Abstract

Endothelial dysfunction has been considered as one of potential mechanisms by which depression and stress might contribute to the development of coronary artery disease (CAD). Recent studies suggest that circulating endothelial progenitor cells (EPCs) and brachial artery flow-mediated dilation (FMD) are related to endothelial function and progression of CAD. We investigated the relationships between the level of circulating CD34/KDR+ EPCs and CD133/KDR+ EPCs, brachial FMD, and scores of depression and stress measured with the Depression Anxiety Stress Scales in 288 stable angina patients without major psychiatric disorders. As defined by the ≥75th percentile, 100 (35%) subjects had high depression score (≥8), and 84 (29%) subjects had high stress score (≥10). Subjects with high depression or stress score had significantly lower FMD (1.86±0.14 vs. 3.63±0.17%, p<0.001; 2.05±0.18 vs. 3.48±0.17%, p<0.001) and percentage of circulating CD34/KDR+ EPCs (0.97±0.11 vs. 1.94±0.17%, p<0.001; 1.09±0.13 vs. 1.68±0.16%, p=0.005), but not CD133/KDR+ EPCs (0.52±0.04 vs. 0.66±0.06%, p=0.057; 0.61±0.05 vs. 0.59±0.05%, p=0.833), as compared with subjects with normal depression or stress score. Multivariate regression analysis indicated that high depression score (OR 1.09, 95% CI: 1.04–1.15, p<0.001), but not stress score or percentage of circulating EPCs, independently predicted impaired brachial FMD. In conclusions, our results demonstrated that in stable angina patients without major psychiatric disorders, a high depression or stress score was related to attenuated brachial FMD and depletion of circulating EPCs. However, only the depression score, but not the stress score or the level of EPCs, was an independent predictor for decreased brachial FMD.

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