To predict CE even in patients who are negative for troponin T. Yet, the complexity of the molecular pathways in the chain of events leading to ACS, as well as the heterogeneity in clinical presentation, imply that a single-marker strategy is most likely inferior to a multi-marker approach. Indeed, multi-marker testing adds useful prognostic information to that of individual markers, both for the prediction of early and long-term outcomes in patients with suspected ACS. However, the potential of different novel cardiac biomarkers in comparison to and combined with clinical assessment in predicting CE in individuals presenting with symptoms suggestive of ACS has not been fully elucidated. This study assessed novel sensitive biomarkers along with established clinical parameters on admission of patients with suspected ACS, for the prediction of CE defined as a composite of early coronary revascularization, myocardial infarction, and cardiovascular death within 30 days. At variance with other biomarker studies, in this analysis CE were prespecified to include immediate revascularization therapy, since in the contemporary setting of primary PCI for ACS, emergency room triage firstly aims at identifying patients in need of PCI or CABG. Acute coronary syndromes presenting as myocardial infarction may be suspected or diagnosed by ECG already at admittance, and diagnosis may be corroborated or not with biomarker testing. Most likely, those patients will undergo cardiac catheterization immediately. But in all patients with suspected ACS, identification and therapy of a culprit lesion nowadays is paramount and complementary to the clinical endpoints of myocardial infarction and cardiovascular death within 30 days, which in turn may reflect both success or failure of therapy, or a missed diagnosis in patients not having undergone coronary angiography. Importantly, this study showed that performance of single biomarkers – notably of hs-cTnT and MPO – depend on the clinical pretest probability of ACS, with hs-cTnT adding to the sensitivity in patients with low and MPO improving the specificity of patients with high clinical risk scores, respectively. Accordingly, identification of those prone to CE was best based on clinical criteria complemented by hs-cTnT based on decision tree analysis. Interestingly, prediction of CE based on the clinical TIMI risk score alone was not improved by adding hs-cTnT to the risk prediction model. Although this study was originally designed also to assess the diagnostic value of MRP 8/14 for early diagnosis of ACS, in the current setting this marker of phagocyte activation did not show sufficient discriminatory performance, notwithstanding its significant elevation in ACS. Scoring systems predicting the patients’ risk of ischemic events and cardiovascular death have been established such as the TIMI risk score for unstable angina/NSTEMI.