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Ultrasound and carotid bifurcation atherosclerosis / , Ultrasound and carotid bifurcation atherosclerosis / , کتابخانه دیجیتال جندی شاپور اهواز

In the 1970s and 1980s, angiography was the standard method used for grading internal carotid artery stenosis. With the introduction of ultrasound in the 1980s and early 1990s, angiography became the gold standard used for the development of duplex velocity criteria for different grades of stenosis.

The predictive ability of intima-media thickness (IMT) and plaque measurements for future cardiovascular events has been discussed in Chaps. 22–26. It has been demonstrated that carotid plaque size (thickness, area, volume) is a stronger predictor of cardiovascular risk than IMT when the latter is measured in the common carotid artery (IMTcc).

The multidisciplinary approach combining angiography, high-resolution ultrasound imaging, transcranial Doppler studies of embolic signals, plaque pathology, histochemistry, coagulation studies, and, more recently, molecular biology has led to a better understanding of the mechanism of carotid plaque rupture, the key mechanism underlying the development of cerebrovascular events1–3 (Chap. 1).

The Asymptomatic Carotid Stenosis and Risk of Stroke (ACSRS) study was a multicenter natural history study. Its primary aim was to identify clinical, biochemical, and plaque features that, when used in combination, would allow risk stratification for ipsilateral carotid territory hemispheric ischemic events, especially stroke. It was planned in 1996, soon after the publication of the Asymptomatic Carotid Atherosclerosis Study (ACAS),1 and recruitment started in 1998. The ACSRS is the largest natural history study of patients with asymptomatic carotid stenosis performed to date with 1,121 patients followed for 6–96 months (mean 48 months). Results of different aspects such as quality control, stenosis and risk, factors associated with cardiovascular mortality, effect of image normalization on carotid plaque classification, silent ipsilateral cerebral embolic infarcts on computed tomography (CT) brain scans and stroke risk, and stroke risk stratification using baseline plaque texture features have already been published.

Despite continuing advances in the sensitivity of diagnostic ultrasound systems, Doppler-based imaging techniques are unable to detect low velocity blood flow in the microcirculation. The main difficulty these techniques share is that blood is a weak reflector of ultrasound with received amplitude 40–60 dB smaller than that of tissue. As a result, Doppler-based techniques rely solely on the movement of red blood cells to differentiate blood flow from tissue. The removal of this tissue signal places a lower limit on the ability to detect low velocity blood flow (

More than 50 years ago, William Kannel1 first popularized the concept of cardiovascular disease risk factors for clinicians and clinical epidemiologists.2 The word “factor” derives from Latin (meaning doer) which implies causality.

In the 1980s and early 1990s, ultrasonic plaque characterization was highly subjective. When the examination was performed in a dimly lit room, the gain was usually reduced by the operator; when it was performed in a brightly lit room, the gain was increased. Although the human eye could adjust to the image brightness to a certain extent, reproducible measurements of echodensity when the same patient was scanned in another room and on different equipment were not possible. Ultrasonic image normalization which has been introduced in the late 1990s has enabled us to overcome this problem.

The principles of 3-dimensional (3D) image reconstruction from a series of consecutive two-dimensional (2D) ultrasound images and the measurement of plaque volume and plaque surface irregularity have been described in Chaps. 16 and 17.

The multidisciplinary approach combining angiography, high-resolution ultrasound, thrombolytic therapy, plaque pathology, histochemistry, coagulation studies, and more recently molecular biology has led to the realization that carotid plaque rupture is a key mechanism underlying the development of cerebrovascular events.1, 2, 3