Abstract
The classical paradigm regarding the mechanism of restenosis after successful coronary intervention has been one of neointimal thickening from the migration, proliferation and extracellular matrix production by smooth muscle cells [1–5]. More recently this paradigm has been challenged by both experimental and human intravascular ultrasound studies which suggest that restenosis is also partly due to unfavourable vascular remodeling and vascular shrinkage as well as neointimal hyperplasia [6–8]. The mechanisms involved in this are also unclear but are thought to involve a combination of vessel wall fibrosis (particularly of the adventitia) in response to deep wall injury, apoptosis (programmed cell death), qualitative and antitative changes in the extracellular matrix and changes in local flow ynamics [9–11]. How we may influence this process also remains completely unknown. Two recent multicenter studies using intracoronary stenting however suggest that the mechanical scaffolding properties of coronary stenting may play a role in this. The STRESS study comprised 407 patients with stable angina randomised to coronary stent implantation using the Palmas-Schatz stent or balloon angioplasty [12]. Quantitative coronary angiographic analysis indicated that following coronary intervention the minimal luminal diameter (MLD) was significantly greater in the stent group than in the balloon angioplasty group (stent; 2.49 ±0.43mm versus balloon angioplasty; 1.99 ±0.47mm, p<.001). This favourable effect continued up to the 6 month follow-up (stent; 1.74 ±0.60mm versus balloon angioplasty; 1.56 ±0.65mm, p<.01).
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Ozaki, Y., Violaris, A.G., Maekawa, M., Kobayashi, T., Serruys, P.W. (1997). Stent: A Mechanical Approach for Remodeling Inhibition. 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_24
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