17β-Estradiol and Restenosis: A Novel Vaso-Protective Role for Estrogen?

Baskaran Chandrasekar, MD

Disclosures

J Invasive Cardiol. 2004;16(12) 

In This Article

Abstract and Introduction

Restenosis is the major limitation of percutaneous transluminal coronary angioplasty. Several therapies to prevent restenosis, pharmacological and non-pharmacological, have shown favorable results in experiments, and a few in clinical trials. Evidence is accumulating that 17β-estradiol, the predominant circulating form of estrogen in premenopausal women, inhibits neointimal formation following arterial injury. Evidence demonstrating the ability of estrogen to suppress neointimal formation and underlying mechanisms are reviewed.

The possible role of estrogen in coronary artery disease (CAD) has been extensively studied. Prospective randomized clinical trials have not substantiated a beneficial role for estrogen in CAD. The Heart and Estrogen/Progestin Study follow-up (HERS II) did not demonstrate a reduced risk of CAD after 6.8 years of hormone replacement therapy.[1] The Women's Health Initiative (WHI) trial has concluded that overall health risks exceeded benefits with the use of hormone replacement therapy for a mean treatment period of 5.2 years.[2] There is no longer any support for systemic estrogens in CAD in clinical practice. The only remaining area of interest, therefore, is local delivery.

The vaso-protective effect of estrogen reaches beyond its effects on plasma lipids and atherosclerosis. Estrogen exerts a marked effect on the vascular endothelium, smooth muscle cells (SMC), and other components involved in tissue repair following arterial injury.

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