Diagnostic ultrasound ( PDFDrive )

CHAPTER 26 The Extracranial Cerebral Vessels 919
intima-media thickness (IMT) to be a surrogate marker for
atherosclerotic disease in the whole arterial system, not only the
cerebrovascular system. 32,33 Some believe that thickening of the
I-M complex greater than 0.8 mm is abnormal and may represent
the earliest changes of atherosclerotic disease. However, because
thickness of the I-M increases with age, absolute measurements
of IMT for any given person may not be a reliable indicator of
atherosclerotic risk factors 34 (Fig. 26.6).
Carotid artery IMT is an independent predictor of new
cardiovascular events in persons without a history of
cardiovascular disease. 35 Numerous studies support the relationship
between IMT and increased risk for myocardial infarction
FIG. 26.5 Normal Intima-Media (I-M) Complex of Common Carotid
Artery. The I-M complex (arrows) is seen in a left common carotid
artery.
or stroke in asymptomatic patient populations. 19,36-43 Assessment
of IMT has been advocated as a means of assessing efectiveness
of medical interventions to reduce the progression of I-M
thickening or even reverse carotid wall thickening. However,
because of concerns regarding minimal impact on prediction
models and diiculty in standardizing measurement technique,
the 2013 American College of Cardiology/American Heart
Association (ACC/AHA) Guideline on the Assessment of
Cardiovascular Risk does not recommend the carotid IMT test. 44
Plaque Characterization
Atheromatous carotid plaques should be carefully evaluated
to determine plaque extent, location, surface contour, and texture,
as well as to assess luminal stenosis. 45 he plaque should be
scanned and evaluated in both the sagittal and the transverse
projections. 46 he most common cause of TIAs is embolism,
not low-limiting stenosis; less than half of patients with documented
TIA have hemodynamically signiicant stenosis. It is
important to identify low-grade atherosclerotic lesions that may
contain hemorrhage or ulceration, which can serve as a nidus
for emboli that cause both TIAs and stroke. 1 Polak et al. 47 showed
that plaque is an independent risk factor for developing a stroke.
Of patients with hemispheric stroke symptoms, 50% to 70%
demonstrate hemorrhagic or ulcerated plaque. Plaque analysis
of CEA specimens has implicated intraplaque hemorrhage as an
important factor in the development of neurologic symptoms. 48-55
However, the relationship between sonographic plaque morphology
and the onset of symptoms is controversial.
Currently, substantial gaps in knowledge of the mechanisms
involved in atherosclerotic plaque rupture exist and this is a
critical barrier to developing methodologies for the prevention
of myocardial infarction and stroke. Myocardial infarction and
stroke, complications of atherosclerosis, are the most common
causes of death in developed countries and are caused by
inlammation-driven rupture of atherosclerotic plaques. Stable
plaques are characterized by a necrotic core with an overlying
ibrous cap composed of vascular smooth muscle cells in a
A
B
FIG. 26.6 Abnormal Intima-Media (I-M) Complex of Common Carotid Artery (CCA). (A) Early I-M hyperplasia with loss of the hypoechoic
component of the I-M complex and thickening (arrows). (B) Thickening of the I-M complex with hyperplasia (arrows).