PURPOSE: Angiopoietin-2 (Ang-2) impairs endothelial integrity. The association of Ang-2 in the presence of oedema and outcome of patients with acute decompensated heart failure (ADHF) has not been investigated. METHODS AND RESULTS: Angiopoietin-2 was measured in 132 ADHF patients, which were included in a monocentric, prospective trial (Clinicaltrials.gov: NCT01429857). Primary endpoint was all-cause death at 6-months. 20 healthy persons served as control group (HC). In ADHF patients, mean Ang-2 concentration at admission was significantly increased compared to HC (2,111 ± 117 vs. 971 ± 46 pg/ml, p = 0.0002). Ang-2 was increased in patients with compared to those without peripheral oedema (2,294 ± 140 vs. 1,540 ± 170 pg/ml; p = 0.009) and in patients with NYHA class III or IV symptoms compared to those with NYHA class II symptoms (2,256 ± 132 vs. 1,341 ± 380 pg/ml, p = 0.023). During the 6-month follow-up, 10 patients died. In survivors, Ang-2 significantly decreased at discharge compared to admission (2,046 ± 118 vs. 1,431 ± 93 pg/ml; p < 0.0001). Non-survivors showed no difference between Ang-2 concentration at admission and discharge (3,296 ± 594 vs. 2,909 ± 536 pg/ml). Ang-2 concentrations at discharge above 2,500 pg/ml were associated with an increased risk of death compared to Ang-2 concentrations below this threshold (Hazard ratio 8.8; 95 % confidence interval; 2.48-31.16, p < 0.001). CONCLUSION: In ADHF patients, Ang-2 is significantly increased compared to healthy controls, shows a relationship in the presence of oedema and is a predictor of poor outcome.
PURPOSE:Angiopoietin-2 (Ang-2) impairs endothelial integrity. The association of Ang-2 in the presence of oedema and outcome of patients with acute decompensated heart failure (ADHF) has not been investigated. METHODS AND RESULTS:Angiopoietin-2 was measured in 132 ADHF patients, which were included in a monocentric, prospective trial (Clinicaltrials.gov: NCT01429857). Primary endpoint was all-cause death at 6-months. 20 healthy persons served as control group (HC). In ADHF patients, mean Ang-2 concentration at admission was significantly increased compared to HC (2,111 ± 117 vs. 971 ± 46 pg/ml, p = 0.0002). Ang-2 was increased in patients with compared to those without peripheral oedema (2,294 ± 140 vs. 1,540 ± 170 pg/ml; p = 0.009) and in patients with NYHA class III or IV symptoms compared to those with NYHA class II symptoms (2,256 ± 132 vs. 1,341 ± 380 pg/ml, p = 0.023). During the 6-month follow-up, 10 patients died. In survivors, Ang-2 significantly decreased at discharge compared to admission (2,046 ± 118 vs. 1,431 ± 93 pg/ml; p < 0.0001). Non-survivors showed no difference between Ang-2 concentration at admission and discharge (3,296 ± 594 vs. 2,909 ± 536 pg/ml). Ang-2 concentrations at discharge above 2,500 pg/ml were associated with an increased risk of death compared to Ang-2 concentrations below this threshold (Hazard ratio 8.8; 95 % confidence interval; 2.48-31.16, p < 0.001). CONCLUSION: In ADHF patients, Ang-2 is significantly increased compared to healthy controls, shows a relationship in the presence of oedema and is a predictor of poor outcome.
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