Abstract
Background: Cardiac collagen remodeling is important in the progression of heart failure. Estimation of cardiac collagen turnover by serum levels of serological markers is used for monitoring cardiac tissue repair and fibrosis. Peritoneal dialysis (PD) is used for the long-term management of refractory congestive heart failure (CHF). In this study, we investigated the effect of PD treatment on circulating fibrosis markers levels in patients with refractory CHF and fluid overload. Methods: Twenty-five patients with refractory CHF treated with PD were prospectively enrolled in the study. Circulating fibrosis markers procollagen type III C-peptide (PIIINP), matrix metalloproteinase 2 (MMP-2), and tissue inhibitor of metalloproteinases I (TIMP-1) levels were checked at baseline and after three and six months of treatment. Results: The clinical benefit of PD manifested by improved NYHA functional class and reduced hospitalization rate. Serum brain natriuretic peptide (BNP) levels decreased significantly during the treatment. Serum MMP-2 and TIMP-1 decreased significantly on PD. Circulating PIIINP showed two patterns of change, either decreased or increased following PD treatment. Patients in whom circulating PIIINP decreased had significantly lower baseline serum albumin, lower baseline mean arterial blood pressure, higher serum CRP, and a less significant improvement in hospitalization rate compared to the patients in whom circulating PIIINP increased. Patients in whom all three markers decreased demonstrated a trend to longer survival compared to patients whose markers increased or did not change. Conclusion: In refractory CHF patients PD treatment was associated with a reduction in circulating fibrosis markers.
Highlights
IntroductionProgressive myocardial fibrosis in response to injury is a hallmark of pathological cardiac remodeling
Cardiac collagen remodeling is important in the progression of heart failure
Degradation of extracellular matrix and deposition of collagen fibers in cardiac tissue are mainly controlled by the expression and activity of matrix metalloproteinases (MMPs) and their endogenous inhibitors
Summary
Progressive myocardial fibrosis in response to injury is a hallmark of pathological cardiac remodeling. It involves myocyte replacement with fibrosis or diffuse deposition of extracellular matrix (ECM). Degradation of extracellular matrix and deposition of collagen fibers in cardiac tissue are mainly controlled by the expression and activity of matrix metalloproteinases (MMPs) and their endogenous inhibitors. We investigated the effect of PD treatment on circulating fibrosis markers levels in patients with refractory CHF and fluid overload. Circulating fibrosis markers procollagen type III C-peptide (PIIINP), matrix metalloproteinase 2 (MMP-2), and tissue inhibitor of metalloproteinases I (TIMP-1) levels were checked at baseline and after three and six months of treatment. Conclusion: In refractory CHF patients PD treatment was associated with a reduction in circulating fibrosis markers
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