Endothelial dysfunction and inflammation in chronic and acute heart failure

Background. There is a neurohormonal an inflammatory activation in heart failure. There is also an endothelial dysfunction. Our objective war to compare both processes ( inflammation and endothelial dysfunction) in patients with heart failure. Material and method. We compared endothelial dysfunction markers (circulating endothelial cells, circulating microparticles and Von Willebrand factor) and inflammatory markers (C reactive protein, interleukin-6 and functional fibrinogen) in 16 patients with acute heart failure (AHF), 16 with stable chronic heart failure (SHF) and 32 healthy controls. Results. The number of circulating endothelial cells was greater in AHF patients than in SHF and controls (115.10 +/- 63.44 vs 19.67 +/- 3.17 vs 11.71 +/- 2.92 cel/mL). The amount of circulating microparticles was greater in the AHF group than in the SHF and in both than controls (9,627 +/- 4,986 vs 3,970 +/- 3,452 vs 1,371 +/- 739 p/mu L). Von Willebrand factor was greater in both heart failure groups than in controls (234.3 +/- 45.31 vs 245.92 +/- 117.89 vs 100.14 +/- 20.7%). C reactive protein was greater in the AHF group than in the SHF group or controls (20.29 +/- 17.56 vs 7.65 +/- 4.27 vs 1.44 +/- 1.10 mg/dL). Interleukin-6 was also higher in the AHF group than in the SHF and in this greater than in controls (9.73 +/- 9.37 vs 1.69 +/- 1.36 vs 1.01 +/- 1.09 pg/mL). Functional fibrinogen was only greater in the AHF group (350 +/- 60.48 vs 264.08 +/- 67.02 vs 254.29 +/- 23.69 mg/dL). Conclusions. Inflammation and endothelial dysfunction run together in heart failure patients. The endothelial dysfunction observed seems to be proportional to the inflammatory state.