Lin Chih-Pei, Lin Wen-Tsai, Leu Hsin-Bang, Wu Tao-Cheng, Chen Jaw-Wen
Department of Pathology, Taipei Veterans General Hospital, 201 Shih-Pai Road Section 2, Taipei, Taiwan 11217, ROC.
Int J Cardiol. 2003 May;89(1):53-62. doi: 10.1016/s0167-5273(02)00428-x.
Circulating mononuclear cells could be activated with endothelial inflammation in patients with coronary artery disease (CAD). In some patients with normal coronary angiograms, myocardial ischemia could also present with coronary microvascular dysfunction (cardiac syndrome X). This study was undertaken to investigate whether mononuclear cell activation and endothelial inflammation can present in syndrome X patients.
We evaluated the biochemical parameters, circulating soluble adhesion molecules, circulating superoxide free radicals, and mononuclear cell activity in 32 patients with syndrome X, 34 with angiographically documented CAD, and 17 age- and gender-matched healthy control subjects.
Compared to that in control subjects, plasma high-density lipoprotein was reduced (P<0.001) and insulin to glucose ratio increased (P=0.02) in CAD patients. Circulating level of soluble intracellular adhesion molecule-1 was significantly higher in both syndrome X and CAD patients than in control subjects (P<0.01), whereas the levels of soluble vascular cell adhesion molecule (P=0.02) and von Willebrand factor (P=0.01) were increased in CAD patients only. The peak (P<0.001) and total counts of superoxide free radicals in whole blood (P<0.001) was significantly higher in syndrome X patients than in the other two groups. However, phorbol-12-myristate-13-acetate-induced superoxide free radical generation of mononuclear cells was increased in CAD (10.5+/-4.6%, P=0.01) but not in syndrome X patients (8.7+/-2.0%) as compared with control subjects (7.7+/-0.5%).
The results indicated that the activity of mononuclear cells was increased with significant endothelial inflammation and injury in CAD patients. In syndrome X patients, though circulating superoxide free radicals were increased, there was minimal endothelial inflammation without mononuclear cell activation. The relatively preserved lipid and metabolic profiles might contribute to less vascular inflammation in syndrome X patients.
冠心病（CAD）患者的循环单核细胞可因内皮炎症而被激活。在一些冠状动脉造影正常的患者中，心肌缺血也可能表现为冠状动脉微血管功能障碍（心脏综合征X）。本研究旨在调查综合征X患者是否存在单核细胞激活和内皮炎症。
我们评估了32例综合征X患者、34例血管造影证实的CAD患者以及17例年龄和性别匹配的健康对照者的生化参数、循环可溶性黏附分子、循环超氧自由基和单核细胞活性。
与对照组相比，CAD患者血浆高密度脂蛋白降低（P<0.001），胰岛素与葡萄糖比值升高（P=0.02）。可溶性细胞间黏附分子-1的循环水平在综合征X患者和CAD患者中均显著高于对照组（P<0.01），而可溶性血管细胞黏附分子（P=0.02）和血管性血友病因子（P=0.01）水平仅在CAD患者中升高。综合征X患者全血中超氧自由基的峰值（P<0.001）和总数（P<0.001）显著高于其他两组。然而，与对照组（7.7±0.5%）相比，CAD患者中佛波酯-12-肉豆蔻酸酯-13-乙酸酯诱导的单核细胞超氧自由基生成增加（10.5±4.6%，P=0.01），而综合征X患者中未增加（8.7±2.0%）。
结果表明，CAD患者单核细胞活性增加，伴有显著的内皮炎症和损伤。在综合征X患者中，尽管循环超氧自由基增加，但内皮炎症轻微，无单核细胞激活。相对保留的脂质和代谢谱可能导致综合征X患者血管炎症较轻。
