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4.15.2008 New Perspectives in the Imaging of Carotid Artery Plaque SPEAKER:
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Carotid artery plaque raises one’s risk of stroke, but not all plaque is equally dangerous. Vulnerable plaque can lead to thrombosis (clotting of the artery) or to the formation of emboli (small clots) that travel to the brain. The pathogenesis of stroke is ischemic, or the result of plaque, in approximately 83% of cases. Studies have shown that fifty asymptomatic patients with carotid artery stenosis (narrowing) of greater than 70% undergo carotid endarterectomy (CEA), a plaque-removing procedure, to prevent one stroke, for three years of follow-up. In asymptomatic patients with carotid artery stenosis of 50-70%, the benefit of CEA is less well understood. In the future, imaging techniques could help doctors predict which people with intermediate levels of stenosis will benefit most from surgery.
Multiple techniques exist to assess unstable plaque. These include ultrasound, angiography, magnetic resonance imaging (MRI), computed tomography (CT), computerized tomographic angiography (CTA), positron emission tomography (PET), and biochemical assays. A large study utilizing ultrasound found that the presence of hypoechoic (non-calcified) plaque and greater than 50% stenosis is connected to increased stroke risk while hyperechoic (calcified) plaque is more stable. Interestingly, in coronary artery disease, highly calcified plaque is associated with a high risk of symptoms while in carotid artery disease, highly calcified plaque is associated with a low risk of symptoms. Studies using MRI have found that the presence of plaques with thin fibrous caps is correlated with symptoms of transient ischemic attack (TIA) and stroke. Biochemical studies done in rabbits fed high cholesterol diets have shown that the enzyme myeloperoxidase, which activated macrophages and neutrophils secrete in response to inflammation, is also secreted by vulnerable plaque prone to rupture.
The lab of Javier Romero is studying the ability of CTA to provide information about plaque vulnerability. Patients with enhancement on CTA of the vasa vasorum (a network of small arterioles, capilllaries, and venules that supply the outer tissues of large blood vessels) at the carotid bifurcation appear more likely to be symptomatic. Romero’s group also compared symptomatic and asymptomatic patients and found that the asymptomatic patients had denser, more calcified plaques than symptomatic patients, a finding that corroborates previous ultrasound data. Plaque density may be a surrogate marker of plaque stability and a potential way to determine whether an asymptomatic patient with carotid artery stenosis should undergo surgical treatment.
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