Plaque burden, arterial remodeling and plaque vulnerability: determined by systemic factors?

Vink, Aryan; Schoneveld, Arjan H.; Richard, Wietske; Kleijn, Dominique P. V. de; Falk, Erling; Borst, Cornelius; Pasterkamp, Gérard

doi:10.1016/s0735-1097(01)01444-9

Cited by 74 publications

(58 citation statements)

References 23 publications

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“…24,25 In any case, whatever the triggers of the increased number of leukocytes may be, these cells exert important atherogenic activities, [26][27][28][29] in particular with respect to plaque destabilization. 30 Furthermore, in our study, the leukocyte count remained an independent predictor of hypoechoic plaques after correction for possible confounding factors (i.e. smoking and diabetes).…”

Section: Inflammation and Unstable Plaquessupporting

confidence: 52%

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

et al. 2009

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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.

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Section: Inflammation and Unstable Plaquessupporting

confidence: 52%

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

et al. 2009

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“…4 Moreover, the simultaneous presence of multiple complex atherosclerotic plaques was also reported in arterial districts other than the coronary arteries. 6,8,24 …”

Section: Multifocal Plaque Instabilitymentioning

confidence: 99%

Inflammation as a Possible Link Between Coronary and Carotid Plaque Instability

Lombardo¹,

Biasucci²,

Lanza³

et al. 2004

Circulation

188

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Background-Multiple complex stenoses, plaque fissures, and widespread coronary inflammation are common in acute coronary syndromes. A systemic cause of atherosclerotic plaque instability is also suggested by studies of ischemic cerebrovascular disease. We investigated the association between coronary and carotid plaque instability and the potential common causal role of inflammation. Methods and Results-The ultrasound characteristics of carotid plaques were evaluated retrospectively in patients scheduled for coronary bypass surgery, 181 with unstable and 92 with stable angina, and prospectively in a similar group of patients, 67 with unstable and 25 with stable angina, in whom serum C-reactive protein levels were also measured. The prevalence of carotid plaques was similar in the retrospective and prospective studies and Ͼ64% in both unstable and stable coronary patients.

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“…Rupture of the plaque surface and subsequent luminal thrombus formation are probably the most important mechanism underlying acute syndromes. The risk of plaque rupture depends on plaque composition, which may be more important than plaque size (5). Other factors are also important; proximity of the necrotic core to the lumen and cellular indicators of plaque neoformation or inflammatory reaction around the fibrous cap are associated with clinical events (6).…”

Section: Introductionmentioning

confidence: 99%

MRI of atherosclerosis in clinical trials

et al. 2006

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Magnetic resonance imaging (MRI) of the arterial wall has emerged as a viable technology for characterizing atherosclerotic lesions in vivo, especially within carotid arteries and other large vessels. This capability has facilitated the use of carotid MRI in clinical trials to evaluate therapeutic effects on atherosclerotic lesions themselves. MRI is specifically able to characterize three important aspects of the lesion: size, composition and biological activity. Lesion size, expressed as a total wall volume, may be more sensitive than maximal vessel narrowing (stenosis) as a measure of therapeutic effects, as it reflects changes along the entire length of the lesion and accounts for vessel remodeling. Lesion composition (e.g. lipid, fibrous and calcified content) may reflect therapeutic effects that do not alter lesion size or stenosis, but cause a transition from a vulnerable plaque composition to a more stable one. Biological activity, most notably inflammation, is an emerging target for imaging that is thought to destabilize plaque and which may be a systemic marker of vulnerability. The ability of MRI to characterize each of these features in carotid atherosclerotic lesions gives it the potential, under certain circumstances, to replace traditional trials involving large numbers of subjects and hard end-points -heart attacks and strokes -with smaller, shorter trials involving imaging end-points. In this review, the state of the art in MRI of atherosclerosis is presented in terms of hardware, image acquisition protocols and post-processing. Also, the results of validation studies for measuring lesion size, composition and inflammation will be summarized. Finally, the status of several clinical trials involving MRI of atherosclerosis will be reviewed.

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Plaque burden, arterial remodeling and plaque vulnerability: determined by systemic factors?

Cited by 74 publications

References 23 publications

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

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

Inflammation as a Possible Link Between Coronary and Carotid Plaque Instability

MRI of atherosclerosis in clinical trials

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