Disease markers · 2015
The Relation between eNOS -786 C/T, 4 a/b, MMP-13 rs640198 G/T, Eotaxin 426 C/T, -384 A/G, and 67 G/A Polymorphisms and Long-Term Outcome in Patients with Coronary Artery Disease.
СтатьяПоддержка 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.
Kincl Vladimír, Máchal Jan, Drozdová Adéla, Panovský Roman, Vašků Anna
Аннотация
AIM: The purpose of this study is to determine the association between eotaxin 426 C/T, -384 A/G, 67 G/A, eNOS -786 T/C, 4 a/b, and MMP-13 rs640198 G/T and prognosis of patients with known CAD.
METHODS: From total of 1161 patients referred to coronary angiography, 532 patients with angiographically confirmed CAD were selected. Their long-term outcome was followed up using hospital database. Subsequent events were assessed in this study: death or combined endpoint-myocardial infarction, unstable angina pectoris, revascularization, heart failure hospitalization, and cardioverter-defibrillator implantation.
RESULTS: The multivariate Cox regression model identified age, smoking, and 3-vessel disease as significant predictors of all-cause death. Further analysis showed that eotaxin 67 G/A (GA + AA versus GG) and eotaxin -384 A/G (GG versus GA + AA) were significant independent prognostic factors when added into the model: HR (95% CI) 2.81 (1.35-5.85), p = 0.006; HR (95% CI) 2.63 (1.19-5.83), p = 0.017; eotaxin -384 A/G was significantly associated with the event-free survival, but it did not provide the prognostic information above the effect of two- or three-vessel disease.
CONCLUSION: The A allele in eotaxin 67 G/A polymorphism is associated with worse survival in CAD patients.
METHODS: From total of 1161 patients referred to coronary angiography, 532 patients with angiographically confirmed CAD were selected. Their long-term outcome was followed up using hospital database. Subsequent events were assessed in this study: death or combined endpoint-myocardial infarction, unstable angina pectoris, revascularization, heart failure hospitalization, and cardioverter-defibrillator implantation.
RESULTS: The multivariate Cox regression model identified age, smoking, and 3-vessel disease as significant predictors of all-cause death. Further analysis showed that eotaxin 67 G/A (GA + AA versus GG) and eotaxin -384 A/G (GG versus GA + AA) were significant independent prognostic factors when added into the model: HR (95% CI) 2.81 (1.35-5.85), p = 0.006; HR (95% CI) 2.63 (1.19-5.83), p = 0.017; eotaxin -384 A/G was significantly associated with the event-free survival, but it did not provide the prognostic information above the effect of two- or three-vessel disease.
CONCLUSION: The A allele in eotaxin 67 G/A polymorphism is associated with worse survival in CAD patients.