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• SuPAR was a strong prognostic biomarker of non-cardiac mortality after STEMI. • The suPAR level was independent of sampling time < 12 h after revascularization. • SuPAR may identify patients in risk of non-cardiac mortality prior to discharge. Identification of patients at high risk of non-cardiac mortality following ST-segment elevation myocardial infarction (STEMI) could guide clinicians to identify patients who require attention due to serious non-cardiac conditions after the acute phase of STEMI. The purpose of this study was to evaluate if the non-specific and prognostic biomarker of inflammation and comorbidity, soluble urokinase receptor (suPAR), could predict non-cardiac mortality in a cohort of STEMI patients. SuPAR was measured in 1,190 STEMI patients who underwent primary percutaneous coronary intervention (pPCI). The primary endpoint was non-cardiac mortality, secondary endpoints were cardiac mortality, all-cause mortality, reinfarction and periprocedural acute kidney injury. Backwards elimination of potential confounders significantly associated with the respective outcome was used to adjust associations. Patients were followed for a median of 3.0 years (interquartile range 2.5– 3.6 years). Multivariate cox regression revealed that a plasma suPAR level above 3.70 ng mL−1 was associated with non-cardiac and cardiac mortality at hazard ratios 3.33 (95% confidence interval 1.67–6.63, p = 0.001, adjusted for age) and 0.99 (0.18–5.30, p = 0.98, adjusted for previous myocardial infarction and left ventricular ejection fraction), respectively. In patients with pPCI treated STEMI, suPAR was an independent prognostic biomarker of non-cardiac but not cardiac mortality and may identify patients with high risk of non-cardiac mortality. [ABSTRACT FROM AUTHOR]

Background Primary percutaneous coronary intervention (pPCI) is recommended in patients presenting with ST-elevation myocardial infarction (STEMI) within <12 h of symptom onset. However, patients-reported symptom duration is not always reliable. Cardiac specific troponin T (cTnT) and the endogenous stress marker copeptin have different temporal release patterns for myocardial infarction MI. We hypothesized that copeptin/troponin-ratio is associated to the duration of coronary occlusion and therefore inversely proportional to myocardial salvage. Method Patients older than 18 years with first time STEMI referred to pPCI were eligible. cTnT and copeptin values were measured at admission. A cardiac magnetic resonance scanning (CMR) was done during the index admission for assessment of area at risk (AAR), and later 3 months to assess final infarct size (FIS). Myocardial salvage index (MSI) was calculated based on these measurements. Results A total of 468 patients were included. The median time from patient-reported onset of symptoms to pPCI was 192 min (IQR 150 min - 290 min). At presentation 416 (89%) patients had hs-cTnT values above the 99th percentile, median hs-cTnT was 53 ng/l (IQR 24 ng/l-146 ng/l) and 318 (68%) patients had copeptin values above the 99th percentile (18.9 pmol/l), median copeptin was 50 pmol/l (IQR 14 pmol/l-131 pmol/l). Symptom duration showed a weak but significant association with AAR (R 2  = 0.02, p  = .04), FIS (R 2  = 0.03, p  < .01) and MSI (R 2  = 0.04, p < .01). Copeptin/troponin-ratio was significantly associated with symptom duration (R 2  = 0.19, p < .01), but not AAR (R 2  = 0.02, p  = .19), FIS (R 2  = 0.02, p  = .12), or MSI (R 2  = 0.01, p  = .25). Conclusion Copeptin/troponin-ratio is associated with patient-reported symptom duration, but there was no association with area at risk, final infarct size or myocardial salvage index. [ABSTRACT FROM AUTHOR]