© 1998 by European Society of Cardiology
Copyright © 1998, European Society of Cardiology
Endothelin and restenosis
Knoll AG, Preclinical Cardiology, PO Box 210805, 67008 Ludwigshafen, Germany
* Corresponding author. Tel.: +49 (621) 589 2879; Fax: +49 (621) 589 3551; E-mail: michael.kirchengast@knoll-ag.de
Received 17 March 1998; accepted 24 April 1998
KEYWORDS Coronary angioplasty; Endothelin; Restenosis; Smooth muscle cell proliferation; Extracellular matrix
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1 Introduction |
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Percutaneous transluminal angioplasty (PTCA) was first introduced into the therapy of patients with coronary artery stenosis in the late seventies [1]. In the two decades since, this method has become standard therapy for patients suffering from all forms of coronary artery disease. The success rate of the procedure itself has increased from 61 percent in the late seventies to well over 90 percent from the mid-eighties onwards [2]. However, long-term success of PTCA remains limited by late restenosis caused by vessel wall proliferation that occurs in 20 to 40 percent of all patients to such an extent that a second PTCA is necessary [2]. As in the mid-90s about 500,000 primary PTCA procedures were carried out in the USA [3]and about 200,000 in Europe [4], this accounts for more than 230,000 patients per year eligible for a second invasive procedure due to recurrent angina. A
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2 Mechanisms of restenosis |
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3 Endothelin in restenosis |
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4 Endothelin antagonism in experimental restenosis |
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5 Conclusions and future directions |
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