European Journal of Vascular and Endovascular Surgery

2007

DOI: 10.1016/j.ejvs.2006.10.021

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Intimal Neovascularisation is a Prominent Feature of Atherosclerotic Plaques in Diabetic Patients with Critical Limb Ischaemia

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Neill J. Turner

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et al.

Abstract: Diabetic patients with critical limb ischaemia requiring amputation demonstrate a greater degree of plaque intimal neovascularisation and inflammatory infiltrate compared to their non-diabetic counterparts. This may explain the greater plaque instability and subsequent cardiovascular complications seen in these patients.

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Clinical Stem Cell Studies In Peripheral Vascular Disease1

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Cited by 16 publications

(7 citation statements)

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“…3, 13 To our knowledge, this is the first demonstration of a significant association of genetic variation specifically with extent of the atherosclerotic disease that develops among patients with DM, where atherosclerosis has been known to display a distinctively aggressive phenotype. 20-22 …”

Section: Discussionmentioning

confidence: 99%

Peroxisome Proliferator-Activated Receptor Pathway Gene Polymorphism Associated With Extent of Coronary Artery Disease in Patients With Type 2 Diabetes in the Bypass Angioplasty Revascularization Investigation 2 Diabetes Trial

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et al. 2011

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Background Coronary artery disease (CAD) is the major cause of death in patients with type 2 diabetes (DM). While demographic and clinical factors associated with extent of CAD in patients with DM have been described, genetic factors have not. We hypothesized that genetic variation in peroxisome proliferator-activated receptor (PPAR)-pathway genes, important in DM and atherosclerosis, would be associated with extent of CAD in patients with DM. Methods and Results 1,043 patients (702 Caucasian; 175 African-Americans) from the Bypass Angioplasty Revascularization Investigation 2 Diabetes (BARI 2D) genetic cohort were genotyped for 3,351 variants in 223 PPAR-pathway genes using a custom targeted-genotyping array. Angiographic endpoints were determined by a core laboratory. In Caucasians, a single variant (rs1503298) in TLL1 was significantly (p = 5.5 × 10−6) associated with extent of CAD, defined as number of lesions with % diameter stenosis (DS) ≥ 20%, after stringent Bonferroni correction for all 3,351 SNPs. This association was validated in the diabetic subgroups of two independent cohorts, the TRIUMPH post-myocardial infarction registry and the prospective Family Heart Study of individuals at risk for CAD. rs1503298 was also significantly associated with extent of severe CAD (≥ 70% DS; p = 3.7 × 10−2) and myocardial jeopardy index (p = 8.7 × 10−4). In general linear regression modeling, rs1503298 explained more variance of extent of CAD than the previously determined clinical factors. Conclusions We identified a variant in one PPAR-pathway gene, TLL1, that is associated with the extent of CAD, independent of clinical predictors, specifically in patients with type 2 DM and CAD.

“…3, 13 To our knowledge, this is the first demonstration of a significant association of genetic variation specifically with extent of the atherosclerotic disease that develops among patients with DM, where atherosclerosis has been known to display a distinctively aggressive phenotype. 20-22 …”

Section: Discussionmentioning

confidence: 99%

Peroxisome Proliferator-Activated Receptor Pathway Gene Polymorphism Associated With Extent of Coronary Artery Disease in Patients With Type 2 Diabetes in the Bypass Angioplasty Revascularization Investigation 2 Diabetes Trial

¹

,

²

,

³

et al. 2011

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Background Coronary artery disease (CAD) is the major cause of death in patients with type 2 diabetes (DM). While demographic and clinical factors associated with extent of CAD in patients with DM have been described, genetic factors have not. We hypothesized that genetic variation in peroxisome proliferator-activated receptor (PPAR)-pathway genes, important in DM and atherosclerosis, would be associated with extent of CAD in patients with DM. Methods and Results 1,043 patients (702 Caucasian; 175 African-Americans) from the Bypass Angioplasty Revascularization Investigation 2 Diabetes (BARI 2D) genetic cohort were genotyped for 3,351 variants in 223 PPAR-pathway genes using a custom targeted-genotyping array. Angiographic endpoints were determined by a core laboratory. In Caucasians, a single variant (rs1503298) in TLL1 was significantly (p = 5.5 × 10−6) associated with extent of CAD, defined as number of lesions with % diameter stenosis (DS) ≥ 20%, after stringent Bonferroni correction for all 3,351 SNPs. This association was validated in the diabetic subgroups of two independent cohorts, the TRIUMPH post-myocardial infarction registry and the prospective Family Heart Study of individuals at risk for CAD. rs1503298 was also significantly associated with extent of severe CAD (≥ 70% DS; p = 3.7 × 10−2) and myocardial jeopardy index (p = 8.7 × 10−4). In general linear regression modeling, rs1503298 explained more variance of extent of CAD than the previously determined clinical factors. Conclusions We identified a variant in one PPAR-pathway gene, TLL1, that is associated with the extent of CAD, independent of clinical predictors, specifically in patients with type 2 DM and CAD.

“…142 Additionally, patients with diabetes mellitus can exhibit several-fold-greater intimal plaque neovascularization by histology and microscopy, a process that has previously been associated with greater plaque instability and cardiovascular events. 143 Despite these challenges, therapeutic benefit can be derived using autologous strategies. 144,145 Reversal of risk factors and modulation of cellular microenvironments, for example, through smoking cessation or use of hyperoxygenation, can overcome intrinsic deficiencies of autologous EPCs.…”

Section: Clinical Stem Cell Studies In Peripheral Vascular Diseasementioning

confidence: 99%

Cell Therapy of Peripheral Arterial Disease

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2013

Circulation Research

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The age-adjusted prevalence of peripheral arterial disease in the US population was estimated to approach 12% in 1985, and as the population ages, the overall population having peripheral arterial disease is predicted to rise. The clinical consequences of occlusive peripheral arterial disease include intermittent claudication, that is, pain with walking, and critical limb ischemia (CLI), which includes pain at rest and loss of tissue integrity in the distal limbs, which may ultimately lead to amputation of a portion of the lower extremity. The risk factors for CLI are similar to those linked to coronary artery disease and include advanced age, smoking, diabetes mellitus, hyperlipidemia, and hypertension. The worldwide incidence of CLI was estimated to be 500 to 1000 cases per million people per year in 1991. The prognosis is poor for CLI subjects with advanced limb disease. One study of >400 such subjects in the United Kingdom found that 25% required amputation and 20% (including some subjects who had required amputation) died within 1 year. In the United States, ≈280 lower-limb amputations for ischemic disease are performed per million people each year. The first objective in treating CLI is to increase blood circulation to the affected limb. Theoretically, increased blood flow could be achieved by increasing the number of vessels that supply the ischemic tissue with blood. The use of pharmacological agents to induce new blood vessel growth for the treatment or prevention of pathological clinical conditions has been called therapeutic angiogenesis. Since the identification of the endothelial progenitor cell in 1997 by Asahara and Isner, the field of cell-based therapies for peripheral arterial disease has been in a state of continuous evolution. Here, we review the current state of that field.

“…9 This angiopathy may also occur in plaque tissue, resulting in the proliferation of immature and fragile intraplaque vessels. 7 Studies addressing this issue are scarce, 10,11 however, and no studies have focused on plaque shoulder vascularization in diabetes and its associations with inflammation and vascular endothelial growth factor (VEGF) and its receptor (VEGFR-2).…”

mentioning

confidence: 99%

Increased vascularization of shoulder regions of carotid atherosclerotic plaques from patients with diabetes

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et al. 2011

Journal of Vascular Surgery

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Diabetes was associated with increased vascularization of the shoulder regions in patients with symptomatic carotid atherosclerotic plaques. This was accompanied by increased expression of VEGFR-2. The increased vascularization of the plaque shoulder regions may help explain why patients with diabetes are at increased risk of atherosclerotic complications.

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