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COMPARATIVE STUDY
JOURNAL ARTICLE
Circulating endothelial progenitor cells in patients with unstable angina: association with systemic inflammation.
European Heart Journal 2004 June
BACKGROUND: Endothelial progenitor cells (EPC) are present in peripheral blood and can develop a functional endothelial phenotype. The number and function of circulating EPCs are altered in atherosclerosis, diabetes, and after myocardial infarction and EPCs have been shown to promote postnatal angiogenesis and vasculogenesis. We investigated the number and adhesive properties of EPCs from patients with unstable angina and no evidence of cardiac necrosis.
METHODS AND RESULTS: Patients were selected with unstable angina (n=29) and no evidence of cardiac necrosis, and controls with stable angina (n=12) and atherosclerotic risk factors, medication use, and coronary vessel involvement similar to patients. Circulating EPC numbers were determined by colony-forming unit assay and their adhesive properties were evaluated by EPC capacity to bind immobilised fibronectin. High-sensitivity C-reactive protein (hsCRP) was determined in all patients. Circulating EPCs were significantly increased in patients with unstable as compared with stable angina (24.5+/-2.6 vs. 13.3+/-2.9, respectively). Seven unstable angina patients followed up for 3 months after clinical stabilisation exhibited a reduction of close to 50% in circulating EPC numbers. The adhesive capacity of EPCs from patients with unstable and stable angina did not differ. A positive correlation was found between systemic CRP levels and circulating EPC numbers, but not their adhesive capacity.
CONCLUSION: Patients with unstable angina and no evidence of cardiac necrosis exhibited increased circulating EPCs. Systemic inflammation, in addition to recognised growth factors, could play a role in the peripheral mobilisation of EPCs in patients with anginal syndromes.
METHODS AND RESULTS: Patients were selected with unstable angina (n=29) and no evidence of cardiac necrosis, and controls with stable angina (n=12) and atherosclerotic risk factors, medication use, and coronary vessel involvement similar to patients. Circulating EPC numbers were determined by colony-forming unit assay and their adhesive properties were evaluated by EPC capacity to bind immobilised fibronectin. High-sensitivity C-reactive protein (hsCRP) was determined in all patients. Circulating EPCs were significantly increased in patients with unstable as compared with stable angina (24.5+/-2.6 vs. 13.3+/-2.9, respectively). Seven unstable angina patients followed up for 3 months after clinical stabilisation exhibited a reduction of close to 50% in circulating EPC numbers. The adhesive capacity of EPCs from patients with unstable and stable angina did not differ. A positive correlation was found between systemic CRP levels and circulating EPC numbers, but not their adhesive capacity.
CONCLUSION: Patients with unstable angina and no evidence of cardiac necrosis exhibited increased circulating EPCs. Systemic inflammation, in addition to recognised growth factors, could play a role in the peripheral mobilisation of EPCs in patients with anginal syndromes.
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