Effects of Percutaneous Coronary Intervention on Serum Angiopoietin-2 in Patients with Coronary Heart Disease

Background： Angiopoietin-2 （Ang-2） plays a crucial role in hypoxia-induced angiogenesis and is expressed only in sites of vascular remodeling. Ang-2 expression can be regulated by hypoxia inducible factors and other regulators with exposure to hypoxia. The objective of this study was to investigate the influence of percutaneous coronary intervention （PCI） on serum Ang-2 concentrations, and analyze the correlation between serum Ang-2 and the severity of coronary artery stenosis in patients with coronary heart disease （CHD）. Methods： Sixty-four patients with CHD were selected as the study group, each undergone PC1. Thirty-two healthy subjects were selected as the control group. Pre-PCI and post-PCl serum Ang-2 were measured by enzyme-linked immunosorbent assay. The severity of coronary artery stenosis was evaluated using angiographic Gensini scores, and the coronary collateral vessels were scored according to Rentrop＇s classification. Results： Concentrations of pre-PCI serum Ang-2 in the study group were significantly higher than those in the control group （4625.06 ~ 1838.06 vs. 1945.74 ：k 1588.17 pg/ml, P 〈 0.01 ）; however, concentrations of post-PCl serum Ang-2 were significantly lower than those of pre-PCI （3042.63 ＋ 1845.33 pg/ml vs. 4625.06 .k 1838.06 pg/ml, P 〈 0.01）. Concentrations of pre-PCl serum Ang-2 were significantly correlated with Gensini scores （r= 0.488, P〈 0.01）; however, the decrease in serum Ang-2 after PC1 was not correlated with Gensini scores, coronary collateral vessel grading, or left ventricular ejection fraction. Conclusions： Serum Ang-2 concentrations significantly increased in patients with CHD, and PCI treatment significantly decreased these concentrations. Serum Ang-2 concentrations, but not the decrease in serum Ang-2 concentrations, were significantly correlated with the severity of coronary artery stenosis. These results suggested that Ang-2 may be a biomarker of myocardial ischemia and vessel remodeling.