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Gremlin-1 identifies fibrosis and predicts adverse outcome in patients with heart failure undergoing endomyocardial
Karin A L Mueller1, Elli Tavlaki, Martina Schneider
1Medizinische Klinik III, Kardiologie und Kreislauferkrankungen, Universitätsklinikum Tübingen, Tübingen, Germany.
Insights
Gremlin-1 (Grem1) expression in heart tissue correlates with fibrosis and dysfunction in nonischemic heart failure (HF). Higher Grem1 levels predict adverse outcomes, including death and rehospitalization, in HF patients.
Area of Science:
- Cardiology
- Molecular Biology
- Pathology
Background:
- Gremlin-1 (Grem1) is implicated in fibrotic conditions in the kidney and lung.
- The role of myocardial Grem1 in heart failure (HF) is not well understood.
Purpose of the Study:
- To investigate the prognostic significance of Grem1 expression in patients with nonischemic heart failure (HF).
Main Methods:
- Assessed Grem1 expression (1-4 score) and myocardial fibrosis in 214 nonischemic HF patients via endomyocardial biopsy.
- Evaluated risk factors including LVEF, LVEDD, NYHA class, and biomarkers.
- Defined study endpoint as all-cause death or HF-related rehospitalization within 3 years.
Main Results:
- Grem1 expression strongly correlated with myocardial fibrosis (r=0.619, P<.0001).
- Highest Grem1 levels were associated with impaired LVEF and increased LVEDD (P<.0001, P=0.030).
- Grem1 expression (HR 7.5) and NYHA class ≥II (HR 2.0) independently predicted adverse outcomes.
Conclusions:
- Myocardial Grem1 expression correlates with fibrosis and left ventricular dysfunction in nonischemic HF.
- Grem1 is an independent predictor of adverse outcomes in this patient population.
Background:
Gremlin-1 (Grem1), an antagonist of bone morphogenetic proteins, is involved in fibrotic tissue formation in kidney and lung. The impact of myocardial Grem1 expression is unknown. We investigated the prognostic value of Grem1 expression in 214 consecutive patients with nonischemic heart failure (HF) undergoing endomyocardial biopsy.
Methods:
In all patients, the following risk factors were assessed: Grem1 expression (semiquantitative score scheme ranging from 1 to 4), presence of inflammatory markers, detection of viral genome, left ventricular ejection fraction (LVEF), left ventricular end-diastolic diameter (LVEDD), New York Heart Association functional class (NYHA), troponin I, and B-type natriuretic peptide. Degree of myocardial fibrosis was defined as an index. Study end point was a combination of all-cause death and HF-related rehospitalization within 3 years of follow-up.
Results:
Grem1 expression significantly correlated with the degree of myocardial fibrosis (correlation coefficient r = 0.619; P < .0001). Patients with the highest Grem1 expression (score 4) showed the most severely impaired LVEF and highest LVEDD (P < .0001 and P = .030, respectively, for comparison of semiquantitative scores). During follow-up, 33 patients (15.4%) reached the study end point. Grem1 expression and NYHA ≥II were independent predictors of the end point (Grem1: hazard ratio [HR] 7.5, 95% confidence interval [CI] 1.8-32.2; P = .006; NYHA ≥II: HR 2.0, 95% CI 1.0-4.1; P = .048).
Conclusions:
Grem1 correlates with the degree of myocardial fibrosis and left ventricular dysfunction and is an independent predictor of adverse outcome in patients with nonischemic HF.
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