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Serial Intravascular Ultrasound Evidence for Arterial Remodeling as a Mechanism of Restenosis Following Interventional Coronary Procedures

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Arterial Remodeling: A Critical Factor in Restenosis

Abstract

Restenosis occurs within the first 6 months after 30% to 50% of transcatheter procedures; it remains the major limitation to percutaneous coronary revascularization (1, 2). The restenotic lesion has been thought to be a proliferative lesion in which an exaggeration of the normal reparative processes following angioplasty-induced local vessel trauma leads to proliferation of both cellular and matrix components causing an increased tissue mass and restenosis (3–7). As the understanding of this process has advanced, attempts have been made to attack restenosis by interfering with this cascade. Although the results in animal models have been impressive, pharmacologic trials using anti-proliferative agents in humans have been strikingly ineffective in humans (8).

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Mintz, G.S., Popma, J.J., Pichard, A.D., Kent, K.M., Satler, L.F., Leon, M.B. (1997). Serial Intravascular Ultrasound Evidence for Arterial Remodeling as a Mechanism of Restenosis Following Interventional Coronary Procedures. 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_7

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  • DOI: https://doi.org/10.1007/978-1-4615-6079-1_7

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