Impaired ability to grow colonies of endothelial stem cells could be the mechanism explaining the high cardiovascular morbidity and mortality of patients with depression.

Abstract

Subjects with depression are more prone to develop cardiovascular complications. Severity of depression is associated with higher rates of cardiovascular mortality and morbidity. Several mechanisms were suggested including accelerated atherosclerosis, alteration of the cardiac autonomic response with a decrease in heart rate variability. There is evidence that circulating endothelial progenitor cells (EPCs) are decreased in patients with major depression. Our hypothesis was that patients with depression would have an impaired ability to build colonies of EPCs. A prospective study enrolled twenty women with a diagnosis of major. All were not treated before for depression. Thirteen healthy age-matched women served as controls. All signed a consent form before recruitment to the study. Peripheral blood was drawn to build colonies of EPCs within 5 days. ELISA methods were used to measure levels of vascular cell adhesion molecule-1 (VCAM-1) and vascular endothelial growth factor (VEGF). Twenty female patients with depression were recruited. The mean age was 43 ± 14 years (vs. controls 41 ± 11 years, P = 0.682), patients' average CFU-EPCs was 7 ± 8 colonies per well (controls 31 ± 11, P = 0.0001), VCAM-1 level was 121.7 ± 3.0 ng/ml (controls 119.3 ± 3.1 pg/ml, P = 0.037), VEGF level was 6.4 ± 0.2 pg/ml (controls 5.2 ± 0.5 pg/ml, P = 0.0001). An inverse correlation was found between VEGF level and EPCs' colonies (r = -0.547, P < 0.001) and between age and CFU-EPCs (r = -0.576, P = 0.008). We found that patients with major depression had high levels of VCAM-1 and VEGF. They also had a significant inhibition of EPCs' colonies. An inverse correlation was found between levels of VEGF and the ability to grow colonies of EPCs in culture.