Department of Cardiology, Koc University School of Medicine and Hospital, Istanbul, Turkey.
Department of Cardiology, Bakirkoy Dr. Sadi Konuk Education and Research Hospital, Istanbul, Turkey.
Microvasc Res. 2019 Mar;122:85-93. doi: 10.1016/j.mvr.2018.11.009. Epub 2018 Nov 28.
Coronary microvascular dysfunction plays a major role in the pathogenesis of microvascular angina (MVA). Along with endothelial dysfunction, microvascular atherosclerosis and inflammation seem to contribute to the development of coronary microvascular dysfunction. Serum soluble ST2 (sST2) and serum soluble CD40 ligand (sCD40L) are two biomarkers associated with inflammation and atherosclerosis. The aim of this study was to investigate the role of these biomarkers in the pathogenesis of MVA and determine their possible association with coronary microvascular dysfunction.
A total of 152 patients were included in the study. Ninety-one patients with MVA {median age 56 years (40-79), of which 55 are women} and sixty-one controls {median age 52 (38-76), of which 29 are women} were included in the study. Serum concentration of sST2 and sCD40L were measured with a commercially available ELISA kit.
Serum sST2 (median 13.6 ng/ml; interquartile range (IQR), 3.5-63.8 ng/ml vs median 10.6 ng/ml; IQR, 2.9-34.2 ng/ml, p < 0.0005) and sCD40L (median 5.3 ng/ml; IQR, 0.5-20.6 ng/ml vs median 2.2 ng/ml; IQR, 0.7-10.8 ng/ml, p < 0.0005) were significantly higher in patients with MVA compared to controls. Analysis of the associations between these biomarkers and potential contributors of MVA revealed that serum sST2 showed a positive correlation with LDL-cholesterol (r = 0.19, p = 0.016) and serum sCD40L concentrations correlated positively with hs-CRP (r = 0.22, p = 0.005). In logistic regression analysis, sCD40L and hs-CRP but not sST2 were found to be significantly associated with MVA.
Higher serum concentrations of sST2 and sCD40L in MVA patients may be associated with inflammatory activation and coronary microvascular dysfunction. Larger studies are required for understanding their role in the pathogenesis of inflammatory and possibly fibrotic process in MVA patients.
冠状动脉微血管功能障碍在微血管性心绞痛（MVA）发病机制中起主要作用。除内皮功能障碍外，微血管粥样硬化和炎症似乎也促成了冠状动脉微血管功能障碍的发展。血清可溶性 ST2（sST2）和血清可溶性 CD40 配体（sCD40L）是与炎症和动脉粥样硬化相关的两种生物标志物。本研究的目的是探讨这些生物标志物在 MVA 发病机制中的作用，并确定它们与冠状动脉微血管功能障碍的可能关联。
共纳入 152 例患者。91 例 MVA 患者[中位年龄 56 岁（40-79 岁），其中 55 例为女性]和 61 例对照组[中位年龄 52 岁（38-76 岁），其中 29 例为女性]纳入研究。使用商业 ELISA 试剂盒测量血清 sST2 和 sCD40L 浓度。
MVA 患者的血清 sST2（中位数 13.6ng/ml；四分位距（IQR），3.5-63.8ng/ml 与中位数 10.6ng/ml；IQR，2.9-34.2ng/ml，p<0.0005）和 sCD40L（中位数 5.3ng/ml；IQR，0.5-20.6ng/ml 与中位数 2.2ng/ml；IQR，0.7-10.8ng/ml，p<0.0005）水平明显高于对照组。对这些生物标志物与 MVA 潜在促成因素之间的关联进行分析显示，血清 sST2 与 LDL-胆固醇呈正相关（r=0.19，p=0.016），血清 sCD40L 浓度与 hs-CRP 呈正相关（r=0.22，p=0.005）。在逻辑回归分析中，sCD40L 和 hs-CRP 而不是 sST2 与 MVA 显著相关。
MVA 患者血清中较高的 sST2 和 sCD40L 浓度可能与炎症激活和冠状动脉微血管功能障碍有关。需要进一步的大型研究来了解它们在 MVA 患者炎症和可能的纤维化过程中的发病机制中的作用。
