Marroquin Oscar C, Kip Kevin E, Mulukutla Suresh R, Ridker Paul M, Pepine Carl J, Tjandrawan Tjendimin, Kelsey Sheryl F, Mankad Sunil, Rogers William J, Merz C Noel Bairey, Sopko George, Sharaf Barry L, Reis Steven E
Cardiovascular Institute, Department of Epidemiology, University of Pittsburgh, Pittsburgh, PA, USA.
Am Heart J. 2005 Jul;150(1):109-15. doi: 10.1016/j.ahj.2004.08.003.
Coronary artery microvascular dysfunction is prevalent in women with chest pain in the absence of obstructive coronary artery disease (CAD) and is manifested by attenuated coronary flow reserve (CFR). Markers of inflammation and endothelial cell activation have been found to be elevated in patients with chest pain but without CAD. The relationship between inflammation, endothelial activation, and CFR is not known.
Ninety-four women with chest pain in the absence of obstructive angiographic CAD underwent catheterization-based assessment of CFR and measurement of levels of inflammatory markers (n = 78) and endothelial cell activation in the NHLBI WISE study.
Coronary flow reserve did not correlate with levels of C-reactive protein (high-sensitivity C-reactive protein) (rs = -0.07, P = .53), interleukin (IL)-6 (rs = -0.12, P = .31), IL-18 (rs = 0.14, P = .23), tumor necrosis factor alpha (rs = -0.09, P = .43), transforming growth factor beta1 (rs = 0.02, P = .84), and soluble intracellular adhesion molecule-1 (rs = 0.04, P = .68). Median levels of markers of inflammation and endothelial cell activation did not differ between the 57 women with abnormal CFR (< 2.5) and the 37 women with normal coronary microvascular function (high-sensitivity C-reactive protein 0.32 vs 0.25 mg/dL, P = .80; IL-6 2.89 vs 2.39 pg/mL, P = .63; IL-18 218 vs 227 pg/mL, P = .59; tumor necrosis factor alpha 2.7 vs 2.4 pg/mL, P = .43; transforming growth factor beta1 9928 vs 12436 pg/mL, P = .76; soluble intracellular adhesion molecule-1 286 vs 287 pg/mL, P = .95). Multivariable models demonstrated no evidence of associations between markers of inflammation and of endothelial cell activation and CFR.
Coronary microvascular dysfunction is not associated with markers of inflammation and endothelial cell activation in women with chest pain in the absence of obstructive CAD. These results suggest that inflammation and endothelial cell activation may not play a pathophysiological role in coronary microvascular dysfunction.
在无阻塞性冠状动脉疾病（CAD）的胸痛女性中，冠状动脉微血管功能障碍很常见，表现为冠状动脉血流储备（CFR）降低。已发现胸痛但无CAD的患者炎症和内皮细胞活化标志物升高。炎症、内皮细胞活化与CFR之间的关系尚不清楚。
在NHLBI WISE研究中，94例无阻塞性血管造影CAD的胸痛女性接受了基于导管插入术的CFR评估以及炎症标志物水平（n = 78）和内皮细胞活化测量。
冠状动脉血流储备与C反应蛋白（高敏C反应蛋白）水平（rs = -0.07，P = 0.53）、白细胞介素（IL）-6（rs = -0.12，P = 0.31）、IL-18（rs = 0.14，P = 0.23）、肿瘤坏死因子α（rs = -0.09，P = 0.43）、转化生长因子β1（rs = 0.02，P = 0.84）和可溶性细胞间黏附分子-1（rs = 0.04，P = 0.68）均无相关性。57例CFR异常（<2.5）的女性与37例冠状动脉微血管功能正常的女性之间，炎症和内皮细胞活化标志物的中位数水平无差异（高敏C反应蛋白分别为0.32 vs 0.25 mg/dL，P = 0.80；IL-6分别为2.89 vs 2.39 pg/mL，P = 0.63；IL-18分别为218 vs 227 pg/mL，P = 0.59；肿瘤坏死因子α分别为2.7 vs 2.4 pg/mL，P = 0.43；转化生长因子β1分别为9928 vs 12436 pg/mL，P = 0.76；可溶性细胞间黏附分子-1分别为286 vs 287 pg/mL，P = 0.95）。多变量模型未显示炎症标志物和内皮细胞活化标志物与CFR之间存在关联的证据。
在无阻塞性CAD的胸痛女性中，冠状动脉微血管功能障碍与炎症和内皮细胞活化标志物无关。这些结果表明，炎症和内皮细胞活化可能在冠状动脉微血管功能障碍中不发挥病理生理作用。
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