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Abstract 13335: Elevated Protease Inhibitor SERPINA3 is Associated With Increased Mortality and Improves Prognostic Stratification in a de novo or Worsened Heart Failure

IntroductionOverexpression of serpin peptidase inhibitor, clade A member 3 (SERPINA3) has been associated with poor prognosis in cancer. HypothesisSERPINA3 in a de novo or worsened heart failure (HF) bears a prognostic information alone and in addition to established biomarkers NT-proBNP and ST2 or...

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Published in:Circulation (New York, N.Y.) N.Y.), 2021-11, Vol.144 (Suppl_1), p.A13335-A13335
Main Authors: Delrue, Leen, Vanderheyden, Marc, Beles, Monika, Dierckx, Riet, verstreken, sofie, Heggermont, Ward, Bartunek, Jozef
Format: Article
Language:English
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Summary:IntroductionOverexpression of serpin peptidase inhibitor, clade A member 3 (SERPINA3) has been associated with poor prognosis in cancer. HypothesisSERPINA3 in a de novo or worsened heart failure (HF) bears a prognostic information alone and in addition to established biomarkers NT-proBNP and ST2 or clinical risk factors. MethodsCirculating SERPINA3 levels were examined in HFpatients who died within 5 years (n=44) and compared with age- and hemodynamically matched survivors (n=39). Prognostic value of circulating SERPINA3 levels alone and in combination with ST2 and NT-proBNP was then analyzed in an independent cohort with a de novo or worsened HF (n=384). ResultsPlasma SERPINA3 levels were significantly higher in HF non-survivors compared to survivors (334.7 ± 138.7 vs 228.2 ± 83.1 μg/mL, p316 μg/mL were associated with increased all-cause mortality (HR (95% CI)2.4 (1.5-3.9), p=0.0002) and its composite with unplanned cardiac admission (HR (95% CI)2.0 (1.2-3.3), p=0.004). In a multivariate analysis, including established clinical risk factors and ST2 and NT-proBNP, SERPINA3 remained independent predictor of all-cause mortality together with age, ST2, glomerular filtration and pulmonary capillary wedge pressure. ConclusionsElevated SERPINA3 appears to provide additional prognostic information in models incorporating clinical, hemodynamic and laboratory risk including ST2 and NT-proBNP by identifying a subgroup of heart failure patients at increased mortality risk.
ISSN:0009-7322
1524-4539
DOI:10.1161/circ.144.suppl_1.13335