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Even in the era of drug eluting stents, in-stent restenosis is likely to remain a significant problem. Restenosis is caused by growth of a neointima, comprised of smooth muscle cells and intercellular matrix. The quantity of neointima is directly proportional to the amount of injury inflicted upon the artery by the stent itself.1 That injury is in the form of either a deep laceration or stretch of the arterial wall. We have previously shown that stretch is ubiquitous after stenting and, even in the absence of deep injury, is an important mediator of neointima formation.2 A few parameters of stent geometry have been shown to have an influence upon neointima formation, including smaller strut number,3 greater strut thickness,4 and increased variation in the angular burden (pointedness) of the stent cross section.5
Therefore, in this study, we aimed to examine the contribution of a wide panel of parameters of stent geometry to the development of neointima in stent sections that displayed stretch but not deep injury.
METHODS
In accordance with UK Home Office regulations, we deployed BiodivYsio stents (3.5 × 15 mm) in 26 coronary arteries of 21 pigs; 17 in the right coronary artery (RCA) and nine in the left anterior descending (LAD). Quantitative coronary angiography identified two …
Footnotes
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Conflict of interest: Dr Gunn has performed paid consultancy work for Abbott Vascular Devices and Biocompatibles (current and previous manufacturers of the BiodivYsio stent). Those companies have also supported several of his research projects.