Abstract
Luminal narrowing in atherosclerosis and the loss of lumen caliber following angioplasty have commonly been attributed to lumen encroachment by intimai growth. This hypothesis has been called into question by the recent observation that lumen narrowing in both atherosclerosis (1,2) and after angioplasty (3) correlates poorly with intimal mass. In the case of restenosis a multitude of drugs that effectively inhibit intimai hyperplasia in animal models of arterial injury (4,5) have consistently failed to prevent restenosis in costly clinical trials (6–8). These failures could be due to: 1) species differences in the regulation of smooth muscle cell growth (9,10); 2) inadequate experimental modeling of advanced human atherosclerosis and as a consequence a poor understanding of the contribution of a pre-existing lesion to the injury response (11); or 3) the intimal hyperplasia hypothesis equating intimal growth with lumen narrowing may simply be wrong (3, 12, 13).
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References
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Geary, R.L., Schwartz, S.M. (1997). Intimal Hyperplasia is the Wrong Target: Restenosis as a Failure of Remodeling. In: Lafont, A., Topol, E.J. (eds) Arterial Remodeling: A Critical Factor in Restenosis. Developments in Cardiovascular Medicine, vol 198. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-6079-1_11
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