2004

DOI: 10.1161/01.cir.0000128522.98016.19

|View full text |Cite

|

Sign up to set email alerts

|

Atherosclerotic Vascular Disease Conference

Mark A. Creager¹,

Daniel W. Jones²,

J. Donald Easton³

et al.

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...

Discussion2

Introduction2

Citation Types

Supporting

3

Mentioning

6

Contrasting

0

Year Published

2006

2006

2012

2012

Publication Types

Select...

Article10

Relationship

Self Cite1

Independent9

Authors

Journals

Cited by 48 publications

(9 citation statements)

References 100 publications

Supporting

3

Mentioning

6

Contrasting

0

Order By: Relevance

“…Furthermore, compared with the CAD alone group, the CAD+PAD group: (1) included a lower number of patients without carotid plaques; (2) tended to have a higher prevalence of carotid stenosis ≥ 50%, although the group difference was not statically significant; and (3) showed a greater number of patients with symptomatic plaques. Collectively, these findings support the concept that PAD is a marker of diffuse atherosclerosis, 18 and that its presence entails more severe vascular lesions in other arterial districts. Indeed, previous studies showed that compared to CAD alone patients, those with concomitant PAD had a greater number of coronary stenoses and unstable lesions.…”

Section: Discussionsupporting

confidence: 80%

Prevalence of hypoechoic carotid plaques in coronary artery disease: relationship with coexistent peripheral arterial disease and leukocyte number

¹

,

²

,

³

et al. 2009

View full text Add to dashboard Cite

In coronary artery disease (CAD), a concomitant peripheral arterial disease (PAD) entails a more severe coronary atherosclerosis. We hypothesized that the severity of carotid artery disease is greater in CAD+PAD than in CAD alone. In 90 CAD and 79 CAD+PAD patients, carotid plaque echolucency was measured by gray-scale median (GSM), and the degree of carotid stenosis by routine Doppler criteria. Plaques were absent in 20 (22.2%) CAD and 8 (10.1%) CAD+PAD patients (p = 0.035), while the prevalence of carotid stenosis ≥ 50% was 16.7% and 25.3%, respectively (p = 0.166). The GSM score was 45.1 [21.7-67.7] in CAD+PAD vs 60.1 [44.9-83.1] in CAD alone (p < 0.001). Consistently, hypoechoic plaques (GSM < 25th percentile) were more common in CAD+PAD than in CAD patients (38.0% vs 11.4%, p < 0.001). On multivariate analysis, CAD+PAD was the only variable significantly associated with hypoechoic plaques (OR = 4.16, 95% CI 1.68-10.28). However, when the leukocyte count was added to the model, it showed the strongest association with hypoechoic plaques (OR = 6.70, 95% CI 2.13-21.10). In conclusion, compared with CAD alone patients, those with concomitant PAD showed a greater prevalence of plaques with characteristics of instability. Thus, our data suggest that in CAD+PAD, evaluation of carotid plaque echogenicity could contribute to improve clinical decision-making and differentiate treatments for individual patients.

“…Furthermore, compared with the CAD alone group, the CAD+PAD group: (1) included a lower number of patients without carotid plaques; (2) tended to have a higher prevalence of carotid stenosis ≥ 50%, although the group difference was not statically significant; and (3) showed a greater number of patients with symptomatic plaques. Collectively, these findings support the concept that PAD is a marker of diffuse atherosclerosis, 18 and that its presence entails more severe vascular lesions in other arterial districts. Indeed, previous studies showed that compared to CAD alone patients, those with concomitant PAD had a greater number of coronary stenoses and unstable lesions.…”

Section: Discussionsupporting

confidence: 80%

Prevalence of hypoechoic carotid plaques in coronary artery disease: relationship with coexistent peripheral arterial disease and leukocyte number

¹

,

²

,

³

et al. 2009

View full text Add to dashboard Cite

In coronary artery disease (CAD), a concomitant peripheral arterial disease (PAD) entails a more severe coronary atherosclerosis. We hypothesized that the severity of carotid artery disease is greater in CAD+PAD than in CAD alone. In 90 CAD and 79 CAD+PAD patients, carotid plaque echolucency was measured by gray-scale median (GSM), and the degree of carotid stenosis by routine Doppler criteria. Plaques were absent in 20 (22.2%) CAD and 8 (10.1%) CAD+PAD patients (p = 0.035), while the prevalence of carotid stenosis ≥ 50% was 16.7% and 25.3%, respectively (p = 0.166). The GSM score was 45.1 [21.7-67.7] in CAD+PAD vs 60.1 [44.9-83.1] in CAD alone (p < 0.001). Consistently, hypoechoic plaques (GSM < 25th percentile) were more common in CAD+PAD than in CAD patients (38.0% vs 11.4%, p < 0.001). On multivariate analysis, CAD+PAD was the only variable significantly associated with hypoechoic plaques (OR = 4.16, 95% CI 1.68-10.28). However, when the leukocyte count was added to the model, it showed the strongest association with hypoechoic plaques (OR = 6.70, 95% CI 2.13-21.10). In conclusion, compared with CAD alone patients, those with concomitant PAD showed a greater prevalence of plaques with characteristics of instability. Thus, our data suggest that in CAD+PAD, evaluation of carotid plaque echogenicity could contribute to improve clinical decision-making and differentiate treatments for individual patients.

“…15 However, our data clearly shows that long-term mortality in PAD subjects with diabetes is worse than subjects without diabetes and lends credence to the ADA recommendation of using presence of PAD as an indicator for screening for asymptomatic CAD. Our data are also useful in supporting recommendations by the American Heart Association for aggressive screening for PAD in high risk subjects 16 -especially the elderly. 17 Our study has several strengths.…”

Section: Discussionsupporting

confidence: 52%

Diabetes and Peripheral Arterial Disease in Men: Trends in Prevalence, Mortality, and Effect of Concomitant Coronary Disease

¹

,

²

2009

Clinical Cardiology

View full text Add to dashboard Cite

Background: Recent data on trends in diabetes mellitus (DM) prevalence and long-term effect on mortality in peripheral arterial disease (PAD) subjects is lacking. Methods: All subjects discharged from any VA medical center between October 1990 to September 1997 with an International Classification of Diseases (ICD)-9 code for PAD and DM in the discharge summary were retrospectively identified. Demographic data were extracted from the database. Mortality data were obtained from the Beneficiary Information and Resource Locator. Outcome measures were age specific DM prevalence over time, and short-term and long-term mortality. Results: Of 33, 629 patients with PAD, 9474 (29%) had DM. Diabetes mellitus subjects were less likely to be white and had more comorbidities. Mean length of hospital stay was greater for DM (22.3 d vs 18.7 days, P < 0.001). Mortality was higher for DM at 180 days (9.8% vs 8.4%, P < 0.001), 1 year (16.4% vs 13.7%, P < 0.001), and continues to increase at 8 years of follow-up. Logistic regression analysis showed no interaction between DM and coronary artery disease (CAD). Conclusions: Diabetes mellitus increases all-cause mortality in subjects with PAD starting at 6 months postdischarge and continues to be higher even at 8 years of follow-up. There was a lack of interaction of DM and CAD on mortality in this cohort of subjects with PAD.

“…The most feared clinical consequence of AAA progression is acute rupture, which accounts for about 15,000 deaths annually in the United States (2). Risk factors for AAA development include cigarette smoking, hypertension, male sex, and a family history of AAA in a male first-degree relative as well as presence of atherosclerosis in other vascular beds (3).…”

Section: Introductionmentioning

confidence: 99%

Inhibition of microRNA-29b reduces murine abdominal aortic aneurysm development

¹

,

Toh³

et al. 2012

J. Clin. Invest.

View full text Add to dashboard Cite

MicroRNAs (miRs) regulate gene expression at the posttranscriptional level and play crucial roles in vascular integrity. As such, they may have a role in modifying abdominal aortic aneurysm (AAA) expansion, the pathophysiological mechanisms of which remain incompletely explored. Here, we investigate the role of miRs in 2 murine models of experimental AAA: the porcine pancreatic elastase (PPE) infusion model in C57BL/6 mice and the AngII infusion model in Apoe -/-mice. AAA development was accompanied by decreased aortic expression of miR-29b, along with increased expression of known miR-29b targets, Col1a1, Col3a1, Col5a1, and Eln, in both models. In vivo administration of locked nucleic acid anti-miR-29b greatly increased collagen expression, leading to an early fibrotic response in the abdominal aortic wall and resulting in a significant reduction in AAA progression over time in both models. In contrast, overexpression of miR-29b using a lentiviral vector led to augmented AAA expansion and significant increase of aortic rupture rate. Cell culture studies identified aortic fibroblasts as the likely vascular cell type mediating the profibrotic effects of miR-29b modulation. A similar pattern of reduced miR-29b expression and increased target gene expression was observed in human AAA tissue samples compared with that in organ donor controls. These data suggest that therapeutic manipulation of miR29b and its target genes holds promise for limiting AAA disease progression and protecting from rupture.

scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.

Contact Info

customersupport@researchsolutions.com

10624 S. Eastern Ave., Ste. A-614

Henderson, NV 89052, USA

Product

Browser Extension Assistant by scite Citation Statement Search Reference Check Visualizations Dashboards Explore Journals Explore Organizations Explore Funders Embedding Badge Embedding Citation Search Pricing

Resources

Blog Help & FAQ Accessibility Statement API Terms For Universities & Governments For Researchers For Publishers For Corporate, Pharma & Enterprise Author Marketing Become an Affiliate Get an organization trial or quote scite Data & Services

About

News & Press Careers Read our Paper Coverage

This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.

Blog Terms and Conditions API Terms Privacy Policy Contact Cookie Preferences Do Not Sell or Share My Personal Information

Copyright © 2024 scite LLC. All rights reserved.

Made with 💙 for researchers

Part of the Research Solutions Family.