Structural and hemodynamic response of peripheral arteries of macaque monkeys to atherogenic diet.

Armstrong, Marc P.; Heistad, Donald D.; Marcus, Melvin L.; Megan, Marjorie B.; Piegors, Donald J.

doi:10.1161/01.atv.5.4.336

Cited by 141 publications

(44 citation statements)

References 22 publications

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“…10 Plaque growth initially leads to a compensatory arterial expansion ("positive remodeling") at sites of lesions, a response pattern that is well demonstrated in animal models of coronary disease. 11 The observation that luminal size is initially unaffected by plaque is well confirmed in necropsy studies in CLINICAL EPIDEMIOLOGY www.jasn.org human coronary arteries. 12 Yet the arterial remodeling process is bidirectional in nature.…”

Section: Relationship Between Imt and Indicators Of Vascular Remodelimentioning

confidence: 78%

Rate of Atherosclerotic Plaque Formation Predicts Cardiovascular Events in ESRD

Benedetto¹,

Tripepi²,

Mallamaci³

et al. 2008

Journal of the American Society of Nephrology

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Carotid intima media thickness (IMT) is a strong, independent predictor of cardiovascular events in both the general population and among those with end-stage renal disease (ESRD), but it is unknown whether changes in IMT or other ultrasound-measured indicators of atherosclerosis over time provide additional prognostic information. The progression of atherosclerosis with carotid ultrasound was followed in a cohort of 135 ESRD patients, 103 of whom had a repeat ultrasound after 15 mo of follow-up. The number of plaques and the proportion of patients with severe atherosclerosis increased substantially during the follow-up period, but IMT, common carotid artery diameter, common carotid artery wall-to-lumen ratio, and cross-sectional area, did not change. The rate of formation of new plaques was a strong, independent predictor of incident cardiovascular events, even after adjusting for baseline plaque burden and other potential confounders. New plaque formation over time was independently predicted by background plaque burden and serum C-reactive protein (P ϭ 0.004 and P ϭ 0.02, respectively). Changes in IMT and the other ultrasound-measured indicators of atherosclerosis progression did not predict cardiovascular outcomes. Therefore, monitoring IMT over time is unlikely to provide additional prognostic information compared with a single measurement, but longitudinal ultrasound monitoring of plaque formation may be useful for cardiovascular risk stratification in the ESRD population.

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Section: Relationship Between Imt and Indicators Of Vascular Remodelimentioning

confidence: 78%

Rate of Atherosclerotic Plaque Formation Predicts Cardiovascular Events in ESRD

Benedetto¹,

Tripepi²,

Mallamaci³

et al. 2008

Journal of the American Society of Nephrology

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“…65 However, the slow and unpredictable progression of atherosclerotic disease makes this impractical and ethically difficult, which emphasizes the importance of good animal models to study geometrical remodeling. Armstrong et al 66 were the first to report that the arterial wall adapts to experimentally induced plaque formation in primates. Two years later, Glagov et al confirmed their results in human cadaver studies, 2 promoting the notion of compensatory enlargement.…”

Section: Expansive Atherosclerotic Remodeling: What Did We Learn Frommentioning

confidence: 99%

Expansive Arterial Remodeling: Location, Location, Location

Pasterkamp

Galis

Kleijn

2004

ATVB

118

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Abstract-The artery is a dynamic organ capable of changing its geometry in response to atherosclerotic plaque formation.Expansion of the vessel diameter retards luminal narrowing and is considered a compensatory response. However, the expansive remodeling response is a "wolf in sheep's clothes," because expansion is associated with the presence of inflammatory cells, proteolysis, and a thrombotic plaque phenotype. The prevalence and clinical presentation of expansively remodeled lesions may differ among vascular beds. However, it is evident that all types of atherosclerotic arterial expansive lesions share the presence of inflammatory cells and subsequent protease activities. The potential role of inflammation and protease activity in the development of the different remodeling modes is discussed. Key Words: remodeling Ⅲ atherosclerosis Ⅲ toll-like receptor Ⅲ inflammation Ⅲ compensatory enlargement P laque formation has long been considered the only determinant of atherosclerotic luminal narrowing. The arterial wall, however, is not a rigid tube, but rather an organ capable of overall reshaping in response to hemodynamic, mechanical, and biochemical stimuli. For instance, the increase in the circumference of the artery can partially or totally compensate for the encroachment of the lumen caused by formation of atherosclerotic plaques or by intimal hyperplasia after arterial injury. 1-3 However, the arterial wall may also respond with constrictive remodeling, thereby aggravating the luminal narrowing response 4,5 (Figure 1).Scientific interest in the role of arterial remodeling in occlusive arterial disease boomed with the upcoming use of the visualization technique of intravascular ultrasound (IVUS). With IVUS, it became apparent just how ubiquitously remodeling can prevent plaque from encroaching on the lumen and also how failure of an expansive remodeling response accelerates luminal stenosis in de novo atherosclerosis. The role of such geometrical remodeling response in relation to plaque formation is currently appreciated but has been traditionally strongly underestimated as a causal factor for arterial occlusive disease. It has recently become clear that the geometrical change in arterial size and plaque area may equally contribute to the luminal narrowing in atherosclerotic disease 6 (Figure 2). For instance, it is possible to demonstrate that in 5% of patients eligible for coronary intervention, the plaque mass at the culprit lesion is actually smaller than that located at the angiographically normal reference site, indicating that in such lesions the degree of luminal narrowing is determined by the differences in vessel size rather than by the plaque mass. 6 In this brief review, an overview of anatomical localization and local morphology of the different remodeling modes is given. We also discuss available results of mechanistic

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“…9 Hypercholesterolemic macaque monkeys, rabbits, and pigs all show arterial compensatory enlargement, whereas highgrade stenosis or a decrease in lumen diameter is hardly ever observed. 10,11 Also, apoE-deficient (apoE Ϫ/Ϫ ) mice, the most frequently used atherosclerotic mouse model, show compensatory enlargement, and when they are fed an extremely high cholesterol diet or infused with angiotensin II, they even demonstrate aneurysm formation. 14 -17 Some apoE Ϫ/Ϫ mice do develop significant stenosis in the external CA but without evidence of ischemia.…”

mentioning

confidence: 99%

Compensatory Enlargement and Stenosis Develop in ApoE ^−/− and ApoE*3-Leiden Transgenic Mice

Lutgens

Muinck

Heeneman

et al. 2001

ATVB

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Abstract-Atherosclerotic mouse models develop little ischemic organ damage and no infarctions, despite the presence of large atherosclerotic lesions. Therefore, we hypothesize that luminal changes do not follow atherosclerotic lesion development. Because a phenomenon that may explain the discrepancy between luminal changes and lesion size is vascular remodeling, we measured parameters of vascular remodeling in the carotid arteries (CAs), thoracic aorta (TA), and abdominal aorta (AA) of apolipoprotein E (apoE)-deficient (apoE Ϫ/Ϫ ) and apoE*3-Leiden mice, 2 well-known mouse models of atherosclerosis. Atherosclerotic lesions were classified (American Heart Association [AHA] types II through V), and plaque thickness, compensatory enlargement versus constrictive remodeling, lumen diameter, stenosis, and media thickness were measured relative to the nondiseased arterial wall. In CAs, plaque thickness increased during atherogenesis. CAs showed compensatory enlargement (apoE Ϫ/Ϫ 55%, apoE*3-Leiden 38%). Regression analysis revealed a positive correlation between plaque and lumen area (for apoE Ϫ/Ϫ , Rϭ0.95; for apoE*3-Leiden, Rϭ0.90). Medial thinning and elastolysis were also observed. During atherogenesis, lumen diameter decreased (apoE Ϫ/Ϫ Ϫ69%, apoE*3-Leiden Ϫ40%), and stenosis Ͼ70% developed. TA and AA showed similar features, but neither developed a progressive decrease in lumen diameter or stenosis Ͼ70%. In CAs, TA, and AA of apoE Ϫ/Ϫ and apoE*3-Leiden mice, atherogenesis is associated with compensatory enlargement, medial thinning, and elastolysis. A progressive decrease in lumen diameter and stenoses Ͼ70% occur only in CAs. Vascular remodeling is more prominent in apoE Ϫ/Ϫ mice.

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Structural and hemodynamic response of peripheral arteries of macaque monkeys to atherogenic diet.

Cited by 141 publications

References 22 publications

Rate of Atherosclerotic Plaque Formation Predicts Cardiovascular Events in ESRD

Rate of Atherosclerotic Plaque Formation Predicts Cardiovascular Events in ESRD

Expansive Arterial Remodeling: Location, Location, Location

Compensatory Enlargement and Stenosis Develop in ApoE ^−/− and ApoE*3-Leiden Transgenic Mice

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Structural and hemodynamic response of peripheral arteries of macaque monkeys to atherogenic diet.

Cited by 141 publications

References 22 publications

Rate of Atherosclerotic Plaque Formation Predicts Cardiovascular Events in ESRD

Rate of Atherosclerotic Plaque Formation Predicts Cardiovascular Events in ESRD

Expansive Arterial Remodeling: Location, Location, Location

Compensatory Enlargement and Stenosis Develop in ApoE −/− and ApoE*3-Leiden Transgenic Mice

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Compensatory Enlargement and Stenosis Develop in ApoE ^−/− and ApoE*3-Leiden Transgenic Mice