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Circulating endothelial cell count, plasma vWF and soluble ICAM-1 levels following primary or elective percutaneous coronary intervention.

作者信息

Vargová K, Toth-Zsamboki E, Beres B J, Bencze J, Kerecsen G, Gulacsi-Bardos P, Kiss R G, Preda I

机构信息

Research Group for Inflammation Biology and Immunogenomics of Hungarian Academy of Sciences and Semmelweis University, 44 Robert Karoly str., 1134 Budapest, Hungary.

出版信息

Atherosclerosis. 2008 Jun;198(2):366-72. doi: 10.1016/j.atherosclerosis.2007.09.005. Epub 2007 Oct 23.

Abstract

BACKGROUND

Percutaneous coronary intervention (PCI) is an important therapeutic strategy in patients with ischaemic heart disease. Our aim was to clarify the extent of endothelial injury induced by PCI in stable angina (SA) or in acute ST-elevation myocardial infarction (STEMI).

METHODS

Circulating endothelial cell (CEC) count, von Willebrand factor (vWF) and soluble intercellular adhesion molecule-1 (sICAM-1) levels were determined pre-, post-, 24 and 96h after PCI in patients with SA (n=23) and with STEMI (n=28). To provide control data regarding the effect of angiography itself stable angina patients with coronarography only (n=23) were enrolled.

RESULTS

PCI and coronarography in stable angina patients caused measurable, but only non-significant elevation of CEC count and plasma vWF (p=NS). In STEMI, significantly higher baseline CEC count (p=0.019) and vWF plasma levels (p=0.046) were found compared to SA with PCI/or coronarography. After PCI, explicit increase in CEC count was observed (significant peak at 24h) (p=0.036). Positive correlation was found between baseline CKMB and CEC count at 24h (r=0.51, p<0.05).

CONCLUSION

Both coronary angiography and elective PCI cause only mild endothelial injury. However, in patients with STEMI, not only the procedure itself but myocardial ischemia and the ongoing atherothrombotic process might be responsible for the prolonged and more pronounced endothelial damage.

摘要

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