Restenosis after successful percutaneous transluminal coronary angioplasty is the major clinical problem limiting the long-term efficacy of this treatment for coronary atherosclerosis. Recent advances in the understanding of the biology of restenosis indicate that intimal hyperplasia of smooth muscle cells is the predominant cause for restenosis. Therefore, therapeutic agents that inhibit vascular smooth muscle cell proliferation should be candidate drugs to prevent restenosis. Heparin has documented antiproliferative effects on smooth muscle cells, and the availability of low molecular weight heparins that lack anticoagulant properties makes them ideal agents. Glucocorticoids have wide effects on inflammatory and wound healing events and inhibit smooth muscle cell growth in culture and in animal models of arterial injury. Recent laboratory data suggest that combination therapy with both low molecular weight heparin and hydrocortisone may be a powerful treatment regimen to limit restenosis. © 1991.
Berk, B. C., Gordon, J. B., & Alexander, R. W. (1991). Pharmacologic roles of heparin and glucocorticoids to prevent restenosis after coronary angioplasty. Journal of the American College of Cardiology, 17(6 SUPPL. 2), 111–117. https://doi.org/10.1016/0735-1097(91)90946-7