Remodeling of In-Stent Neointima, Which Became Thinner and Transparent Over 3 Years

Asakura, Masanori; Ueda, Yasunori; Nanto, Shinsuke; Hirayama, Atsushi; Adachi, Takahiro; Kitakaze, Masafumi; Hori, Masatsugu; Kodama, Kazuhisa

doi:10.1161/01.cir.97.20.2003

Cited by 124 publications

(65 citation statements)

References 12 publications

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“…In the previous studies, MLD was shown to improve from 6 months to 3 to 4 years after coronary stenting or balloon coronary angioplasty, 8,9,17 which was confirmed in this study. Fibrotic scar formation associated with maturation of smooth muscle cells and reduction in matrix proteoglycans was suggested as one of the possible mechanisms of late angiographic regression, protecting the TLs from atherosclerotic progression or plaque rupture after both balloon coronary angioplasty and coronary stenting.…”

Section: Discussionsupporting

confidence: 88%

“…Medium-term follow-up studies at 3 to 5 years revealed a paucity of late clinical stent-related problems 4 -8 and even angiographic regression of the stented lesions. 8,9 Recently, Choussat et al 10 reported clinical stability of the stented target site at 8 to 10 years after coronary stenting. However, there is still no long-term angiographic data supporting sustained patency of the stented target site and absence of local complications specific for permanent implantation of metallic prosthesis.…”

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confidence: 99%

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Long-Term Clinical and Angiographic Follow-Up After Coronary Stent Placement in Native Coronary Arteries

et al. 2002

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Background — Although coronary stents have been proved effective in reducing clinical cardiac events for up to 3 to 5 years, longer term clinical and angiographic outcomes have not yet been fully clarified. Methods and Results — To evaluate longer term (7 to 11 years) outcome, clinical and angiographic follow-up information was analyzed in 405 patients with successful stenting in native coronary arteries. Primary or secondary stabilization, which was defined as freedom from death, coronary artery bypass grafting, and target lesion-percutaneous coronary intervention (TL-PCI) during the 14 months after the initial procedure or after the last TL-PCI, was achieved in 373 patients (92%) overall. Only 7 patients (1.7%) underwent TL-PCI more than twice. After the initial 14-month period, freedom from TL-PCI reached a plateau at 84.9% to 80.7% over 1 to 8 years. However, quantitative angiographic analysis in 179 lesions revealed a triphasic luminal response characterized by an early restenosis phase until 6 months, an intermediate-term regression phase from 6 months to 3 years, and a late renarrowing phase beyond 4 years. Minimal luminal diameter in 131 patients with complete serial data were 2.62±0.4 mm immediately after stenting, 2.0±0.49 mm at 6 months, 2.19±0.49 mm at 3 years, and 1.85±0.56 mm beyond 4 years ( P <0.0001). Conclusions — The efficacy and safety of coronary stenting seemed to be clinically sustained at 7 to 11 years of follow-up. However, late luminal renarrowing beyond 4 years was common, which demonstrates the need for further follow-up.

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Section: Discussionsupporting

confidence: 88%

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confidence: 99%

Long-Term Clinical and Angiographic Follow-Up After Coronary Stent Placement in Native Coronary Arteries

et al. 2002

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“…40 Thinning of the in-stent neointima (increased transparency) 3 years after stenting has been visualized by coronary angioscopy. 41 The present study provides pathological insights into these observations of neointimal regression; beyond 18 months, the stent neointima becomes less cellular (potentially via SMC apoptosis) and richer in type I collagen.…”

Section: Neointimal Regressionmentioning

confidence: 67%

Extracellular Matrix Changes in Stented Human Coronary Arteries

et al. 2004

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Background-Restenosis after stenting occurs secondary to the accumulation of smooth muscle cells (SMCs) and extracellular matrix (ECM), with the ECM accounting for Ͼ50% of the neointimal volume. The composition of the in-stent ECM has not been well characterized in humans. Methods and Results-Postmortem human coronary arteries (nϭ45) containing stents underwent histological assessment of neointimal proteoglycans, hyaluronan, collagen (types I and III), SMCs, and CD44 (a cell surface receptor for hyaluronan). The mean duration of stent implantation was 18.7 months; stents in place Ն3 to Ͻ9 months (nϭ17) were assigned to group 1, stents Ն9 to Ͻ18 months old (nϭ19) to group 2, and stents Ն18 months old (nϭ9) to group 3. In groups 1 and 2, neointimal versican and hyaluronan staining was strongly positive, colocalized with ␣-actin-positive SMCs, and was greater in intensity compared with group 3. Conversely, decorin staining was greatest in group 3. The neointima of both group 1 and 2 stents was rich in type III collagen, with reduced staining in group 3. Type I collagen staining was weakest in group 1 stents, with progressively stronger staining in groups 2 and 3. SMC density and stent stenosis were significantly reduced in group 3 stents compared with groups 1 and 2. CD44 staining colocalized with macrophages and was associated with increased neointimal thickness. Conclusions-The ECM within human coronary stents resembles a wound that is not fully healed until 18 months after deployment, followed by neointimal retraction. ECM contraction may be a target for therapies aimed at stent restenosis prevention.

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“…Like angioplasty, stent placement also initially stimulates intimal hyperplasia in animal models and human arteries. Intimal atrophy occurs spontaneously in stented arteries after 6 months in humans (Asakura et al 1998) and 2 months in rats (Finn et al 2002, Langeveld et al 2004. At these late times during regression, the extracellular matrix (ECM) shows a relative loss of versican and a gain of collagen compared to earlier times (Chung et al 2002, Finn et al 2002, Langeveld et al 2004, Farb et al 2004.…”

Section: Versican Metabolism In Intimal Regressionmentioning

confidence: 99%

Versican Degradation and Vascular Disease

Kenagy

Plaas

Wight³

2006

Trends in Cardiovascular Medicine

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Versican is an abundant proteoglycan in the blood vessel wall that is increased after vascular injury and accumulates in advanced atherosclerotic plaques. Versican is a large molecule with domains that mediate binding to cytokines, enzymes, lipoproteins, other extracellular matrix molecules, and signaling receptors. There is evidence that versican exists in the normal, as well as the diseased, vessel wall as discrete fragments, which represent these functional domains. We review the literature on versican degradation in vascular tissue and the function of versican domains, all of which suggest that proteolytic modification of versican may have physiologic as well as pathologic implications for the vascular system.

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Remodeling of In-Stent Neointima, Which Became Thinner and Transparent Over 3 Years

Abstract: The neointima became thick and nontransparent until 6 months and then became thin and transparent by 3 years. We conclude that neointimal remodeling exists after stenting and plays a major role in the alteration of coronary luminal diameter after stenting.

Cited by 124 publications

References 12 publications

Long-Term Clinical and Angiographic Follow-Up After Coronary Stent Placement in Native Coronary Arteries

Long-Term Clinical and Angiographic Follow-Up After Coronary Stent Placement in Native Coronary Arteries

Extracellular Matrix Changes in Stented Human Coronary Arteries

Versican Degradation and Vascular Disease

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