BACKGROUND: Cardiac inflammation has been suggested to play a critical role in the pathogenesis of inflammatory cardiomyopathy as well as in progressive heart failure (HF). CXC motif ligand 16 (CXCL16) is a recently discovered chemokine produced by several inflammatory cells and representing an important pathogenic mediator in the development of HF. The present study evaluates the diagnostic and prognostic relevance of CXCL16 expression in endomyocardial biopsies of consecutive patients with congestive HF. METHODS AND RESULTS: 174 patients (age 54.4±14.6 years) with congestive HF undergoing endomyocardial biopsy for diagnostic reasons were prospectively enrolled. Biopsies were analyzed using established histopathological and immunohistological criteria together with CXCL16 staining. CXCL16 was significantly enhanced in patients with inflammatory cardiomyopathy (78/127, 61.4%) as compared to patients with non-inflammatory cardiomyopathy (17/47, 36.2%, p=0.003). During a mean follow-up of 27.5 months, 20 patients (11.5%) reached the primary endpoint (death of all causes). Of all clinical (age, gender, NYHA functional class, systolic pulmonary artery pressure, left ventricular ejection fraction), laboratory (brain natriuretic peptide) and immunohistological (CXCL16) parameters tested, CXCL16 was the only independent predictor of death (hazard ratio 5.4; 95% confidence interval 1.2 to 24.0; p=0.027). Subgroup analysis revealed CXCL16 as a predictor of death in both patients with inflammatory and with non-inflammatory cardiomyopathy. CONCLUSION: According to the present observations CXCL16 is enhanced in inflammatory cardiomyopathy and turned out as an independent predictor of death in patients with HF undergoing endomyocardial biopsy.
BACKGROUND:Cardiac inflammation has been suggested to play a critical role in the pathogenesis of inflammatory cardiomyopathy as well as in progressive heart failure (HF). CXC motif ligand 16 (CXCL16) is a recently discovered chemokine produced by several inflammatory cells and representing an important pathogenic mediator in the development of HF. The present study evaluates the diagnostic and prognostic relevance of CXCL16 expression in endomyocardial biopsies of consecutive patients with congestive HF. METHODS AND RESULTS: 174 patients (age 54.4±14.6 years) with congestive HF undergoing endomyocardial biopsy for diagnostic reasons were prospectively enrolled. Biopsies were analyzed using established histopathological and immunohistological criteria together with CXCL16 staining. CXCL16 was significantly enhanced in patients with inflammatory cardiomyopathy (78/127, 61.4%) as compared to patients with non-inflammatory cardiomyopathy (17/47, 36.2%, p=0.003). During a mean follow-up of 27.5 months, 20 patients (11.5%) reached the primary endpoint (death of all causes). Of all clinical (age, gender, NYHA functional class, systolic pulmonary artery pressure, left ventricular ejection fraction), laboratory (brain natriuretic peptide) and immunohistological (CXCL16) parameters tested, CXCL16 was the only independent predictor of death (hazard ratio 5.4; 95% confidence interval 1.2 to 24.0; p=0.027). Subgroup analysis revealed CXCL16 as a predictor of death in both patients with inflammatory and with non-inflammatory cardiomyopathy. CONCLUSION: According to the present observations CXCL16 is enhanced in inflammatory cardiomyopathy and turned out as an independent predictor of death in patients with HF undergoing endomyocardial biopsy.
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