(Circulation. 2001;103:1330.)
© 2001 American Heart Association, Inc.
Current Perspectives |
Long-Term Efficacy of Intracoronary Irradiation in Inhibiting In-Stent Restenosis
From the Center for Radiological Research, Columbia University, New York, NY.
Correspondence to David J. Brenner, DSc, Center for Radiological Research, Columbia University, 630 W 168th St, New York, NY 10032. E-mail djb3{at}columbia.edu
Background—Intracoronary irradiation is a promising modality for inhibition of in-stent restenosis. Results of randomized clinical trials at 6 months after gamma ray irradiation are highly encouraging. The first results at 3 years after irradiation, while still showing benefit, have shown significant late loss. The probable mechanism of the radiation is to inactivate (prevent from dividing) most cells that otherwise could proliferate to produce neointimal formation. We measured the proportion of cells that survive with their clonogenic potential intact after the doses and dose rates used in the randomized trials, and we then modeled the subsequent repopulation of the surviving cells that might cause late restenosis.
Methods and
Results—Human aortic smooth muscle cells were
irradiated with gamma rays, including the doses and dose rates used in
current trials, and clonogenic surviving fractions were measured. The
subsequent repopulation of the surviving cells was modeled with the
assumption that the repopulation kinetics were similar to those in
unirradiated cells. The radiation is expected to delay the time to
restenosis by factors of 
6 to 8, depending on the dose, shifting the
delay from a median of 6 months (for no irradiation) to median values
from 36 months (for a nominal 13 Gy) to 43 months (for a nominal 15
Gy).
Conclusions—These results and predictions are quantitatively consistent with clinical results and suggest that clonogenic inactivation (prevention of cellular division) is the dominant mechanism of radiation action in the delay of restenosis. Intracoronary radiotherapy is a very promising modality for significantly delaying, although probably not preventing, in-stent restenosis.
Key Words: radiotherapy • stents • coronary disease • restenosis
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