Soluble ST2 for Prediction of Clinical Outcomes in Patients with ST-Segment Elevation Myocardial Infarction Receiving Primary PCI.

Soluble suppression of tumorigenicity 2 (sST2), a biomarker representing myocardial fibrosis and inflammation, has been applied in risk stratification of patients with myocardial infarction (MI). However, whether primary PCI (PPCI) will eliminate the predictive value of sST2 in STEMI patients has not been well studied. Here, we conducted a prospective clinical trial to evaluate the correlation between sST2 and prognosis in STEMI patients undergoing PPCI. sST2 levels were measured in 295 STEMI patients (60.2 ± 10.8 years) at admission using a high sensitivity assay. Baseline sST2 levels were significantly associated with heart function, biomarkers of inflammation, and myocardial injury. During a 12-month follow-up, 19 patients had major adverse cardiovascular events (MACEs). Greater sST2 was continuously associated with a higher risk of incident MACEs. Such association remained even after adjusting for other risk factors in a multivariate Cox analysis. A baseline sST2 level in the highest quartile (≥ 58.7 ng/mL) was independently associated with mortality (HR: 5.01, 95%CI: 1.02-16.30, P = 0.048). More incident heart failure was seen in the group with greater sST2, however, the association was not significant after adjustment. Therefore, baseline sST2 may be useful to predict MACEs, especially mortality, in STEMI patients receiving PPCI.

Evaluation of D-dimer in the diagnosis of suspected aortic dissection.

BACKGROUND: The goal of this study was to evaluate plasma D-dimer as a diagnostic marker for exclusion of suspected aortic dissection (AD). METHODS: Two-hundred and sixty suspected AD patients were enrolled, including acute AD, n=107; chronic AD, n=17; acute myocardial infarction (AMI), n=70; pulmonary embolism (PE), n=18; non-ST elevation myocardial infarction (NSTEMI), n=28; and unstable angina (UA), n=20. All patients had D-dimer testing performed (Roche Diagnostics GmbH) immediately following admission. RESULTS: The D-dimer concentrations in both the acute AD group [median: 3.47; 95% confidence interval (CI): 2.43-4.50 µg/mL] and chronic AD group (median: 1.09; 95% CI: 0.36-3.81 µg/mL) were significantly higher than those in patients in the AMI, NSTEMI and UA groups (p=0.000), but not when compared to the PE group. One (0.8%) patient was identified in the acute AD group who presented with a low D-dimer value (0.04 µg/mL), indicating the existence of intramural hematoma as demonstrated by CT. CONCLUSIONS: D-dimer may be used as a potential marker for suspected AD, with high sensitivity of up to 99.2% (1/124). Regardless of the cut-off threshold selected, the sensitivity of D-dimer was unable to reach 100%. Further examinations, including imaging technology, were necessary to diagnose the suspected AD patients who had negative D-dimer result.