Reduced incidence of clinical restenosis with newer generation stents, stent oversizing, and high‐pressure deployment: Single‐operator experience

Manolis, Antonis S.

doi:10.1002/clc.4960240205

Cited by 9 publications

(6 citation statements)

References 29 publications

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“…38,39 Results to date, including those of the current study, do not indicate that the CETP TaqIB polymorphism is a pertinent factor in this regard. However, if the response to statin therapy is affected by the TaqIB genotype, TaqIB could be important in predicting which patients are likely to benefit from therapy with this drug class.…”

Section: Resultscontrasting

confidence: 72%

Lack of Association Between the Cholesteryl Ester Transfer Protein Gene—TaqIB Polymorphism and Coronary Restenosis Following Percutaneous Transluminal Coronary Angioplasty and Stenting: A Pilot Study

et al. 2009

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Section: Resultscontrasting

confidence: 72%

Lack of Association Between the Cholesteryl Ester Transfer Protein Gene—TaqIB Polymorphism and Coronary Restenosis Following Percutaneous Transluminal Coronary Angioplasty and Stenting: A Pilot Study

et al. 2009

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“…To evaluate the impact of stent overdilation on wall mechanics and intimal hyperplasia, our experimental study was designed to mimic the clinical practice of high-pressure deployment to obtain a sufficiently large lumen and avoid restenosis. [20][21][22] We purposefully overdilated the stents by 130% after initial deployment, using 2 successive balloon inflations. However, the fact that we implanted stents in normal arteries is a limitation of our study.…”

Section: Discussionmentioning

confidence: 99%

Wall Mechanics of the Stented Rabbit Aorta: Long-Term Study and Correlation with Histological Findings

et al. 2003

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“…[1][2][3][4][5][6][7] On the basis of these risk factors, patients enrolled in both nonrandomized studies and clinical trials have been classified as having a high, intermediate, or low risk of restenosis. Therefore, the binary restenosis rates (Ͼ50% diameter stenosis angiographically) and major adverse cardiac event (MACE) rates in human studies vary greatly depending on the overall risk profile of patients enrolled in these studies.…”

Section: Human Studiesmentioning

confidence: 99%

Coated Stents for the Prevention of Restenosis: Part II

2002

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T his is the second part of a 2-part article that reviews the literature on coated stents and their effects on in-stent restenosis after percutaneous coronary intervention (PCI). Part I of this review discussed the pathophysiology of in-stent restenosis, specific stent coatings, and animal studies investigating coated stents. Part II discusses nonrandomized studies and clinical trials in humans. Studies in humans have examined stents coated with biocompatible materials and drug-eluting stents. Complications and controversies associated with this new technology are also addressed. Human StudiesThe risk of developing in-stent restenosis is related to a variety of factors, both clinical and procedural. [1][2][3][4][5][6][7] On the basis of these risk factors, patients enrolled in both nonrandomized studies and clinical trials have been classified as having a high, intermediate, or low risk of restenosis. Therefore, the binary restenosis rates (Ͼ50% diameter stenosis angiographically) and major adverse cardiac event (MACE) rates in human studies vary greatly depending on the overall risk profile of patients enrolled in these studies. Non-Randomized Studies Stents Coated with Biocompatible MaterialsThe biocompatibility of stents coated with several materials, including carbon, gold, silicon carbide, and phosphorylcholine, has been investigated in humans. The Carbostent (Sorin Biomedica Cardio) is a metal stent coated with a carbon film that is thought to be less thrombogenic than uncoated steel stents. 8 Antoniucci et al 9 investigated the long-term biocompatibility of the Carbostent in a group of 112 patients with an intermediate risk of developing restenosis. Six-month follow-up revealed low MACE and restenosis rates of 12% and 11%, respectively. A second study in another group of 112 patients at high risk for restenosis resulted in a MACE rate of 20% and a binary restenosis rate of 25% by 6 months. 10 These results suggest that the Carbostent is well tolerated in vivo and possibly inhibits neointimal hyperplasia, especially in high-risk patients (Table 1).Gold has been touted as a biocompatible material and has been thought to be ideal for coating coronary stents because of its radio-opaque properties. 1 Two studies evaluating the biocompatibility of gold-coated stents suggested equivalency with uncoated steel stents. 11,12 However, two other studies concluded that these stents may increase neointimal hyperplasia compared with uncoated stents, although patients at a higher risk for restenosis were enrolled. 13,14 Follow-up angiography at 6 months demonstrated a relatively high lumen late loss (postintervention minimum luminal diameter minus the minimum luminal diameter at follow-up) and diameter stenosis in both studies (Table 1). Overall, there have been conflicting results in observational studies examining goldcoated stents, and the restenosis rates seem to be no better than those obtained with uncoated steel stents.Silicon carbide is an inert semiconductor that can be coated onto prosthetic surfaces and has be...

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Reduced incidence of clinical restenosis with newer generation stents, stent oversizing, and high‐pressure deployment: Single‐operator experience

Cited by 9 publications

References 29 publications

Lack of Association Between the Cholesteryl Ester Transfer Protein Gene—TaqIB Polymorphism and Coronary Restenosis Following Percutaneous Transluminal Coronary Angioplasty and Stenting: A Pilot Study

Lack of Association Between the Cholesteryl Ester Transfer Protein Gene—TaqIB Polymorphism and Coronary Restenosis Following Percutaneous Transluminal Coronary Angioplasty and Stenting: A Pilot Study

Wall Mechanics of the Stented Rabbit Aorta: Long-Term Study and Correlation with Histological Findings

Coated Stents for the Prevention of Restenosis: Part II

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