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Rivista di Angiologia
Official Journal of the , the International Union of Phlebology and the
Indexed/Abstracted in: BIOSIS Previews, Current Contents/Clinical Medicine, EMBASE, PubMed/MEDLINE, Science Citation Index Expanded (SciSearch), Scopus
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International Angiology 2001 March;20(1):51-7
Carotid plaque echogenicity and types of silent CT-brain infarcts. Is there an association in patients with asymptomatic carotid stenosis?
Sabetai M. M., Tegos T. J., Clifford C., Dhanjil S., Belcaro G., Kakkos S., Kalodiki E., Stevens J. M. *, Nicolaides A. N.
From the Irvine Laboratory for Cardiovascular Investigation and Research, Imperial College School of Medicine at St. Mary’s Hospital, Department of Vascular Surgery, London
* Department of Radiology, Imperial College School of Medicine at St. Mary’s Hospital, London, UK
Background. The aim of this study was to identify the differences in echogenicity and the degree of stenosis of asymptomatic carotid plaques associated with different types of ipsilateral silent CT-brain infarcts.
Methods. Some 273 asymptomatic carotid plaques (218 patients) causing 50 to 99% stenosis were studied with high-resolution ultrasound. B-mode images were digitised and normalised by assigning certain grey values to blood and adventitia. The grey scale median (GSM) of the plaque in the normalised image was used to quantify echogenicity. Every patient had a CT-brain scan which an independent neuroradiologist read. The presence of 1) non-lacunar and 2) lacunar silent CT-brain infarcts ipsilateral to the carotid plaque was noted.
Results. The mean GSM of plaques associated with non-lacunar silent CT-brain infarcts was 19.6, of plaques associated with lacunar infarcts was 35.5 and of those associated with no infarcts was 32 (p=0.008, ANOVA). The mean degree of stenosis was 79%, 72% and 73% respectively (p=0.1, ANOVA). Plaque echogenicity (p=0.007) and not the degree of stenosis (p=0.07) predicted the presence of non-lacunar silent CT-brain infarcts (logistic regression).
Conclusions. Carotid bifurcation plaques, which are associated with non-lacunar silent CT-brain infarcts, are significantly more hypoechoic than those associated with lacunar or no infarcts. Plaques associated with lacunar silent infarcts and no infarcts have the same echogenicity and degree of stenosis. These findings suggest an embologenic mechanism of non-lacunar silent CT-brain infarcts that may have prognostic implications in patients with asymptomatic carotid stenosis. Prospective studies of asymptomatic carotid stenosis should assess the significance of 1) plaque echogenicity and 2) the presence of different types of silent CT-brain infarcts and atheroembolic stroke.