Endothelial Cell Activation in Patients With Decompensated Heart Failure

Abstract

Clinical decompensation in CHF is associated with activation of the venous endothelium. Return to a compensated state after short-term inotropic therapy results in a significant reduction in endothelial nitrotyrosine formation, COX-2, and iNOS expression.

Acute heart failure as “acute endothelitis” — Interaction of fluid overload and endothelial dysfunction

“…Using a novel approach that involves sampling of venous endothelial cells and quantification of protein expression by quantitative immunofluorescent analysis [21,22], we observed an increase in endothelial oxidative stress that eventually justifies this decline in vascular NO bioactivity (Fig. 1) [20]. The increase in venous endothelial oxidative stress partially subsided with clinical improvement during the index hospitalisation.…”

“…We recently reported a particularly severe impairment in endothelium NO-dependent vasodilation in patients hospitalised with AHF [19,20]. Using a novel approach that involves sampling of venous endothelial cells and quantification of protein expression by quantitative immunofluorescent analysis [21,22], we observed an increase in endothelial oxidative stress that eventually justifies this decline in vascular NO bioactivity (Fig.…”

Cardiorenal Syndrome

“…In addition to its effects on renal hemodynamics, high systemic venous congestion can activate endothelial dysfunction with production of reactive oxygen species, TNFa, endothelin-1, IL-6, and other inflammatory cytokines (46,47), all of which worsen nitric oxide dysregulation, resulting in additional neurohormonal activation and renal dysfunction. Venous congestion may also trigger production of systemic endotoxins from the gut, and superimposed infection may also contribute to renal dysfunction (48).…”

Lack of Diagnostic and Prognostic Utility of Circulating Plasma Myeloperoxidase Concentrations in Patients Presenting with Dyspnea

“…Higher MPO concentrations are also associated with an increased prevalence of severe diastolic dysfunction and right ventricular systolic dysfunction (11 ). Furthermore, plasma markers of oxidative stress are increased in acute decompensated heart failure (ADHF) (12,13 ). The purposes of this study were first to investigate the diagnostic and prognostic value of circulating MPO concentrations in patients presenting with dyspnea to the emergency department (ED) and, second, to evaluate the additive prognostic value of MPO concentration in combination with established natriuretic peptide biomarkers and measures of cardiac function.…”