PURPOSE: 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. METHODS: 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. RESULTS: Median TGF-beta 1 levels were lower in patients with AF (21.0 ng/ml, interquartile range (IR) 15.4-27.6 ng/ml, n = 107) compared to those without (25.0 ng/ml, IR 18.5-31.6 ng/ml, n = 294) (p = 0.009). Patients with aCHF had lower TGF-beta 1 levels (median 22.0 ng/ml, IR 15.6-27.1 ng/ml, n = 122) than those without (median 24.9 ng/ml, IR 18.1-31.9 ng/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). CONCLUSIONS: 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.
PURPOSE: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. METHODS: 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. RESULTS: Median TGF-beta 1 levels were lower in patients with AF (21.0 ng/ml, interquartile range (IR) 15.4-27.6 ng/ml, n = 107) compared to those without (25.0 ng/ml, IR 18.5-31.6 ng/ml, n = 294) (p = 0.009). Patients with aCHF had lower TGF-beta 1 levels (median 22.0 ng/ml, IR 15.6-27.1 ng/ml, n = 122) than those without (median 24.9 ng/ml, IR 18.1-31.9 ng/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). CONCLUSIONS: 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.
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