Fig. 1.

Proposed relationship between venous congestion, endothelial activation, and decompensation in CHF: venous congestion ↔ inflammation. ECs sense both biochemical stimuli and biomechanical forces, and translate both types of signals into genetic regulatory events. When exposed to biomechanical stress (circumferential stretch associated with venous congestion), ECs release pro-oxidant, proinflammatory, and vasoconstricting mediators, which contribute to the development of ADHF. Antioxidant enzymes are the primary defense mechanism against oxidative and inflammatory damage. ADHF—acute decompensated heart failure; CHF—chronic heart failure; COX—cyclo-oxygenase; CuZnSOD—copper-zinc superoxide dismutase; EC—endothelial cell; eNOS—endothelial nitric oxide synthase; ET—endothelin; GPx1—glutathione peroxidase; ICAM—intercellular adhesion molecule; iNOS—inducible nitric oxide synthase; MnSOD—manganese superoxide dismutase; TNF—tumor necrosis factor