Key result
Pirfenidone reduces circulating endotrophin, a potential biomarker for myocardial fibrosis in HFpEF.
Why the study?
Does pirfenidone reduce circulating endotrophin levels, and is endotrophin associated with myocardial ECV in patients with HFpEF?
Does pirfenidone reduce circulating endotrophin levels, and is endotrophin associated with myocardial ECV in patients with HFpEF?
Circulating endotrophin is a promising biomarker for myocardial fibrosis burden that is sensitive to antifibrotic therapy with pirfenidone in HFpEF.
May facilitate monitoring of fibrosis in HFpEF without repeat imaging; extends evidence for endotrophin as dynamic biomarker responsive to anti-fibrotics.
In patients with heart failure with preserved ejection fraction, treatment with pirfenidone was associated with a sustained reduction in circulating levels of endotrophin from 13 weeks. Circulating endotrophin was also independently associated with both baseline myocardial ECV and change in myocardial ECV. Endotrophin shows high potential as a circulating biomarker reflective of myocardial fibrosis burden and sensitive to change in myocardial fibrosis over time.
No takes yet. Share an insight, caveat, or question.
Black et al. (2026) studied this question. Circulating endotrophin correlates with myocardial extracellular volume and is reduced by pirfenidone therapy, highlighting its potential as a biomarker for myocardial fibrosis in HFpEF.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: