期刊论文详细信息
Growth factors in the collateral circulation of chronic total coronary occlusions - Relation to duration of occlusion and collateral function
Article
关键词: THERAPEUTIC ANGIOGENESIS;    ANGIOGRAPHIC ASSESSMENT;    MYOCARDIAL-INFARCTION;    ARTERY OCCLUSION;    BLOOD-FLOW;    ARTERIOGENESIS;    ISCHEMIA;    EXPRESSION;    MODULATION;    MECHANISMS;   
DOI  :  10.1161/01.CIR.0000143624.72027.11
来源: SCIE
【 摘 要 】

Background - Despite extensive animal experimental evidence, there are few data on the relation of growth factors and collateral function in humans. Methods and Results - In 104 patients with a chronic total coronary occlusion (CTO; > 2 weeks' duration), collateral function was assessed invasively during recanalization by intracoronary Doppler and pressure recordings. A collateral resistance index, R-Coll, was calculated. Blood samples were drawn from the distal coronary bed supplied by the collaterals and from the aortic root to measure basic fibroblast growth factor ( bFGF), monocytic chemotactic protein-1 (MCP-1), transforming growth factor-beta (TGF-beta), placenta growth factor (PlGF), and tumor necrosis factor-alpha (TNF-alpha). The bFGF concentration in the collateralized artery was higher than in the aortic root (34 +/- 20 versus 18 +/- 14 pg/mL; P < 0.001). bFGF was highest in recent occlusions ( 2 to 12 weeks) with the highest RColl. Higher collateral concentrations were also observed for MCP-1, TGF-beta, and PlGF, but without a close relation to the duration of occlusion. TNF-alpha was not increased in collaterals compared with the systemic circulation. MCP-1, PlGF, and TGF-beta were significantly increased in small collaterals with the highest shear stress. Diabetic patients had lower bFGF and higher MCP-1 levels than nondiabetics. Conclusions - In CTOs, the continuous release of bFGF into collaterals showed a close relation to the duration of occlusion and collateral function, which underscores its therapeutic potential. Other factors influencing growth factor release appeared to be shear stress for MCP-1, TGF-beta, and PlGF and the presence of diabetes.

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