Suppression of Tumorigenicity 2 in Heart Failure With Preserved Ejection Fraction

DSpace/Manakin Repository

Suppression of Tumorigenicity 2 in Heart Failure With Preserved Ejection Fraction

Citable link to this page


Title: Suppression of Tumorigenicity 2 in Heart Failure With Preserved Ejection Fraction
Author: AbouEzzeddine, Omar F.; McKie, Paul M.; Dunlay, Shannon M.; Stevens, Susanna R.; Felker, G. Michael; Borlaug, Barry A.; Chen, Horng H.; Tracy, Russell P.; Braunwald, Eugene; Redfield, Margaret M.

Note: Order does not necessarily reflect citation order of authors.

Citation: AbouEzzeddine, Omar F., Paul M. McKie, Shannon M. Dunlay, Susanna R. Stevens, G. Michael Felker, Barry A. Borlaug, Horng H. Chen, Russell P. Tracy, Eugene Braunwald, and Margaret M. Redfield. 2017. “Suppression of Tumorigenicity 2 in Heart Failure With Preserved Ejection Fraction.” Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease 6 (2): e004382. doi:10.1161/JAHA.116.004382.
Full Text & Related Files:
Abstract: Background: Soluble suppression of tumorigenicity 2 (sST2) receptor is a biomarker that is elevated in certain systemic inflammatory diseases. Comorbidity‐driven microvascular inflammation is postulated to play a key role in heart failure with preserved ejection fraction (HFpEF) pathophysiology, but data on how sST2 relates to clinical characteristics or inflammatory conditions or biomarkers in HFpEF are limited. We sought to determine circulating levels and clinical correlates of sST2 in HFpEF. Methods and Results: At enrollment, patients (n=174) from the Phosphodiesterase‐5 Inhibition to Improve Clinical Status And Exercise Capacity in Diastolic Heart Failure (RELAX) trial of sildenafil in HFpEF had sST2 levels measured. Clinical characteristics; cardiac structure and function; exercise performance; and biomarkers of neurohumoral activation, systemic inflammation and fibrosis, and myocardial necrosis were assessed in relation to sST2 levels. Median sST2 levels in male and female HFpEF patients were 36.7 ng/mL (range 30.9–49.2 ng/mL; reference range 4–31 ng/mL) and 30.8 ng/mL (range 25.3–39.3 ng/mL; reference range 2–21 ng/mL), respectively. Among HFpEF patients, higher sST2 levels were associated with the presence of diabetes mellitus; atrial fibrillation; renal dysfunction; right ventricular pressure overload and dysfunction; systemic congestion; exercise intolerance; and biomarkers of systemic inflammation and fibrosis, neurohumoral activation, and myocardial necrosis (P<0.05 for all). sST2 was not associated with left ventricular structure or left ventricular systolic or diastolic function. Conclusions: In HFpEF, sST2 levels were associated with proinflammatory comorbidities, right ventricular pressure overload and dysfunction, and systemic congestion but not with left ventricular geometry or function. These data suggest that ST2 may be a marker of systemic inflammation in HFpEF and potentially of extracardiac origin. Clinical Trial Registration URL: Unique identifier: NCT00763867.
Published Version: doi:10.1161/JAHA.116.004382
Other Sources:
Terms of Use: This article is made available under the terms and conditions applicable to Other Posted Material, as set forth at
Citable link to this page:
Downloads of this work:

Show full Dublin Core record

This item appears in the following Collection(s)


Search DASH

Advanced Search