The purpose of this study was to determine the cerebrovascular risk stratification potential of baseline degree of stenosis, clinical features, and ultrasonic plaque characteristics in patients with asymptomatic internal carotid artery (ICA) stenosis

The size of a JBA is linearly related to the risk of stroke and can be used in risk stratification models. These findings need to be confirmed in future prospective studies or in the medical arm of randomized controlled studies in the presence of optimal medical therapy. In the meantime, the JBA may be used to select asymptomatic patients at high stroke risk for carotid endarterectomy and spare patients at low risk from an unnecessary operation.

Genetic discoveries of Alzheimer’s disease are the drivers of our understanding, and together with polygenetic risk stratification can contribute towards planning of feasible and efficient preventive and curative clinical trials. We first perform a large genetic association study by merging all available case-control datasets and by-proxy study results (discovery n = 409,435 and validation size n = 58,190). Here, we add six variants associated with Alzheimer’s disease risk (near APP, CHRNE, PRKD3/NDUFAF7, PLCG2 and two exonic variants in the SHARPIN gene). Assessment of the polygenic risk score and stratifying by APOE reveal a 4 to 5.5 years difference in median age at onset of Alzheimer’s disease patients in APOE ɛ4 carriers. Because of this study, the underlying mechanisms of APP can be studied to refine the amyloid cascade and the polygenic risk score provides a tool to select individuals at high risk of Alzheimer’s disease.

Linearity between ECST per cent stenosis and risk makes this method for grading stenosis more amenable to risk prediction without any transformation not only in clinical practice but also when multivariable analysis is to be used. Identification of additional risk factors provides a new approach to risk stratification and should help refine the indications for carotid endarterectomy.

Background and Purpose-We sought to assess the reproducibility, interobserver variability, and application to clinical studies of a new method for the quantitative assessment of carotid plaque echogenicity. Methods-Carotid plaques were scanned with the use of ultrasound, and their images were stored in a computer. They were normalized by assigning certain gray values to blood and adventitia, and the gray scale median (GSM) was used to quantify their echogenicity. The variability between storage media, between degrees of magnification, and between probes was assessed. The method was applied to 232 asymptomatic carotid plaques causing 60% to 99% stenosis in relation to the presence of ipsilateral CT-demonstrated brain infarcts. In all parts of the study the plaque GSM was measured before and after normalization to evaluate its effect. Interobserver agreement for the scanning process was assessed. Results-The GSM mean difference before and after normalization for variability studies of storage media, degrees of magnification, and probes was Ϫ14.5 and Ϫ0.12, 2.24 and 1.68, and Ϫ8.3 and Ϫ0.7, respectively. The median GSM of plaques associated with ipsilateral nonlacunar silent CT-demonstrated brain infarcts was 14, and that of plaques that were not so associated was 30 (Pϭ0.003). The interobserver GSM difference was Ϫ0.05 (95% CI, Ϫ1.7 to 1.6). Conclusions-Our method decreases the variability between storage media and between probes but not the variability between degrees of magnification. It separates echomorphologically the carotid plaques associated with silent nonlacunar CT-demonstrated brain infarcts from plaques that are not so associated.

The presence of silent embolic infarcts can identify a high-risk group for ipsilateral hemispheric neurologic events and stroke and may prove useful in the management of patients with moderate asymptomatic carotid stenosis.

Carotid atherosclerotic disease constitutes a major modern health problem whose diagnosis primarily relies on imaging. Grading of stenosis has been long used as the main factor for risk stratification and guiding of management. Nevertheless, increasing evidence has shown that additional plaque characteristics such as plaque composition and surface morphology play an important role in the occurrence of symptoms, justifying the term “vulnerable plaque”. Carotid plaque surface characteristics either in the form of surface irregularities or ulceration represent an important factor of vulnerability and are associated with the occurrence of neurologic symptoms. The delineation of the carotid plaque surface can be performed with virtually all imaging modalities including ultrasound, contrast-enhanced ultrasound, multi-detector computed tomography angiography, magnetic resonance angiography and the traditional reference method of angiography. These techniques have shown varying levels of diagnostic accuracy for the identification of ulcerated carotid plaques or plaque surface irregularities. As a consequence and given its high clinical significance, radiologists should be familiar with the various aspects of this entity, including its definition, classification, imaging findings on different imaging modalities and associations. The purpose of this review is to present the current literature regarding carotid plaque ulcerations and present illustrative images of ulcerated carotid plaques.Teaching Points • Plaque surface and ulceration represent risk factors for stroke in carotid disease. • Characterisation of the plaque surface and ulcerations can be performed with every modality. • US is the first-line modality for carotid disease and identification of ulcerations. • The administration of microbubbles increases US accuracy for diagnosis of carotid ulceration. • MDCTA and MRA are valuable for diagnosing ulceration and evaluating plaque composition.

Atherosclerosis constitutes the most common medical and surgical problem. This can be manifested clinically as stroke, coronary artery disease, or peripheral vascular disease. In the present review the microscopic appearance of the normal arterial wall, the definition of atherosclerosis and the five theories of atherogenesis are described. These are: the lipid theory, the hemodynamic theory, the fibrin incrustation theory, the nonspecific mesenchymal hypothesis and the response to injury hypothesis. Based on the above theories the sequence of events in atherogenesis is analyzed. The classification of the atherosclerotic lesions according to Stary (types I-VI) and their characteristics appear in a table. The epidemiology and the role of the following risk factors are presented in detail: age, sex, lipid abnormalities, cigarette smoking, hypertension, diabetes mellitus, physical inactivity, alcohol consumption, obesity, and hemostatic factors. In addition, less common genetically determined associations like homocystinuria, Tangier disease, Hutchinson-Gilford syndrome (progeria), Werner's syndrome, radiation induced atherosclerosis and the implications of Chlamydia pneumoniae on the arterial wall are discussed.