ObjectivesST2 is a receptor for interleukin (IL)-33. We investigated an association of soluble ST2 (sST2) and IL-33 serum levels with different clinical stages of coronary artery disease. We assessed the predictive value of sST2 and IL-33 in patients with stable angina, non-ST elevation myocardial infarction (NSTEMI) and ST elevation myocardial infarction (STEMI).MethodsWe included 373 patients of whom 178 had stable angina, 97 had NSTEMI, and 98 had STEMI. Patients were followed for a mean of 43 months. The control group consisted of 65 individuals without significant stenosis on coronary angiography. Serum levels of sST2 and IL-33 were measured by ELISAs.ResultssST2 levels were significantly increased in patients with STEMI as compared to patients with NSTEMI and stable angina as well as with controls. IL-33 levels did not differ between the four groups. During follow-up, 37 (10%) patients died and the combined endpoint (all cause death, MI and rehospitalisation for cardiac causes) occurred in 66 (17.6%) patients. sST2 serum levels significantly predicted mortality in the total cohort. When patients were stratified according to their clinical presentation, the highest quintile of sST2 significantly predicted mortality in patients with STEMI, but not with NSTEMI or stable coronary artery disease. sST2 was a significant predictor for the combined endpoint in STEMI patients and in patients with stable angina. Serum levels of IL-33 were not associated with clinical outcome in the total cohort, but the highest quintile of IL-33 predicted mortality in patients with STEMI.ConclusionsSerum levels of sST2 are increased in patients with acute coronary syndromes as compared to levels in patients with stable coronary artery disease and in individuals without coronary artery disease. sST2 and IL-33 were associated with mortality in patients with STEMI but not in patients with NSTEMI or stable angina.

AimsCopeptin, the C-terminal part of the vasopressin pro-hormone, is elevated after myocardial infarction and predicts adverse outcome. In the present study we investigated whether the complementary role of copeptin and cardiac troponin T (cTnT) could be used for identification of high-risk patients with chronic stable heart failure. Methods and resultsWe measured copeptin and high-sensitivity cTnT (hs-cTnT) levels in 172 consecutive patients with stable chronic heart failure. Patients were followed for all-cause mortality and hospitalization due to heart failure for a median of 1301 days (interquartile range: 707 -1636). In univariate analysis, plasma copeptin showed a moderate but significant correlation with hs-cTnT (r ¼ 0.40 P , 0.001), age (r ¼ 0.36 P , 0.001), creatinine (r ¼ 0.52 P , 0.001), and aminoterminal pro-B type natriuretic peptide (NT-proBNP; r ¼ 0.42 P , 0.001). Both copeptin (P ¼ 0.002) and hs-cTnT (P ¼ 0.005) concentrations were significantly increased in patients with higher New York Heart Association classes. While 109 (58%) patients had hs-cTnT concentrations above normal (.14 pg/mL) 104 patients (55%) had copeptin concentrations above normal (16.4 pmol/L). In survival analysis, both elevated copeptin and hs-cTnT concentrations were significant predictors of outcome (P , 0.001 for both). The combination of both markers showed a graded and highly significant association with impaired clinical outcome, which was independent of plasma NT-proBNP levels (adjusted hazard ratios 1.40, 95% CI, 1.20-1.70; P , 0.001). Adding copeptin concentrations to a prediction model with NT-proBNP and hs-cTnT resulted in significant improvement in model performance (net reclassification improvement 0.208; P , 0.05). ConclusionOur data suggest that the combined use of hs-cTnT and copeptin might predict clinical outcome of patients with chronic stable heart failure.--

Background-Contrast-induced acute kidney injury (CI-AKI) after percutaneous coronary intervention is associated with adverse short-and long-term outcomes. However, identification of patients at risk for CI-AKI is challenging. Using a large contemporary randomized trial database of patients with ST-segment-elevation myocardial infarction, we therefore sought to examine whether admission B-type natriuretic peptide (BNP) levels predict the development of CI-AKI. Methods and Results-A total of 979 ST-segment-elevation myocardial infarction patients enrolled in the HarmonizingOutcomes with Revascularization and Stents in Acute Myocardial Infarction (HORIZONS-AMI) trial had BNP levels measured in the emergency room prior to primary percutaneous coronary intervention as part of the study protocol. CI-AKI was defined as a relative increase in serum creatinine of ≥25%, or an absolute increase of ≥0.5 mg/dL, occurring within 48 hours after contrast administration. Logistic regression analysis was used to estimate the association of admission BNP with development of CI-AKI. CI-AKI occurred in 131 patients (13.3%). Baseline BNP was a significant univariable correlate of CI-AKI (odds ratio 1.31, 95% confidence interval, 1.14-1.51; P=0.0001). After multivariable adjustment for clinical, laboratory, and angiographic variables, BNP remained a significant independent predictor of CI-AKI (1.29 [1.10, 1.51]; P<0.001). Significant net reclassification improvement was achieved by addition of BNP to the current clinical risk prediction model (net reclassification improvement=0.177; P<0.001) and to the Mehran Risk Score (net reclassification improvement=0.100; P=0.015). Conclusions-Measurement

ST-elevation in lead aVR is associated with a more severe course of APE, especially in patients with intermediate-risk. Therefore, aVR-ST-elevation might be useful in risk stratification of APE.

In these patients with NSTE-ACS women were less likely to undergo an early invasive therapy compared with men due to their higher age and the higher rate of renal insufficiency. After adjustment for age, comorbidities and treatment female sex was not associated with worse long-term outcome.