Abstract 15077: SuPAR Predicts Cardiovascular Outcomes in Heart Failure Independently of High Sensitivity Troponin I
Introduction: Soluble urokinase-type plasminogen activator receptor (suPAR) is a novel biomarker that reflects immune activation, and predicts adverse outcomes including incident heart failure (HF) in the general population.
Hypothesis: We hypothesized that suPAR levels will be elevated in HF, and associated with adverse outcomes including incident HF, independent of myocardial-specific biomarkers such as high-sensitivity troponin I (hs-TnI).
Methods: We measured plasma suPAR and hs-TnI levels in 5001 patients undergoing cardiac catheterization and enrolled in the Emory Cardiovascular Biobank. Patients were followed for a median of 5 years for adverse events including death, myocardial infarction, hospitalization for HF, and incident HF. Survival analyses using Cox regression were performed after adjusting for clinical characteristics including coronary artery disease severity, medications and hs-TnI levels.
Results: We identified 1501 patients with HF (mean age 64±13, 66% male, 26% African American, 31% with reduced ejection fraction, 58% with ischemic cardiomyopathy). Median suPAR levels were significantly higher in patients with HF compared to those without HF (3344 [IQR 2540, 4600] vs. 2862 [IQR 2242, 3711] pg/mL, respectively, P<0.001) and correlated with NYHA class (r=0.15, P<0.001). In patients with HF, SuPAR levels were independently associated with all-cause death (HR 2.37, 95%CI[1.92-2.92]), cardiovascular death (HR 2.09, 95%CI[1.60, 2.72]), incident myocardial infarction (HR 2.08 95%CI[1.29, 3.35]), and hospitalization for HF (HR 1.70, 95%CI[1.32, 2.20]). Addition of SuPAR to clinical risk factors improved the c-statistic (Δ=0.058,P <0.001) and was additive to hs-TnI. Lastly, in patients without known HF (n=3168), those in the highest suPAR quartile (>3724 pg/mL) had a 3.3-fold increase in the incidence of HF.
Conclusions: SuPAR levels are higher in HF, and are predictive of adverse cardiovascular outcomes, independent of, and in addition to hs-TnI levels. Importantly, suPAR is associated with an increased risk of incident HF. As a marker of immune activation, suPAR likely reflects upstream pathologic processes leading to HF. Whether suPAR levels are modified by therapy and reclassifies risk remains to be determined.
Author Disclosures: S.S. Hayek: None. Y. Ko: None. M. Awad: None. A. Kalogeropoulos: None. K. Hosny: None. K. Patel: None. S. Zheng: None. R. Bhimani: None. J. Hartsfield: None. J. Kim: None. P. Wilson: None. L. Shaw: None. M. Tracy: None. C. Wei: None. J. Reiser: None. A. Quyyumi: None.
- © 2016 by American Heart Association, Inc.