作者: Victoria L. M. Herrera , Joseph A. Vita
DOI: 10.1007/978-1-60327-179-0_13
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摘要: Endothelial cell (EC) activation mediates inflammation and involves several effectors such as E-selectin, P-selectin, ICAM-1, VCAM-1. These EC markers are detected to be significantly increased in clinical coronary artery disease (CAD), mildly subclinical CAD compared with non-disease reference groups. Because is implicated all stages of thought underlie plaque destabilization rupture, monitoring the increase could a surrogate endpoint (subCAD) progression, and/or response prevention/intervention strategies. While progression complex, requires contemporaneous analysis multi-pathway markers, provide insight into subCAD especially when levels approach those acute syndromes (ACS). Clearly, mechanism-based deductions compelling evidence that should integrated management subCAD; however, much study remains done.