Carotid rupture and intraplaque hemorrhage: Immunophenotype and role of cells involved

Milei, José; Parodi, Juan C.; Alonso, Graciela Fernández; Barone, Andrea; Grana, Daniel; Matturri, Luigi

doi:10.1016/s0002-8703(98)70169-3

Cited by 89 publications

(77 citation statements)

References 22 publications

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“…Gross and microscopic pathological investigations suggested that IPH occurs more often in symptomatic patients undergoing CEA and that the age of the hematoma correlates with the timing of the symptoms [44,45]. Histopathological examinations have revealed the association between IPH and the presence of neovessels [46]. Particularly, a study suggested the possible rupture of neovessels as cause of production and expansion of IPH [47].…”

Section: Intraplaque Hemorrhagementioning

confidence: 99%

Imaging of the Carotid Artery Vulnerable Plaque

Saba¹,

Anzidei

Marincola

et al. 2013

Cardiovasc Intervent Radiol

111

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Atherosclerosis involving the carotid arteries has a high prevalence in the population worldwide. This condition is significant because accidents of the carotid artery plaque are associated with the development of cerebrovascular events. For this reason, carotid atherosclerotic disease needs to be diagnosed and those determinants that are associated to an increased risk of stroke need to be identified. The degree of stenosis typically has been considered the parameter of choice to determine the therapeutical approach, but several recently published investigations have demonstrated that the degree of luminal stenosis is only an indirect indicator of the atherosclerotic process and that direct assessment of the plaque structure and composition may be key to predict the development of future cerebrovascular ischemic events. The concept of ''vulnerable plaque'' was born, referring to those plaque's parameters that concur to the instability of the plaque making it more prone to the rupture and distal embolization. The purpose of this review is to describe the imaging characteristics of ''vulnerable carotid plaques.''

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Section: Intraplaque Hemorrhagementioning

confidence: 99%

Imaging of the Carotid Artery Vulnerable Plaque

Saba¹,

Anzidei

Marincola

et al. 2013

Cardiovasc Intervent Radiol

111

View full text Add to dashboard Cite

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“…2,3 Furthermore, microvessels play a role in plaque hemorrhage associated with the development of symptoms in cerebrovascular disease. 4,5 In addition, microvessels are increased in coronary lesions from patients with acute myocardial infarction, suggesting a potential role for microvessels in plaque rupture. 6,7 Histological features associated with plaque rupture include a large lipid core, thin fibrous cap, and increased inflammation.…”

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confidence: 99%

Plaque Neovascularization Is Increased in Ruptured Atherosclerotic Lesions of Human Aorta

et al. 2004

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Background-Growth of atherosclerotic plaques is accompanied by neovascularization from vasa vasorum microvessels extending through the tunica media into the base of the plaque and by lumen-derived microvessels through the fibrous cap. Microvessels are associated with plaque hemorrhage and may play a role in plaque rupture. Accordingly, we tested this hypothesis by investigating whether microvessels in the tunica media, the base of the plaque, and the fibrous cap are increased in ruptured atherosclerotic plaques in human aorta. Methods and Results-Microvessels, defined as CD34-positive tubuloluminal capillaries recognized in cross-sectional and longitudinal profiles, were quantified in 269 advanced human plaques by bicolor immunohistochemistry. Macrophages/T lymphocytes and smooth muscle cells were defined as CD68/CD3-positive and ␣-actin-positive cells. Total microvessel density was increased in ruptured plaques when compared with nonruptured plaques (Pϭ0.0001). Furthermore, microvessel density was increased in lesions with severe macrophage infiltration at the fibrous cap (Pϭ0.0001) and at the shoulders of the plaque (Pϭ0.0001). In addition, microvessel density was also increased in lesions with intraplaque hemorrhage (Pϭ0.04) and in thin-cap fibroatheromas (Pϭ0.038). Logistic regression analysis identified plaque base microvessel density (Pϭ0.003) as an independent correlate to plaque rupture. Conclusions-Thus, neovascularization as manifested by the localized appearance of microvessels is increased in ruptured plaques in the human aorta. Furthermore, microvessel density is increased in lesions with inflammation, with intraplaque hemorrhage, and in thin-cap fibroatheromas. Microvessels at the base of the plaque are independently correlated with plaque rupture, suggesting a contributory role for neovascularization in the process of plaque rupture. (Circulation.

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“…These plaques, as well as those with large amounts of lipid and thin fibrous caps, are 'plaques at risk'. Intraplaque hemorrhage without plaque rupture is characterized by neovascularization of the plaque, and is caused by the breakdown of neoformed vessels in the core and periphery of the plaque (5). In complicated plaques and at the cap regions, trisomy and tetrasomy of chromosome 7, monosomy of chromosome 11, amplifications of fibroblast growth factor 3 and apoptosis, as well as overexpression of p53 protein, proliferating cell nuclear antigen (PCNA) and c-fos positivity, were observed in smooth muscle cells (SMCs) (4,(6)(7)(8) -main factors in atherosclerosis (5,6).…”

mentioning

confidence: 99%