Circulation, Vol 90, 2956-2963, Copyright © 1994 by American Heart Association
TA Fischell, BK Kharma, DR Fischell, PG Loges, CW Coffey 2nd, DM Duggan and AJ Naftilan
BACKGROUND: Restenosis after catheter-based revascularization has been
demonstrated to be primarily caused by medial and/or intimal smooth muscle
cell (SMC) proliferation. The objective of this study was investigate the
ability of local emission of beta-particles from a 32P- impregnated
titanium "stent" wire source to inhibit vascular SMC and endothelial cell
proliferation in cell culture and to determine the dose-response
characteristics of this inhibition. METHODS AND RESULTS: A series of
experiments were performed using 0.20-mm-diameter titanium wires that were
impregnated with varying low concentrations of 32P (activity range, 0.002
to 0.06 microCi/cm wire, n = 47) or 31P (nonradioactive control, n = 28) in
cultures of rat and human aortic SMCs and in cultured bovine aortic
endothelial cells. The zone of complete cell growth inhibition (in
millimeters from stent wire) was measured using light microscopy in the
cultures exposed to the radioactive (32P) or control (31P) wires at 6 and
12 days after plating. In both rat and human SMC cultures there was a
distinct 5.5- to 10.6-mm zone of complete SMC inhibition at wire activity
levels > or = 0.006 microCi/cm. In contrast, there was no zone of
inhibition surrounding the control (31P impregnated) wires (P < .001
versus 32P wires at all wire activities > or = 0.006 microCi/cm for
human and rat SMCs). Proliferating bovine endothelial cells were more
radioresistant than SMCs, with no zone of inhibition observed at wire
activity levels up to 0.019 microCi/cm (P < .001 versus SMCs at 0.006
microCi/cm and 0.019 microCi/cm). CONCLUSIONS: We conclude that very low
doses of beta- particle emission from a 32P-impregnated stent wire
(activity levels as low as 0.006 microCi/cm of wire) completely inhibit the
growth and migration of both rat and human SMCs within a range of 5.5 to
10.6 mm from the wire. Endothelial cells appear to be much more
radioresistant than SMCs. These data suggest that an intra-arterial stent
impregnated with a low concentration of 32P may have a salutary effect on
the restenosis process. Whether this approach can be used successfully and
safely to inhibit restenosis in vivo and in the clinical setting is under
investigation.
ARTICLES
Low-dose, beta-particle emission from 'stent' wire results in complete, localized inhibition of smooth muscle cell proliferation
Division of Cardiology, Vanderbilt University School of Medicine, Nashville, TN 37232-2170.
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