(Circulation. 2000;101:2130.)
© 2000 American Heart Association, Inc.
Editorials |
Prevention of Coronary Restenosis
The Evolving Evidence Base for Radiation Therapy
From the Cardiovascular Divisions of the Brigham and Women’s Hospital (R.E.K.) and the Beth Israel Deaconess Medical Center (D.S.B.) and Harvard Medical School (R.E.K., D.S.B.), Boston, Mass.
Correspondence to Donald S. Baim, MD, Cardiovascular Division, Beth Israel Deaconess Medical Center, East Campus, 330 Brookline Avenue, Boston, MA 02215. E-mail dbaim@bidmc.harvard.edu
Key Words: Editorials • restenosis • radiation • brachytherapy
Restenosis, the time-limited renarrowing of the lumen of a coronary artery, affects 20% to 40% of patients in the months after an initially successful intervention.1 2 As such, it represents the extreme form of the healing response that produces a normally distributed amount of late loss in lumen diameter at all interventional sites.3 To some extent, the percentage of patients who develop renarrowing can be reduced by acutely achieving the largest possible lumen diameter (as by stenting) via the "bigger is better" principle. Stenting can also prevent any late loss caused by vascular contraction,4 although it does not reduce (and, in fact, increases) the amount of late loss due to excessive intimal hyperplasia. To lower the restenosis rate further and to provide durable treatment for in-stent restenosis when it occurs, potent treatments to blunt this late loss are thus required.
Although a number of pharmacological approaches have been tried to limit late loss, only a few have shown even preliminary efficacy. However, radiation therapy seems to provide an interesting, nonpharmacological approach to controlling this excessive response to injury response that is analogous to its role in limiting the growth of many rapidly proliferating neoplasms and non-neoplastic conditions of excessive proliferation (eg, exophthalmos of Grave’s disease or keloid scar formation).
There are some concerns with this hypothesis. First, the number of
proliferating cells in an active restenosis lesion is generally
small, and such cells are virtually absent in a de novo lesion that
might undergo prophylactic radiation at the time of
original
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