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Aortic Arch Artherosclerotic Disease
Introduction
Ischemic stroke etiologies can be classified into thrombotic, embolic, or cerebral infarcts secondary to systemic hypoperfusion. Aortic arch disease has been a subject of study for many years as a potential source of embolic stroke and is common in individuals over 60 years of age. Complex, ulcerated plaques are common, and mural thrombi can superimpose upon ulcers. Mural thrombi can occasionally be loosely adherent and mobile, increasing the risk of embolization to the brain, retina, or peripheral organs. Large plaques, defined as those ≥4 mm in size, have been shown to further increase the risk of stroke and have been linked to a 2.5- to 9-fold increase in stroke risk in case–control studies . The presence of complex features such as ulceration has also been suggested to further increase the risk of stroke in individuals with aortic arch disease . Atherosclerotic disease of the aortic arch has thus been considered a potential source of cerebral ischemia in patients with cryptogenic stroke.
Varying degrees of aortic arch disease are found in about 1 in 4 patients with an embolic event . The advanced use of transesophageal echocardiography (TEE)—the gold standard for evaluating aortic arch disease—has enhanced the ability to detect and characterize aortic arch plaques. Atherosclerosis burden of the thoracic aorta, particularly in lesions with complex characteristics and size of >4 mm, has been considered a major risk factor for both cerebral ischemia and peripheral embolization . Interestingly, lesions in the descending thoracic aorta, located distal to the anatomical branch points of the great vessels, have been considered a potential source of cerebral embolism through retrograde aortic flow . Retrograde flow-related emboli have been suggested as a potential cause of retinal or cerebral infarcts in 24% of patients with cryptogenic stroke . Stroke prevention in patients with atherosclerotic burden of the aortic arch has been controversial, and there is no known optimal stroke prevention strategy. In this chapter, we will summarize some seminal studies along with some of the most recent studies investigating aortic arch disease as a source of ischemic stroke. Stroke treatment and prevention strategies will also be discussed.
Aortic Arch Plaques as a Risk Factor for Ischemic Stroke
Aortic arch plaques >4 mm in thickness are found in one-third of patients with stroke of an unknown source, which accounts for about one-third of the total ischemic stroke population over the age of 60 years . Amarenco et al. found that the presence of ulcerated plaques in the aortic arch is associated with stroke of an unknown cause. It has also been reported that the association between aortic arch atheroma and stroke is stronger when the size of plaque is ≥4 mm . Moreover, Jones et al. demonstrated that the presence of aortic arch atheromas with a size of ≥5 mm or with mobile elements is an independent risk factor for ischemic stroke. Louis R. Caplan reports that large protruding plaques in the ascending aorta and transverse arch are a major source of aortoembolic stroke, and the risk increases with mobile plaques.
Disparities concerning the underlying relationship between aortic arch disease and stroke have also been described. Petty et al. conducted a population-based study of 1135 subjects and found that complex aortic atherosclerotic plaques of ≥4 mm in thickness, with or without mobile debris, was not a significant risk factor for stroke of unknown source or transient ischemic attack. They did, however, report an association between complex aortic plaques and noncryptogenic stroke and, in general, concluded that the presence of aortic arch debris is an indicator for generalized atherosclerosis and increases the risk of cerebrovascular disease .
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