Clinical and Angiographic Factors Associated With Asymptomatic Restenosis After Percutaneous Coronary Intervention

Ruygrok, Peter; Webster, Mark; Valk, Vincent de; Es, Gerrit‐Anne van; Ormiston, John A.; Morel, Marie‐Angèle; Serruys, Patrick W.

doi:10.1161/hc4401.098294

Cited by 70 publications

(46 citation statements)

References 34 publications

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“…In addition, quartiles of CRP concentrations were not associated with a consistent increase in ISR rates. Considering the fact that, in general, the clinically driven target revascularization rate is often ϳ50% of the angiographic ISR rate (22 ), a lack of association between CRP values and TLR was not unexpected in our study. In contrast to TLR, there was a trend toward a higher incidence of nonfatal myocardial infarction in patients with CRP concentration Ͼ3 mg/L, which is in accordance with previous reports (23 -25 ).…”

Section: Discussionmentioning

confidence: 47%

Preprocedural C-Reactive Protein Is Not Associated with Angiographic Restenosis or Target Lesion Revascularization after Coronary Artery Stent Placement

Rittersma¹,

Winter²,

Koch³

et al. 2004

Clinical Chemistry

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Section: Discussionmentioning

confidence: 47%

Preprocedural C-Reactive Protein Is Not Associated with Angiographic Restenosis or Target Lesion Revascularization after Coronary Artery Stent Placement

Rittersma¹,

Winter²,

Koch³

et al. 2004

Clinical Chemistry

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“…(3) The appreciation that a considerable atherosclerosis burden, including plaques vulnerable to rupture or susceptible to erosion, can be accommodated in the vessel wall without impingement on the lumen has lead to a new imperative for direct plaque imaging. (4) In fact, 4-16% of patients suffer from "silent" lesions that do not restrict blood flow but are still vulnerable to rupture (5).…”

Section: Introductionmentioning

confidence: 99%

Development of Contrast Agents Targeted to Macrophage Scavenger Receptors for MRI of Vascular Inflammation

2006

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Atherosclerosis is a leading cause of death in the U.S. Because there is a potential to prevent coronary and arterial diseases through early diagnosis, there is a need for methods to image arteries in the subclinical stage as well as clinical stage using various non-invasive techniques, including Magnetic Resonance Imaging (MRI). We describe a development of a novel MRI contrast agent targeted to plaques that will allow imaging of lesion formation. The contrast agent is directed to macrophages, one of the earliest components of developing plaques. Macrophages are labeled through the macrophage scavenger receptor A, a macrophage specific cell surface protein, using an MRI contrast agent derived from scavenger receptor ligands. We have synthesized and characterized these contrast agents with a range of relaxivities. In vitro studies show that the targeted contrast agent accumulates in macrophages and solution studies indicate that micromolar concentrations are sufficient to produce contrast in an MR image. Cell toxicity and initial biodistribution studies indicate low toxicity, no detectable retention in normal blood vessels, and rapid clearance from blood. The promising performance of this contrast agent targeted towards vascular inflammation opens doors to tracking of other inflammatory diseases such as tumor immunotherapy and transplant acceptance using MRI.

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“…1,2 This can result in renarrowing of the target vessel, which is termed restenosis and limits therapeutic revascularization. 3 Initial endothelial denudation leads to an exposure of subendothelial matrix, which precipitates the adhesion of activated platelets and fibrin deposition, supporting the inflammatory recruitment of leukocytes. 4 The progress of neointimal hyperplasia is attributable to the accumulation of dedifferentiated smooth muscle cells (SMCs), which by far constitute the majority of neointimal cells.…”

mentioning

confidence: 99%

Expression of HIF-1α in Injured Arteries Controls SDF-1α–Mediated Neointima Formation in Apolipoprotein E–Deficient Mice

Karshovska

Zernecke

Sevilmis

et al. 2007

ATVB

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Objective-Hypoxia-inducible factor (HIF)-1␣ is the regulatory subunit of a transcriptional complex, which controls the recruitment of multipotent progenitor cells and tissue repair in ischemic tissue by inducing stromal cell-derived factor (SDF)-1␣ expression. Because HIF-1␣ can be activated under normoxic conditions in smooth muscle cells (SMCs) by platelet products, we investigated the role of HIF-1␣ in SDF-1␣-mediated neointima formation after vascular injury. Methods and Results-Wire-induced injury of the left carotid artery was performed in apolipoprotein E-deficient mice.HIF-1␣ expression was increased in the media as early as 1 day after injury, predominantly in SMCs. Nuclear translocation of HIF-1␣ and colocalization with SDF-1␣ was detected in neointimal cells after 2 weeks. HIF-1␣ mRNA expression was induced at 6 hours after injury as determined by real-time RT-PCR. Inhibition of HIF-1␣ expression by local application of HIF-1␣-siRNA reduced the neointimal area by 49% and significantly decreased the neointimal SMCs content compared with control-siRNA. HIF-1␣ and SDF-1␣ expression were clearly diminished in neointimal cells of HIF-1␣-siRNA treated arteries. Key Words: atherosclerosis Ⅲ restenosis Ⅲ vascular biology Ⅲ chemokines Ⅲ progenitor cells Ⅲ smooth muscle cells N eointima formation and inward remodeling are the basic mechanisms of the vascular response to mechanical injury, eg, by balloon angioplasty or stent implantation in obstructive coronary artery disease. 1,2 This can result in renarrowing of the target vessel, which is termed restenosis and limits therapeutic revascularization. 3 Initial endothelial denudation leads to an exposure of subendothelial matrix, which precipitates the adhesion of activated platelets and fibrin deposition, supporting the inflammatory recruitment of leukocytes. 4 The progress of neointimal hyperplasia is attributable to the accumulation of dedifferentiated smooth muscle cells (SMCs), which by far constitute the majority of neointimal cells. 5 The traditional idea of neointima formation focused on the concept that neointimal SMCs originate from medial cells within the vessel wall, which migrate into the intima and start to proliferate. 5,6 In recent years, evidence has accumulated that bone marrow-derived vascular progenitor cells participate significantly to neointima formation after selective recruitment to the injury site, thereby directing the vascular wound healing. 7 Smooth muscle progenitor cells (SPCs) have been detected in the peripheral blood of humans 8 and appear to be the critical vascular stem cell subtype for vascular repair after mechanical injury. Neointimal lesions after endothelial denudation consist of approximately 50% to 60% bone marrow-derived SMCs. 7 Among the multiple chemokines directing vascular cell trafficking, the CXC chemokine stromal cell-derived factor (SDF)-1␣ and its receptor CXCR4 represent an important molecular signaling axis for the mobilization and recruitment of SPCs. 9,10 In a "remote control" function, upregulation of SDF...

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Clinical and Angiographic Factors Associated With Asymptomatic Restenosis After Percutaneous Coronary Intervention

Cited by 70 publications

References 34 publications

Preprocedural C-Reactive Protein Is Not Associated with Angiographic Restenosis or Target Lesion Revascularization after Coronary Artery Stent Placement

Preprocedural C-Reactive Protein Is Not Associated with Angiographic Restenosis or Target Lesion Revascularization after Coronary Artery Stent Placement

Development of Contrast Agents Targeted to Macrophage Scavenger Receptors for MRI of Vascular Inflammation

Expression of HIF-1α in Injured Arteries Controls SDF-1α–Mediated Neointima Formation in Apolipoprotein E–Deficient Mice

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