Letters to the Editor |
From the Methodist Hospital Research Institute, Houston, Tex.
Correspondence to Juan F. Granada, Methodist Hospital Research Institute, 6565 Fannin B563, Houston, TX 77584. E-mail jgranada@tmh.tmc.edu
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
We appreciate the interest of Dr Virmani and her colleagues in our article. The study of vulnerable plaque remains controversial and is thus open to dynamic and creative insights. We hoped that our paper would be provocative and initiate some discussion in that regard.
As Dr Virmani implies, the argument concerning the adequacy of currently available animal models of atherosclerosis will likely never be settled. As we point out in our discussion, we do not contest the biological limitations of animal models of atherosclerosis. However, if research on vulnerable plaque is to proceed, some animal models will be needed; we firmly believe that the one we have used in our study is the first step toward the development of this goal. We also recognize the different utility of various models; perhaps there will never be a single perfect model for all atherosclerosis research needs. The model remains a work in progress, and we continually strive to improve and advance the model itself as well as the techniques used to evaluate it. We agree that the model used in this study included young pigs (12 weeks old) displaying early stage fibro-proliferative lesions that are still not representative of complex human atherosclerosis. Longer-term studies in our atherosclerotic model are currently being conducted and use several noninvasive imaging techniques that will help evaluate the natural evolution of these lesions. We are learning to improve our histological techniques and are glad to clarify that by protocol, all lesions found after endovascular imaging undergo frozen
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