Huang Po-Hsun, Chen Yung-Hsiang, Chen Yuh-Lien, Wu Tao-Cheng, Chen Jaw-Wen, Lin Shing-Jong
Institute of Clinicial Medicine and [corrected] Cardiovascular Research Center, National Yang-Ming University, Taipei, Taiwan.
Heart. 2007 Sep;93(9):1064-70. doi: 10.1136/hrt.2006.107763. Epub 2007 May 8.
Endothelial dysfunction and microvascular abnormalities have been reported in patients with cardiac syndrome X (CSX), but the underlying mechanisms are unclear. Recent insights suggest that the injured endothelial monolayer is regenerated by circulating bone marrow-derived endothelial progenitor cells (EPCs).
To test the hypothesis that the biology of altered EPCs might contribute to the pathophysiology of CSX.
34 subjects (mean (SD) age: 62 (7) years) were enrolled in the study, including 12 patients with CSX, 12 stable subjects with coronary artery disease (CAD) and 10 healthy controls. The number and adhesive function of EPCs were measured in peripheral-blood samples from these study participants.
The baseline characteristics in patients with CSX and CAD were enhanced Framingham risk scores, more hypertension and lower high-density lipoproteins than the controls. Patients with CSX and CAD had significantly decreased endothelium-dependent flow-mediated vasodilation (FMD) compared with normal controls (normal controls vs CSX vs CAD: 10.6% (3.5%) vs 6.1% (1.8%) vs 4.1% (1.9%), p<0.001), but the difference was not found in endothelium-independent nitroglycerine-mediated vasodilation (p = 0.159). Reduced numbers of colony-forming units (CFU) of EPCs were noted in patients with CSX and CAD (normal vs CSX vs CAD: 41 (9) vs 30 (7) vs 14 (7) CFU/well, p<0.001). Levels of EPCs were shown to be associated with FMD (r = 0.557, p = 0.001) and high-density lipoprotein (r = 0.339, p = 0.049). Also, attenuated fibronectin adhesion function of EPCs was found in patients with CSX and CaD compared with normal subjects (104 (12) vs 80 (20) vs 65 (13)/well, p<0.001).
This study clearly showed for the first time that compared with normal subjects, patients with CSX have decreased levels and adhesive function of circulating EPCs. These findings may explain the underlying mechanisms which contribute to the endothelial dysfunction and microvascular abnormalities observed in patients with CSX.
心脏X综合征（CSX）患者中已报道存在内皮功能障碍和微血管异常，但其潜在机制尚不清楚。最近的研究表明，受损的内皮单层可由循环中的骨髓源性内皮祖细胞（EPCs）再生。
验证改变的EPCs生物学特性可能导致CSX病理生理学改变这一假说。
34名受试者（平均（标准差）年龄：62（7）岁）纳入本研究，包括12例CSX患者、12例稳定型冠心病（CAD）患者和10名健康对照者。检测这些研究参与者外周血样本中EPCs的数量和黏附功能。
CSX患者和CAD患者的基线特征为Framingham风险评分升高、高血压更多且高密度脂蛋白水平低于对照组。与正常对照相比，CSX患者和CAD患者的内皮依赖性血流介导的血管舒张（FMD）显著降低（正常对照vs CSX vs CAD：10.6%（3.5%）vs 6.1%（1.8%）vs 4.1%（1.9%），p<0.001），但在非内皮依赖性硝酸甘油介导的血管舒张方面未发现差异（p = 0.159）。CSX患者和CAD患者的EPCs集落形成单位（CFU）数量减少（正常vs CSX vs CAD：41（9）vs 30（7）vs 14（7）CFU/孔，p<0.001）。EPCs水平与FMD（r = 0.557，p = 0.
