(Circulation. 1999;99:192-194.)
© 1999 American Heart Association, Inc.
Editorials |
From Andreas Gruentzig Cardiovascular Center, Emory University Hospital, Atlanta, Ga.
Correspondence to Spencer B. King III, MD, Andreas Gruentzig Cardiovascular Center, Emory University Hospital, 1364 Clifton Rd NE, Suite F606, Atlanta, GA 30322.
Key Words: Editorials restenosis angioplasty radioisotopes coronary disease
Na sarandisis" is an ancient Greek admonition, which loosely translated means, "When meeting someone you are attracted to, wait 40 days and 40 nights prior to making the commitment." In the attempt to control restenosis, love at first sight has frequently led to disappointing and expensive outcomes. Endovascular radiation therapy to prevent restenosis has appeared very attractive, and Teirstein et al, in this issue of Circulation,1 have contributed some of the "na sarandisis."
Endovascular radiation therapy has been shown by preclinical evaluation to have an effect not previously seen with other agents. From this experience, we have learned several things regarding the nature of restenosis. Initially we were taught that restenosis was primarily a proliferation of smooth muscle cells creating an endoluminal narrowing. Later it was suggested that a major component of restenosis was "negative remodeling" of the artery. Another paradigm suggested that a space-occupying thrombus was necessary for restenosis to occur and that it was subsequently replaced by in-growth of smooth muscle cells. These concepts all led to different approaches to suppress the restenotic process.
The success of endovascular radiation therapy to control
arterial renarrowing in preclinical models2 3 4 5 6
has strongly supported the concept of restenosis as primarily a
wound-healing phenomenon. Serial experimental observations with animal
models of balloon-overstretch angioplasty and endovascular radiation
therapy failed to show bulky thrombotic lesions, although luminal
platelet and fibrin deposition was common.4
Endoluminal neointima formation was dramatically inhibited,
and the chronic contracture of arteries was suppressed and sometimes
reversed, probably owing to an
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