Transforming growth factor beta 1 (TGF-beta 1) in atrial fibrillation and acute congestive heart failure

Abstract

Atrial fibrillation (AF) and acute congestive heart failure (aCHF) are characterized by an adverse cardiac remodeling. Arrhythmogenic or structural remodeling can be caused by interstitial fibrosis. Transforming growth factor beta 1 (TGF-beta 1) represents a central regulator of cardiac fibrosis. This study investigates serum levels of TGF-beta 1 in patients with AF and aCHF. 401 patients presenting with symptoms of dyspnea or peripheral edema were prospectively enrolled. Blood samples for measurement of TGF-beta 1 (R&D Systems, Inc.) and amino-terminal pro-brain natriuretic peptide (NT-proBNP) (DadeBehring ltd.) were collected after the initial clinical evaluation. Median TGF-beta 1 levels were lower in patients with AF (21.0ng/ml, interquartile range (IR) 15.4-27.6ng/ml, n=107) compared to those without (25.0ng/ml, IR 18.5-31.6ng/ml, n=294) (p=0.009). Patients with aCHF had lower TGF-beta 1 levels (median 22.0ng/ml, IR 15.6-27.1ng/ml, n=122) than those without (median 24.9ng/ml, IR 18.1-31.9ng/ml, n=279) (p=0.0005). In logistic regression models TGF-beta 1 was still associated with AF (odds ratio (OR) 3.00, 95% CI 1.37-6.61, p=0.0001) and aCHF (OR 3.98, 95% CI 1.55-10.19, p=0.004). TGF-beta 1 inversely correlated with left atrial diameter (r=-0.30, p=0.007) and NT-proBNP (r=-0.14, p=0.007). Low serum levels of TGF-beta 1 are associated with AF and aCHF. This decrease may result from a higher consumption of TGF-beta 1 within the impaired myocardium or antifibrotic functions of natriuretic peptides.