Abstract

Background: Patients with type 2 diabetes mellitus (T2DM) may develop cardiomyopathy and microvascular disease and oxidative stress may contribute to it. Endothelial progenitor cells (EPCs) is responsible for angiogenesis and has been shown to be closely correlated with oxidative stress. Accordingly, the aim of the study is to evaluate the role of EPCs and oxidative stress in relation with the left ventricular (LV) function in patients with T2DM. Methods: Ninety patients(62±9years, 39% male) with T2DM without coronary artery disease were recruited. Transthoracic echocardiography and detailed evaluation of LV systolic function by 2D speckle tracking derived strain analysis was performed. Four subpopulation of EPCs including CD34+, CD133+, CD34+/kinase insert domain-containing receptor (KDR) + and CD133+/KDR+ EPCs were measured by flow cytometry. Furthermore, oxidative stress was assessed by superoxide dismutase (SOD). Results: The mean HbA1c% was 7.76% and 18.9% were on insulin therapy. Global circumferential strain was associated with CD34+ EPCs (r=-0.22 , P=0.04) and SOD (r=-0.32 , P=0.01 ) but not the other EPCs. Patients were subsequently dichotomized according to the median level of CD34+ EPCs. The two groups of subjects had similar LV ejection fraction (63±7% vs. 65±8%, P=0.30). Importantly, patients with low level of CD34+EPCs had impaired LV global longitudinal strain (-16.7±2.7% vs. -18.1±2.2%, P<0.01), circumferential strain (-17.2±2.1% vs. -18.3±2.2%, P=0.02) and radial strain (30.2±9.3% vs. 37.4±11.6%, P<0.01) compared to those with high level of CD34+EPCs. After multivariate linear regression, CD34+ EPCs was an independent predictor of the circumferential strain (β=-0.22, 95%CI -25.2∼-0.70, P=0.04) and radial strain (β=0.27, 95%CI 17.2∼139.5, P=0.02). furthermore, SOD was an independent predictor of the circumferential strain (β=-0.32, 95%CI -13.7∼-1.7, P=0.01) Conclusions : Both CD34+ EPCs and SOD correlated with global circumferential strain. Importantly, the number of CD34+ EPCs and SOD is independently associated with LV systolic dysfunction in patients with T2DM. The present results thus suggested that EPCs and oxidative stress contributed to the development of diabetic cardiomyopathy.

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