Effect of external beam irradiation on neointimal hyperplasia after experimental coronary artery injury
Author + information
- Received July 3, 1991
- Revision received November 4, 1991
- Accepted November 19, 1991
- Published online April 1, 1992.
Author Information
- Robert S. Schwartz, MD, FACC∗,a,b,
- Thomas M. Koval, PhDa,b,
- William D. Edwards, MD, FACCa,b,
- Allan R. Camrud, RNa,b,
- Kent R. Bailey, PhDa,b,
- Kevin Browne, MD, FACCa,b,
- Ronald E. Vlietstra, MB, BCh, FACCa,b and
- David R. Holmes Jr., MD, FACCa,b
- ↵∗Address for reprints: Robert S. Schwartz, MD, Division of Cardiovascular Diseases, Mayo Clinic, 200 First Street SW, Rochester, Minnesota 55905.
Abstract
Human coronary artery restenosis after percutaneous revascularization is a response to mechanical injury. Smooth muscle cell proliferation is a major component of restenosis, resulting in obstructive neointimal hyperplasia. Because ionizing radiation inhibits cellular proliferation, this study tested in a porcine coronary injury model the hypothesis that the hyperplastic response to coronary artery injury would be attenuated by X-irradiation.
Deep arterial injury was produced in 37 porcine left anterior descending coronary artery segments with overexpanded, percutaneously delivered tantalum wire coils. Three groups of pigs were irradiated with 300-kV X-rays after coil injury: Group I (n = 10), 400 cGy at 1 day; Group II (n = 10), 400 cGy at 1 day and 400 cGy at 4 days and Group III (n = 9), 800 cGy at 1 day. Eight pigs in the control group underwent identical injury but received no radiation. Treatment efficacy was histologically assessed by measuring neointimal thickness and percent area stenosis.
Mean neointimal thickness in all irradiated groups was significantly higher than in the control groups and thickness was proportional to X-ray dose.
X-irradiation delivered at these doses and times did not inhibit proliferative neointima. Rather, it accentuated the neointimal response to acute arterial injury and may have potentiated that injury.
Footnotes
☆ This study was supported by grants from USCI, a Division of C. R. Bard Inc., Billerica, Massachusetts, and the J. Holden DeHaan Foundation, Indianapolis, Indiana.
- Received July 3, 1991.
- Revision received November 4, 1991.
- Accepted November 19, 1991.