Objective Endothelial dysfunction and microvascular abnormalities have been reported in patients with cardiac syndrome X (CSX), but the underlying mechanisms remain unclear. Recent insights suggest that the injured endothelial monolayer is regenerated by circulating bone marrow-derived endothelial progenitor cells (EPCs). Here, we tested the hypothesis that altered EPCs biology might contribute to the pathophysiology of CSX.
Methods Totally, 34 subjects (mean age: 62±7 years) were enrolled in the study, including 12 CSX patients, 12 stable coronary artery disease (CAD) subjects, and 10 healthy controls. The number and adhesive function of EPCs were measured in peripheral-blood samples from these study participants.
Results The baseline characteristics in patients with CSX and CAD had 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 to 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 than in normal subjects (104±12 vs 80±20 vs 65±13/well, p<0.001).
Conclusions This study clearly showed for the first time that compared to 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.
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