 95% CI 1.61-2.95, P < .001) at 1 year. With quantitative assessment, the gradient of mortality risk with increasing cTn level was not evident after adjusting for other prognosticators. Quantitative (compared to qualitative) assessment of cTn level did not improve either the GRACE risk model discrimination for 1-year death.
CONCLUSIONS: Any cTn elevation is associated with higher rate of death at 1 year, but its quantitative assessment did not prove as important as its mere presence as an independent long-term prognosticator in a nonclinical trial, "real-world" NSTE ACS population.