Endothelial progenitor cells and aptoptosis in patients with heart failure

Objective: One the main features of heart failure is endothelial disfunction and some authors claimed this is caused by endothelial cell apoptosis. Scope of the study is to evaluate in a group of patients with heart failure the number of EPC (endothelial progenitor cells) both ex vivo and in culture in parallel with the assessment of EPC apoptosis and the echocardiographic evaluation of systolic and diastolic left ventricular function. Design and Method: We studied 30 patients with congestive heart failure (CHF) and 16 healthy control subjects CS) by measuring the number of EPC both ex vivo and after 4 days in culture. We measured also EPC apoptosis together with echocardiographic parameters of systolic and diastolic left ventricular function. Results and Conclusion: The EPC count measured both ex vivo (CD34+/KDR+; M ± ES, CHF, 9.5 ± 1.1%, CS, 5.1 ± 0.8%, p < 0.02) and after culture (KDR+/CD34+; M ± ES, CHF, 51.2 ± 6.6%; CS, 23.5 ± 8.8%, p < 0.0001) was significantly increased in CHF patients as compared to CS. In CHF patients EPC number measured in culture is directly correlated with hs-CRP (p = 0.035, r = 0.497). The EPC apoptosis does not show any statistically difference between CHF patients and CS. In CHF patients the number of apoptotic EPC was inversely correlated with total (r = −0.418, p = 0.02) and LDL cholesterol (r = −0.399, p = 0.03). We hypnotize that the increased oxidative stress characterizing heart failure may explain the increased EPC number which may have a compensatory significance for endothelial dysfunction as EPC number is directly linked to a crucial flogistic parameter as CRP. EPC apoptosis is not altered in CHF patients and does not seem to be related with the increased EPC number. The inverse correlation between EPC apoptosis and LDL cholesterol may represent the clinical equivalent of the in vitro ability of oxidized LDL to inhibit the macrophage binding to apoptotic endothelial cells.