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. Methods: A total of 3641 consecutive patients with CAD were prospectively enrolled into the study and followed up for major adverse cardiovascular events (MACEs) and all-cause death up to 5.3-7.6 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 prognostic value of GDF-15 level with MACEs and all-cause death was evaluated. Results: 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. Cox regression analysis indicated that GDF-15 > 1800 ng/L were independently associated with the composite of 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, GDF-15 significantly improved the C-statistic (area under the curve, 0.583 [95% CI 0.559-0.606] to 0.628 [0.605-0.651]; P < 0.001), net reclassification index (0.578; P = 0.031), and integrated discrimination index (0.021; P = 0.027). For all-cause death, GDF-15 significantly improved the C-statistic (0.728 [95% CI 0.694-0.761] to 0.817 [0.781-0.846]; P < 0.001), net reclassification index (0.629; P = 0.001), and integrated discrimination index (0.035; P = 0.002). Conclusions: In the setting of CAD, GDF-15 is associated with long-term MACEs and all-cause death, and provides incremental prognostic value beyond traditional risks factors.
Background Soluble suppression of tumorigenesis-2 (sST2) is implicated in myocardial overload and has long been recognized as an inflammatory marker related to heart failure and acute coronary syndrome, but data on the prognostic value of sST2 in patients with coronary artery disease (CAD) remain limited. This study sought to investigate the prognostic value of sST2 in patients with established CAD and its predictive value in CAD patients with and 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 sST2 and outcomes was investigated using multivariable Cox regression. Results During a median follow-up of 6.4 years, MACEs occurred in 775 patients, and 275 patients died. Multiple Cox regression models showed that a higher level of sST2 was an independent predictor of MACEs development (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 sST2 to established risk factors significantly improved risk prediction of the composite outcome of MACEs and all-cause death (C-index, net reclassification index, and integrated discrimination improvement, all p < 0.05). In subgroup analysis depending on diabetes status, the diabetes group had a significantly higher level of sST2, which remained a significant predictor of MACEs and all-cause death in patients with and without T2DM in multivariable models. The area under the curve (AUC) of CAD patients with diabetes mellitus was significantly higher than that of those without T2DM. For MACEs, the AUC was 0.737 (patients with T2DM) vs 0.620 (patients without T2DM). For all-cause death, the AUC was 0.923 (patients with T2DM) vs 0.789 (patients without T2DM). Conclusions A higher level of sST2 is significantly associated with long-term MACEs and all-cause death in CAD patients with and without T2DM. sST2 has strong predictive value for cardiovascular adverse events in CAD patients with T2DM, and these results provide new evidence for the role of sST2.
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 Abdominal obesity as a predominant comorbidity has played a key role in the incidence and worsening of heart failure with preserved ejection fraction (HFpEF), and waist-to-height ratio (WHtR) behaves better than waist circumference or body mass index in evaluating abdominal obesity. While the association between WHtR and all-cause death in Chinese patients with HFpEF remains unclear. Methods Patients with stable HFpEF (N = 2041) who presented to our hospital from January 2008 to July 2019 were divided into low-WHtR (< 0.5, N = 378) and high-WHtR (≥ 0.5, N = 1663). Multivariable Cox proportional-hazard models were used to examine the association of WHtR with all-cause death. Results The average age was 76.63 ± 11.44 years, and the mean follow-up was 4.53 years. During follow-up, 185 patients (9.06%) reached the primary outcome of all-cause death. As for the secondary outcome, 79 patients (3.87%) experienced cardiovascular death, 106 (5.19%) had non-cardiovascular death, and 94 (4.61%) had heart failure rehospitalization. After multivariable adjustment, a higher WHtR was significantly associated with the increased risks of all-cause death [adjusted hazard ratios (HR) 1.91, 95% confidence interval (CI) 1.06–3.45, p = 0.032], cardiovascular death (adjusted HR 2.58; 95% CI 1.01–6.67, p = 0.048), and HF rehospitalization (adjusted HR 3.04; 95% CI 1.26–7.31, p = 0.013). Conclusions Higher WHtR is an independent risk factor for all-cause death in Chinese patients with HFpEF.
BackgroundFrailty has been recognized as an important prognostic indicator in patients with acute myocardial infarction (AMI). However, no study has focused on critical AMI patients. We aimed to determine the impact of frailty on short- and long-term mortality risk in critical AMI patients.MethodsData from the Medical Information Mart for Intensive Care (MIMIC)-IV database was used. Frailty was assessed using the Hospital Frailty Risk Score (HFRS). Outcomes were in-hospital mortality and 1-year mortality. Logistic regression and Cox proportional-hazards models were used to investigate the association between frailty and outcomes.ResultsAmong 5,003 critical AMI patients, 2,176 were non-frail (43.5%), 2,355 were pre-frail (47.1%), and 472 were frail (9.4%). The in-hospital mortality rate was 13.8%, and the 1-year mortality rate was 29.5%. In our multivariable model, frailty was significantly associated with in-hospital mortality [odds ratio (OR) = 1.30, 95% confidence interval (CI): 1.20–1.41] and 1-year mortality [hazard ratio (HR) = 1.29, 95% CI: 1.24–1.35] as a continuous variable (per five-score increase). When assessed as categorical variables, pre-frailty and frailty were both associated with in-hospital mortality (OR = 2.80, 95% CI: 2.19–3.59 and OR = 2.69, 95% CI: 1.93–3.73, respectively) and 1-year mortality (HR = 2.32, 95% CI: 2.00–2.69 and HR = 2.81, 95% CI: 2.33–3.39, respectively) after adjustment for confounders. Subgroup analysis showed that frailty was only associated with in-hospital mortality in critically ill patients with non-ST-segment elevation myocardial infarction (STEMI) but not STEMI (p for interaction = 0.012). In addition, frailty was associated with 1-year mortality in both STEMI and non-STEMI patients (p for interaction = 0.447). The addition of frailty produced the incremental value over the initial model generated by baseline characteristics for both in-hospital and 1-year mortality.ConclusionFrailty, as assessed by the HFRS, was associated with both in-hospital and 1-year mortality in critical AMI patients. Frailty improves the prediction of short- and long-term mortality in critical AMI patients and may have potential clinical applications.
The latest consensus has changed CYP2D6 genotyping among Chinese population, while its impact on metoprolol tolerance and adverse events in elderly Chinese patients with cardiovascular diseases remains unclear. In this study, we prospectively included elderly patients who started metoprolol treatment for cardiovascular indications. According to the latest consensus on CYP2D6 genotype-to-phenotype translation, the patients were categorized as normal, intermediate, or poor metabolizers (NMs, IMs, or PMs, respectively) by detecting the presence of the CYP2D6*1, *2, *5, *10, and *14. Logistic regression model was used to analyze the correlation between the CYP2D6 phenotype and incidence of adverse events, which were assessed over a 12-week period. In this study, there were 651 (62.7%) NMs, 385 (37.1%) IMs, and 3 (0.3%) PMs. After 12 weeks of follow-up, compared with NMs, IMs had the lower maintenance dose [50.0 (25.0–50.0) mg/day vs. 25.0 (25.0–50.0) mg/day, p < 0.001] and lower weight-adjusted maintenance doses (0.52 ± 0.25 mg/day/kg vs. 0.42 ± 0.22 mg/day/kg, p < 0.001), and had higher incidence of postural hypotension (6.0% vs. 10.9%, p = 0.006), bradycardia (21.5% vs. 28.6%, p = 0.011), asystole (0.8% vs. 3.1%, p = 0.009) and syncope (2.0% vs. 6.2%, p = 0.001). In logistic regression model, the overall incidence of adverse events was 1.37-fold larger in IMs than in NMs (odds ratio = 1.37, 95% confidence interval = 1.05–1.79, p = 0.021). We conclude that IMs have lower tolerance and higher incidence of metoprolol-related adverse events than NMs in elderly Chinese patients with cardiovascular diseases. CYP2D6 genotyping is justifiable in elderly patients to minimize the risk of adverse events and ensure the benefits of metoprolol.
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