Imaging of Carotid Plaque Angiogenesis

Vicenzini, Edoardo; Giannoni, Maria Fabrizia; Benedetti-Valentini, F; Lenzi, Gian Luigi

doi:10.1159/000203126

Cited by 41 publications

(28 citation statements)

References 65 publications

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“…Contrast-enhanced ultrasound is a reliable tool to identify neoangiogenesis and remodeling in carotid artery plaques [11,12]. In our patients, the follow-up of internal carotid artery retrograde thrombosis showed with this approach that not only the vessel may unevenly reopen after complete occlusion, but also that thrombus remodeling can still be visible up to 2 years from the first event.…”

Section: Discussionmentioning

confidence: 67%

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Predictors and Timing of Recanalization in Intracranial Carotid Artery and Siphon Dissection: An Ultrasound Follow-up Study

Vicenzini¹,

Toscano²,

Maestrini³

et al. 2013

Cerebrovasc Dis

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Background: Intra- and extracranial internal carotid artery dissections (ICD) are two different pathological conditions. Extracranial dissection is considered to be among the most frequent causes of stroke in the young and the segment generally reopens in 2 out of 3 cases, completely or partially, within 6 months. Intracranial ICD (IICD) is considered a rare occurrence in stroke and, accordingly, there are few systematic published data. However, it is a clinically significant condition that may cause severely disabling ischemic stroke or subarachnoid hemorrhage. In the past, sole availability of invasive imaging methods for its detection may have induced an underreporting. The aim of the study was to analyze ultrasound findings, timing and predictors of recanalization in patients with IICD. Methods: IICD acute patients admitted to our Stroke Unit were submitted to carotid sonographic seriated monitoring, daily for the 1st week after symptom onset, at day 14, at month 1 and every 3 months thereafter up to a follow-up of 4 years. Contrast carotid ultrasound was performed in patients with persistent occlusion after month 1. Results: Fourteen acute patients with IICD were enrolled. Extracranial internal carotid patency was observed in 8 patients at first ultrasound scans; all of these showed complete intracranial recanalization within the 1st week and oral anticoagulants were withdrawn after 6 months. Conversely, in 6 patients retrograde extracranial internal carotid thrombosis was immediately observed, since the first ultrasound scans. In 4 of these the occlusion persisted after 4 years while 2 of them had only a partial recanalization, with evidence at contrast ultrasound of still late remodeling processes in the extracranial thrombus up to 2 years after the first observation; for this reason, in these 2 patients anticoagulation was not discontinued, while in the 4 patients with persistent, stable, occlusion, therapy was suspended 1 year after the diagnosis. Conclusions: Identification of the site of dissection - i.e. extra- versus intracranial - is fundamental in clinical studies for outcome and prognosis evaluation. Carotid ultrasound strict surveillance is important to monitor eventual recanalization in patients with ICD, even in a late phase. Retrograde internal carotid thrombosis seems to be correlated with persistent occlusion and partial recanalization. Remodeling of thrombotic material in the internal carotid artery may, however, continue for up to 2 years. In these cases, contrast ultrasound evidence of thrombus morphological changes may support the decision to continue anticoagulation.

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Section: Discussionmentioning

confidence: 67%

“…After the 1st month, in patients who showed persistence of occlusion with retrograde extracranial internal carotid artery thrombosis, contrast carotid ultrasound (SonoVue 1/2 fl i.v. and real-time CPS real-time contrast software) was performed to evaluate neoangiogenesis in the thrombotic material [11,12,13]. …”

Section: Methodsmentioning

confidence: 99%

Predictors and Timing of Recanalization in Intracranial Carotid Artery and Siphon Dissection: An Ultrasound Follow-up Study

Vicenzini¹,

Toscano²,

Maestrini³

et al. 2013

Cerebrovasc Dis

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“…Carotid atherosclerotic plaques from symptomatic patients contain increased capillary vessels and demonstrate significantly increased expression of angiogenesis-related genes compared with plaques from asymptomatic patients [29,33,34,35]. MACs, attracted by oxidized low-density lipoprotein, are responsible for cytokine production driving neovessel growth [36,37]; an increased density of vasa vasorum is correlated strongly with the number of infiltrating mononuclear cells [33].…”

Section: Discussionmentioning

confidence: 99%

Toll-Like Receptor 4 Immunohistochemical Expression Is Enhanced in Macrophages of Symptomatic Carotid Atherosclerotic Plaques

Katsargyris

Tsiodras²,

Theocharis³

et al. 2010

Cerebrovasc Dis

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Background: A growing body of evidence supports a role for Toll-like receptor 4 (TLR4), a primary receptor of the innate immune system, in atherosclerosis initiation and progression. Carotid atheroma macrophages (MACs) and smooth muscle cells (SMCs) express TLR4; nevertheless, correlations with epidemiological and clinical variables and especially cerebrovascular symptomatology remain unsettled. Methods: Carotid atherosclerotic plaques were obtained by standard carotid endarterectomy on 157 patients with carotid artery disease (84 asymptomatic – 73 symptomatic). TLR4 expression in MACs and SMCs of carotid atheroma was detected by immunohistochemistry techniques. TLR4 positivity, overexpression and intensity of immunostaining in MACs and SMCs were correlated with cerebrovascular symptomatology, epidemiological and clinical variables. Results: MAC TLR4 positivity was noted in 129 (82.2%) patients. Patients receiving statins had significantly lower TLR4 expression. Rates of MAC TLR4 positivity were higher among symptomatic patients (odds ratio, OR = 5.1; 95% confidence interval, CI = 1.8–14.3; p < 0.001); the association was stronger for transient ischemic attacks. TLR4 overexpression was also significantly enhanced among symptomatic patients (OR = 2.3; 95% CI = 1.02–5.03; p < 0.05). No correlations were detected between SMC TLR4 expression and cerebrovascular symptoms. In multivariate models adjusting for age, gender, body mass index, hyperlipidemia and smoking, MAC TLR4 positivity was associated with a cerebrovascular event during the last 6 months (OR = 4; 95% CI = 1.2–13.3; p = 0.02). Conclusions: Symptomatic carotid artery plaques are characterized by increased expression of TLR4 in macrophages supporting a potential role for TLR4 in the pathophysiology and clinical presentation of cerebrovascular disease. Further investigation is warranted.

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“…Several promising studies have targeted pathologic processes with contrast-enhanced ultrasound (Lindner, 2009;Voigt, 2009), such as angiogenesis (by targeting endothelial integrins) (Lerman & Zeiher, 2005), thrombus (by targeting IIbIIIa receptors or fibrinogen) (Alonso et al, 2007), inflammation (by targeting ICAM-1, VCAM-1 P-and L-selectin) and plaque (by targeting ICAM-1, VCAM-1 and several angiogenesis markers) (Voigt, 2009). In fact, it is believed that by targeting plaque inflammation and neovascularization we could identify patients at high risk for cardiovascular events well before angiography (Lindner, 2009;Voigt, 2009) or even recognise "vulnerable plaques" and begin early treatment (Vicenzini et al, 2009). Several future promising therapeutic applications of microbubbles are under research.…”

Section: Contrast-enhanced Ultrasoundmentioning

confidence: 99%