Mechanisms and prevention of restenosis after coronary angioplasty

The success of PTCA is limited by late restenosis, which occurs in 30-50% of all cases, chiefly within the first six months after the intervention. Restenosis is due to the proliferation of smooth muscle cells and especially to overproduction of extracellular matrix in the arterial wall. The coronar...

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Bibliographic Details
Published inSchweizerische medizinische Wochenschrift Vol. 128; no. 13; p. 497
Main Authors Drechsel, S, Bertel, O, Lafont, A
Format Journal Article
LanguageGerman
Published Switzerland 28.03.1998
Subjects
Angioplasty, Balloon, Coronary - methods
Angiotensin-Converting Enzyme Inhibitors - administration & dosage
Animals
Anticoagulants - administration & dosage
Coronary Disease - pathology
Coronary Disease - prevention & control
Coronary Vessels - pathology
Endothelium, Vascular - pathology
Estrogens - administration & dosage
Extracellular Matrix - pathology
Humans
Premedication
Recurrence
Stents
Steroids - administration & dosage
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Summary:The success of PTCA is limited by late restenosis, which occurs in 30-50% of all cases, chiefly within the first six months after the intervention. Restenosis is due to the proliferation of smooth muscle cells and especially to overproduction of extracellular matrix in the arterial wall. The coronary intervention is followed by a not fully defined constrictive process of wound healing, so-called remodeling. Various alternative intervention techniques were investigated but did not show any clear advantage concerning restenosis compared to PTCA. Although the rate of restenosis is reduced by stent implantation, which hinders remodeling, the remaining intimal hyperplasia often leads to restenosis. In spite of promising results in animal models, to date no effective human pharmacological therapy has been found to prevent restenosis. To determine whether antioxidants, endovascular radiation or gene therapy show any benefit will require further, larger trials.
ISSN:0036-7672