Background: Growth differentiation factor-15 (GDF-15) is a marker of inflammation, oxidative stress and it is associated with adverse prognosis in cardiovascular disease. The aim of the present cohort study is to investigate the prognostic value of GDF-15 in patients with coronary artery disease (CAD) during long-term follow up.Method: A total of 3641 consecutive patients with CAD were prospectively enrolled into the study and followed up for all cause death and major adverse cardiovascular events (MACEs) up to 6.4 years. Plasma GDF-15 was measured and clinical data and long-term events were registered. The patients were subsequently divided into three groups by the levels of GDF-15 and the association of GDF-15 level with MACEs was evaluated.Result: After a median follow-up at 6.4 years later, 775 patients (event rate of 21%) had developed MACEs and 275 patients died (event rate of 7.55%). Kaplan–Meier analysis indicated that the patients with GDF-15 > 1800 ng/L were significantly associated with an increased risk of MACEs and all cause death. After adjustment for potential confounders, GDF-15 > 1800 ng/L. were independently associated with the composite of major adverse cardiovascular events (MACEs) (HR 1.74; 95% CI: 1.44–2.02; p<0.001) and all-cause death (HR 2.04; 95% CI 1.57– 2.61; p<0.001). For MACEs a significant increase of receiver operator characteristic curve (ROC)curve was seen after addition of GDF-15 to a clinical model 0.628(95% CI 0.605–0.651; p <0.001).For long-term all-cause death a significant increase of ROC curve was seen after addition of GDF-15 to a clinical model 0.817(95% CI 0.787–0.846; p<0.001).Conclusions: In the setting of CAD, GDF-15 is associated with long-term all-cause death, MACEs and provides incremental prognostic value beyond traditional risks factors.
Background: Suppression of tumorigenesis-2 (ST2) is implicated in myocardial overload and has long been recognized as an inflammation marker related to heart failure and acute coronary syndromes, but data on the prognostic value of ST2 in patients with coronary artery disease (CAD) remain limited. This study sought to investigate the prognostic value of ST2 in patients with established coronary artery disease and its predictive value in CAD patients with or without type 2 diabetes mellitus (T2DM).Methods: A total of 3641 consecutive patients were included in this prospective cohort study. The primary end point was major adverse cardiovascular events (MACEs). The secondary end point was all-cause death. The association between ST2 and outcomes was investigated using multivariable Cox regression.Results: During a median follow-up of 6.4 years, 775 patients had the occurrence of MACEs and 275 patients died. Kaplan-Meier survival estimates indicated that the patients with higher levels of ST2 (ST2> 19 ng/ml) had a significantly increased risk of MACEs (log-rank p<0.001) and all-cause death (log-rank p<0.001). Multiple Cox regression models showed that higher level of ST2 was an independent predictor for MACEs developments (HR=1.36, 95% CI 1.17-1.56, p<0.001) and all-cause death (HR=2.01, 95% CI 1.56-2.59, p<0.001). The addition of ST2 to established risk factors significantly improved risk prediction of the composite outcome of MACEs and all-cause death (C-statistic, net reclassification index, and integrated discrimination improvement, all p<0.05). Subgroup analyses showed that ST2 remained a significant predictor of MACEs and all-cause death in patients with and without T2DM in multivariable models.Conclusions: A higher level of ST2 is significantly associated with long-term MACEs and all-cause death in CAD patients with and without T2DM. ST2 may provide incremental prognostic value beyond traditional risk factors.
Background: Suppression of tumorigenesis-2 is implicated in the myocardial overload and it was long been recognized as an inflammation marker related to heart failure and acute coronary syndromes, but the data on prognostic value of suppression of tumorigenesis-2 on patients with coronary artery disease remains limited. The study ought to investigate the prognostic value of suppression of tumorigenesis-2 in patients with established coronary artery disease.Methods: In this prospective cohort study, a total of 3641 consecutive patients were included. The primary end point was major adverse cardiovascular events. Kaplan-Meier survival estimates indicated that the patients with higher levels of ST2 (ST2> 19 ng/ml) had a significantly increased risk of MACEs (log-rank p<0.001) and all-cause death (log-rank p<0.001). The secondary end point was all-cause death. The association between suppression of tumorigenesis-2 and outcomes was investigated using multivariable COX regression.Results: During a median follow up of 6.4 years, there were 775 patients had the occurrence of major adverse cardiovascular events and 275 patients died. Kaplan-Meier survival estimates indicated that the patients with higher levels of ST2 (ST2> 19 ng/ml) had a significantly increased risk of MACEs (log-rank p<0.001) and all-cause death (log-rank p<0.001). Multiple COX regression models showed that higher level of suppression of tumorigenesis-2 was an independent predictor in developing major adverse cardiovascular events (HR=1.36, 95% CI 1.17-1.56, p<0.001) and all-cause death (HR=2.01, 95%CI 1.56-2.59, p<0.001). The addition of suppression of tumorigenesis-2 to established risk factors significantly improved risk prediction of the composite outcome of major adverse cardiovascular events and all-cause death (c-statistic, net reclassification index, and integrated discrimination improvement, all p<0.05).Conclusions: Higher level of suppression of tumorigenesis-2 is significantly associated with long-term all-cause death and major adverse cardiovascular events. Suppression of tumorigenesis-2 may provide incremental prognostic value beyond traditional risk factors.
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