Editorial
Stent magic! The genie has escaped from the bottle
| The first 150 words of the full text of this article appear below. |
A response to injury leading to intimal thickening and subsequent "restenosis" has limited the clinical efficiency of percutaneous coronary interventions ever since they have been used to treat symptomatic coronary artery disease. During the recent two decades a lot has been learned about the pathophysiology of the response to injury following different kinds of interventions. The predominant mechanism is activation of cells within the arterial wall, the adventitial layer, and the blood, namely arterial smooth muscle cells, fibroblasts, endothelial cells, monocytes, lymphocytes, and leucocytes. Once activated by arterial injury, most of these cells will undergo a change of phenotype and express a variety of growth factors and hormones leading to complex interactions, which result in cellular migration and proliferation. As a result, much research has focused on modulation or inhibition of cell proliferation and, although some compounds were effective in animal models, they were not successful in human restenosis trials.
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