Remodeling of Human Coronary Arteries Undergoing Coronary Angioplasty or Atherectomy

Kimura, Takeshi; Kaburagi, Satoshi; Tamura, Takashi; Yokoi, Hiroyoshi; Nakagawa, Yoshihisa; Yokoi, Hiroatsu; Hamasaki, Naoya; Nosaka, Hideyuki; Nobuyoshi, Masakiyo; Mintz, Gary S.; Popma, Jeffery J.; Leon, Martin B.

doi:10.1161/01.cir.96.2.475

Cited by 207 publications

(107 citation statements)

References 36 publications

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“…In a study by Nagai et al [5], the incidence of RAO was found to be 5% by evaluation of the radial artery at 95 ± 29 days following the procedure. This short period of follow up equals with the ongoing process of both remodeling and intimal thickening [11,12]. Likewise, chronic phase vascular complications such as diffuse stenosis and loss of forward flow may mimic the same physiopathology of restenosis related to angioplasty [13,14].…”

Section: Discussionmentioning

confidence: 99%

The long-term incidence and predictors of radial artery occlusion following a transradial coronary procedure

et al. 2014

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Section: Discussionmentioning

confidence: 99%

The long-term incidence and predictors of radial artery occlusion following a transradial coronary procedure

et al. 2014

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“…The mean luminal loss observed after DCA by the core laboratory was 0.81 mm, 14,16 which is Ͼ2 times the average after balloon angioplasty. 2,3,14,16 Before intravascular ultrasound (IVUS) studies, which changed our perception of restenosis, [21][22][23] we assumed this renarrowing was due to neointimal hyperplasia. 24 For this reason, the investigation of an agent with antioxidant, antichemotactic, and direct antiproliferative effects seemed ideally suited to an atherectomytreated patient population.…”

Section: Appropriateness Of Dca-treated Patients For This Trialmentioning

confidence: 99%

“…24 For this reason, the investigation of an agent with antioxidant, antichemotactic, and direct antiproliferative effects seemed ideally suited to an atherectomytreated patient population. IVUS studies have since demonstrated that vessel remodelling may account for Ͼ50% of the luminal renarrowing response after DCA, 21,22 which reduces the target for antiproliferative drugs. However, if the report by Côté et al 6 on probucol is correct, the antioxidant effects of carvedilol should have the potential to inhibit vascular remodelling as well as inflammation such that a general reduction of the response to injury could have been reasonably expected.…”

Section: Appropriateness Of Dca-treated Patients For This Trialmentioning

confidence: 99%

Carvedilol for Prevention of Restenosis After Directional Coronary Atherectomy

et al. 2000

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on behalf of the EUROCARE study groupBackground-In addition to its known properties as a competitive, nonselective ␤ and ␣-1 receptor blocker, carvedilol directly inhibits vascular myocyte migration and proliferation and exerts antioxidant effects that are considerably greater than those of vitamin E or probucol. This provides the basis for an evaluation of carvedilol for the prevention of coronary restenosis. Methods and Results-In a prospective, double-blind, randomized, placebo-controlled trial, 25 mg of carvedilol was given twice daily, starting 24 hours before scheduled directional coronary atherectomy and continuing for 5 months after a successful procedure. The primary end point was the minimal luminal diameter as determined during follow-up angiography 26Ϯ2 weeks after the procedure. Of 406 randomized patients, 377 underwent attempted atherectomy, and in 324 (88.9%), a Յ50% diameter stenosis was achieved without the use of a stent. Evaluable follow-up angiography was available in 292 eligible patients (90%). No differences in minimal luminal diameter (1.99Ϯ0.73 mm versus 2.00Ϯ0.74 mm), angiographic restenosis rate (23.4% versus 23.9%), target lesion revascularization (16.2 versus 14.5), or event-free survival (79.2% versus 79.7%) between the placebo and carvedilol groups were observed at 7 months. Conclusions-The maximum recommended daily dose of the antioxidant and ␤-blocker carvedilol failed to reduce restenosis after successful atherectomy. These findings are in contrast to those of the Multivitamins and Probucol Trial, which raises doubts regarding the validity of the interpretation that restenosis reduction by probucol was via antioxidant effects. The relationship between antioxidant agents and restenosis remains to be elucidated. (Circulation.

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“…It has been well established that formation of neointima in vascular diseases is associated with impaired assembly of tropoelastin into insoluble elastin (1)(2)(3)(4)(5)(6) and with extensive degradation of the elastin-rich extracellular matrix by numerous proteinases leaking from the serum and secreted from the infiltrating platelets, leukocytes, and activated vascular cells (7)(8)(9)(10). It has also been suggested that local accumulation of non-assembled tropoelastin and small elastin-derived peptides may constitute an important factor in the activation of the normally quiescent medial SMC 1 into the proliferative and migratory phenotype, which participates in the formation of the occlusive neointima in vascular diseases (2,3,(11)(12)(13)(14)(15).…”

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confidence: 99%

Signaling Pathways Transduced through the Elastin Receptor Facilitate Proliferation of Arterial Smooth Muscle Cells

Mochizuki

Brassart

Hinek

2002

Journal of Biological Chemistry

214

148

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In this report we demonstrate that soluble peptides, elastin degradation products stimulate proliferation of arterial smooth muscle cells. We show that these effects are due to generation of intracellular signals transduced through the cell surface elastin receptor, which consists of peripheral 67-kDa elastin-binding protein (EBP) (spliced variant of ␤-galactosidase), immobilized to the transmembrane sialidase and the protective protein. We found that elastin receptor-transduced signaling triggers activation of G proteins, opening of L-type calcium channels, and a sequential activation of tyrosine kinases: FAK, c-Src, platelet-derived growth factorreceptor kinase and then Ras-Raf-MEK1/2-ERK1/2 phosphorylation cascade. This, in turn, causes an increase in expression of cyclins and cyclin-dependent kinases, and a consequent increase in cellular proliferation. The EBP-transduced signals also induce tyrosine kinase-dependent phosphorylation of ␤-tubulin, LC3, microtubule-associated protein 1, and ␣-actin and troponin-T, which could be linked to reorganization of cytoskeleton. We have also disclosed that induction of these signals can be abolished by anti-EBP antibody or by galactosugars, which cause shedding of EBP from the cell surface. Moreover, elastin-derived peptides did not induce proliferation of EBP-deficient cells derived from patients bearing a nonsense mutation of the ␤-galactosidase gene or sialidase-deficient cells from patients with congenital sialidosis.It has been well established that formation of neointima in vascular diseases is associated with impaired assembly of tropoelastin into insoluble elastin (1-6) and with extensive degradation of the elastin-rich extracellular matrix by numerous proteinases leaking from the serum and secreted from the infiltrating platelets, leukocytes, and activated vascular cells (7-10). It has also been suggested that local accumulation of non-assembled tropoelastin and small elastin-derived peptides may constitute an important factor in the activation of the normally quiescent medial SMC 1 into the proliferative and migratory phenotype, which participates in the formation of the occlusive neointima in vascular diseases (2,3,(11)(12)(13)(14)(15) Elastin does not contain the RGD sequence and does not interact with cell surface integrins. Our previous studies demonstrated that numerous cell types, including vascular myocytes, express the cell surface elastin receptor complex, which consists of three subunits (25,26), and that the average cell contains ϳ2 ϫ 10 6 elastin binding sites with the binding affinity (K d ) of 8 nM (27). We found that two of those subunits (55-and 61-kDa) are anchored to the plasma membrane, whereas the third, a peripheral 67-kDa protein, actually binds elastin (25). This major functional component of the receptor complex was named the elastin binding protein (EBP). The repeat hexapeptide in tropoelastin, VGVAPG, has been identified as a chief ligand for high affinity binding to this cell surface receptor (25-27). It has been later established t...

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Remodeling of Human Coronary Arteries Undergoing Coronary Angioplasty or Atherectomy

Cited by 207 publications

References 36 publications

The long-term incidence and predictors of radial artery occlusion following a transradial coronary procedure

The long-term incidence and predictors of radial artery occlusion following a transradial coronary procedure

Carvedilol for Prevention of Restenosis After Directional Coronary Atherectomy

Signaling Pathways Transduced through the Elastin Receptor Facilitate Proliferation of Arterial Smooth Muscle Cells

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