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Am J Physiol Heart Circ Physiol (January 5, 2007). doi:10.1152/ajpheart.01116.2006
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Submitted on October 12, 2006
Accepted on January 2, 2007

Release of TNF{alpha} during stent implantation into saphenous vein aortocoronary bypass grafts and its relation to plaque extrusion and restenosis

Dirk Böse1, Kirsten Leineweber2, Thomas Konorza1, Andreas Zahn3, Martina Bröcker-Preuss4, Klaus Mann5, Michael Haude6, Raimund Erbel6, and Gerd Heusch3*

1 Cardiology, University of Essen, Essen, Germany
2 Pathophysiology, University of Essen, Essen, Germany
3 Essen, Germany; Pathophysiology, University of Essen, Essen, Germany
4 Clinical Chemistry, University of Essen, Essen, Germany
5 Essen, Germany; Clinical Chemistry, University of Essen, Essen, Germany
6 Cardiology, University of Essen, Essen, Germany; Essen, Germany

* To whom correspondence should be addressed. E-mail: gerd.heusch{at}uk-essen.de.

The reduction in plaque volume during stent implantation is associated with the release of particulate debris and plaque-derived soluble substances. We studied the potential release of the pro-inflammatory cytokine tumor necrosis factor-{alpha} (TNF{alpha}) into the coronary circulation and whether such release is related to the reduction in plaque volume and possibly a predictor for restenosis. In eighteen male patients (=24 stents) with a severe stenosis in their saphenous vein aortocoronary bypass graft (SVG) we used a distal balloon occlusion/aspiration device during stenting. The aspirate TNF{alpha} levels were determined before and after stenting and related to the angiographic and intravascular ultrasound-assessed severity of stenosis and to restenosis. We found that TNF{alpha} is indeed released into the aspirate of stented SVG (TNF{alpha} in pg/ml, before: 9±1 vs. after stenting: 28±3; with p<0.0001) and that such release is related to the reduction in plaque volume (r=0.88, p<0.0001) and associated with restenosis after five months (r=0.71, p=0.001). The periprocedural release of plaque-derived TNF{alpha} possibly represents the amount and activity of the atherosclerotic process and might be a predictor for restenosis.




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