No abstract

Background: Circulating soluble (s) cell adhesion molecules (CAMs) are elevated in patients with congestive heart failure (CHF) and may play an important role in the pathogenesis of CHF by mediating the cell-cell interactions of the immune response. However, clinical data about the prognostic value of sCAMs are sparse. The purpose of this study is to determine whether various sCAMs can provide prognostic information in patients with CHF. Methods: We measured circulating levels of three sCAMs (vascular cell adhesion molecule-1, intercellular adhesion molecule-1, and sP-selectin) in 74 patients with symptomatic chronic CHF and left ventricular ejection fraction (LVEF) -50%. We compared these levels with those of a group of 19 age-matched control subjects. Major adverse cardiac events (death, heart transplantation or hospitalization with worsening CHF) during a median follow-up period of 240 days were determined. Results: The concentrations of the three sCAMs in the 74 patients with CHF were significantly associated with one another. Their levels were higher than those of the control subjects and increased with the severity of CHF. Significantly higher sCAM levels were noted in those patients who had major adverse cardiac events during the follow-up period. There were significant negative correlations between LVEF and sCAMs. However, only high levels of sP-selectin were found to be an independent significant predictor of CHF by Cox proportional hazards analysis. Conclusions: These findings indicate that the levels of these three sCAMs increase with the severity of CHF and are related to clinical outcomes. Among them, high levels of sP-selectin can provide prognostic information independently in patients with CHF.

Objectives: Endothelin-1 (ET-1) induces cardiac hypertrophy, whereas adiponectin may elicit protective effects in the vasculature and myocardium. We therefore evaluated the relationship between plasma ET-1 and adiponectin levels in heart failure (HF) patients, and the association between adiponectin expression and ET-1-induced hypertrophy of human cardiomyocytes (HCM) in vitro. Methods: One hundred seventeen patients with chronic HF were enrolled into this study. A group of 7 patients with end-stage HF undergoing heart transplantation was included in the histopathological study. Baseline clinical evaluations and laboratory measurements were performed. HCM cultures were studied to investigate the effect of ET-1 on cell size and adiponectin expression. Results: Plasma ET-1, adiponectin, and N-terminal pro-B-type natriuretic peptide (NT-proBNP) increased with the severity of HF. Higher New York Heart Association functional class, plasma ET-1, adiponectin, and NT-proBNP levels were significant predictors of adverse outcomes in these patients. The myocardial expression of adiponectin was significantly higher in the recipient hearts of patients undergoing emergency or urgent heart transplantation. In cell culture, ET-1 significantly increased cell size and adiponectin expression in HCM. Conclusions: Adiponectin was significantly elevated in HF and was significantly associated with ET-1. The study provides a basis for further investigation of ET-1 and adiponectin modulation as a therapeutic strategy for ventricular remodeling in HF.

Our results parallel the demonstration of a U-shaped relationship between alcohol consumption and cardiovascular mortality, and suggest that anti-inflammatory effects of moderate alcohol intake may partly be linked to a low cardiovascular and overall mortality.

The fenofibrate directly inhibits monocyte binding by TNF-alpha-activated HAECs, probably through preventing up-regulation of cell adhesion molecules by endothelial cells in response to inflammatory stimuli. This PPARalpha activator may have the potential to ameliorate vascular inflammation in patients with CHF.