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Circulation. 1999;100:2366-2372

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(Circulation. 1999;100:2366.)
© 1999 American Heart Association, Inc.


Basic Science Reports

Long-Term Coronary Vascular Response to 32P ß-Particle–Emitting Stents in a Canine Model

Presented at the 71st Scientific Sessions of the American Heart Association, Dallas, Tex, November 11, 1998.

Allen J. Taylor, MD; Patrick D. Gorman, MD; Andrew Farb, MD; Timothy G. Hoopes, MD; Renu Virmani, MD

From the Division of Hematology and Vascular Biology, Walter Reed Army Institute of Research and the Cardiovascular Division, Armed Forces Institute of Pathology, Washington, DC.

Correspondence to Renu Virmani, MD, Chairperson, Cardiovascular Division, Armed Forces Institute of Pathology, 14th Street and Alaska Avenue, NW, Washington, DC 20306. E-mail virmani{at}afip.osd.mil

Background—The arterial placement of 32P ß-particle–emitting stents in various experimental animal models results in discordant effects on neointimal formation. We studied the vascular effects of ß-particle–emitting stents in normal canine coronary arteries because compared with pigs and rabbits, the canine model may more closely mimic the vascular response of humans.

Methods and Results—Thirty stents (control nonradioactive, n=10; low-activity 32P, 3.5 to 6.0 µCi, n=11; high-activity 32P, 6.5 to 14.4 µCi, n=8) were implanted in normal canine coronary arteries through the use of a single balloon inflation at nominal pressure. Histological analysis after 15 weeks included the measurement of neointimal and adventitial area and thickness. Neointimal fibrin area was measured with the use of computer-assisted color segmentation on Movat pentachrome sections. Luminal stenosis was significantly increased in 32P stents compared with control stents (44.6±16.8% versus 32.7±10.8%; P=0.05) and was highest in the high-activity group (45.5±24.3%). No evidence of an "edge effect" was seen in adjacent, nonstented coronary segments. All 32P stents showed incomplete vascular healing as indicated by a dose-dependent increase in fibrin area with increasing stent activity. Arterial radiation resulted in a decrease in adventitial size, which was maximal for high-activity 32P stents, indicating an inhibitory effect on the adventitial response to injury.

Conclusions32P ß-particle–emitting stents have adverse vascular effects at 15 weeks in the canine normal coronary artery model. Vascular brachytherapy with this device causes increased neointimal formation and prominent, dose-dependent lack of healing.


Key Words: stents • radiotherapy • radioisotopes • restenosis • revascularization




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