scholarly journals Soluble Urokinase Plasminogen Activator Receptor Level Is an Independent Predictor of the Presence and Severity of Coronary Artery Disease and of Future Adverse Events

Author(s):  
Danny J. Eapen ◽  
Pankaj Manocha ◽  
Nima Ghasemzadeh ◽  
Riyaz S. Patel ◽  
Hatem Al Kassem ◽  
...  
2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
J E Walter ◽  
M Amrein ◽  
L Koechlin ◽  
J Du Fay De Lavallaz ◽  
T Zimmermann ◽  
...  

Abstract Background The urokinase system is pivotal in the pathogenesis of atherosclerosis. Therefore, soluble urokinase plasminogen activator receptor (suPAR) concentrations may help in the detection of functionally relevant coronary artery disease (fCAD). Purpose To evaluate suPAR as diagnostic marker for fCAD. Methods Among consecutive patients with symptoms suggestive of fCAD, fCAD was adjudicated blinded to suPAR concentrations in two domains: first, diagnosis of fCAD according to myocardial perfusion single photon emission tomography (MPI-SPECT) and coronary angiography; second, fCAD according to cardiovascular death, non-fatal acute myocardial infarction (AMI) and all-cause death during 2-year follow-up. Results Among 968 patients, symptoms were adjudicated to be causally related to fCAD in 26% (255/968). SuPAR concentrations were higher in patients with fCAD as compared to those without (3.45 ng/mL versus 3.20 ng/mL, p=0.007), but overall had only low diagnostic accuracy (area under the curve [AUC]: 0.56, 95% CI 0.52–0.60) and were not independent predictors of fCAD after multivariable adjustment. Circulating suPAR concentrations were modestly correlated with high-sensitivity cardiac troponin (hs-cTn) T (Spearman's rho 0.393, p<0.001), NT-proBNP (Spearman's rho 0.327, p<0.001) and age (Spearman's rho 0.364, p<0.001), but only weakly correlated with the extent of coronary atherosclerosis as quantified by perfusion defects (Spearman's rho 0.123, p<0.001). Prognostically, suPAR concentrations had moderate-to-high accuracy in the prediction of cardiovascular death (AUC 0.72, 95% CI 0.62–0.81) and all-cause death (AUC 0.72, 95% CI 0.65–0.79) at 2-years, and remained a significant predictor for all-cause death after multivariable adjustment (p=0.001). SuPAR concentrations did not predict non-fatal AMI. Conclusions SuPAR is an independent predictor of death, but not helpful in the detection of fCAD. Acknowledgement/Funding European Union, Swiss National Science Foundation, the Swiss Heart Foundation, the Cardiovascular Research Foundation Basel, the University of Basel,


Biomolecules ◽  
2020 ◽  
Vol 10 (6) ◽  
pp. 909
Author(s):  
Georgiana-Aura Giurgea ◽  
Katrin Zlabinger ◽  
Alfred Gugerell ◽  
Dominika Lukovic ◽  
Bonni Syeda ◽  
...  

In our prospective non-randomized, single-center cohort study (n = 161), we have evaluated a multimarker approach including S100 calcium binding protein A12 (S100A1), interleukin 1 like-receptor-4 (IL1R4), adrenomedullin, copeptin, neutrophil gelatinase-associated lipocalin (NGAL), soluble urokinase plasminogen activator receptor (suPAR), and ischemia modified albumin (IMA) in prediction of subsequent cardiac adverse events (AE) during 1-year follow-up in patients with coronary artery disease. The primary endpoint was to assess the combined discriminatory predictive value of the selected 7 biomarkers in prediction of AE (myocardial infarction, coronary revascularization, death, stroke, and hospitalization) by canonical discriminant function analysis. The main secondary endpoints were the levels of the 7 biomarkers in the groups with/without AE; comparison of the calculated discriminant score of the biomarkers with traditional logistic regression and C-statistics. The canonical correlation coefficient was 0.642, with a Wilk’s lambda value of 0.78 and p < 0.001. By using the calculated discriminant equation with the weighted mean discriminant score (centroid), the sensitivity and specificity of our model were 79.4% and 74.3% in prediction of AE. These values were higher than that of the calculated C-statistics if traditional risk factors with/without biomarkers were used for AE prediction. In conclusion, canonical discriminant analysis of the multimarker approach is able to define the risk threshold at the individual patient level for personalized medicine.


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