Aortic atherosclerotic plaques are a manifestation of systemic atherosclerosis. They are associated with general risk factors for atherosclerotic disease, including age, hypertension, and hypercholesterolemia, and are more common in patients with coronary artery disease [1,2].
Aortic atherosclerotic plaques are an important source of emboli, leading to cerebral (eg, transient ischemic attack, stroke), extremity or visceral embolization (picture 1) [3-6]. Embolic events can occur spontaneously or can be induced by interventions including cardiac catheterization, arteriography, peripheral interventions, intraaortic balloon pumping, and cardiac or vascular surgery [7,8].
The general manifestations and treatment of cholesterol crystal embolism, diagnosis and medical and surgical management will be reviewed. Thromboembolism from unstable aortic plaques is discussed elsewhere. (See "Embolism from aortic plaque: Thromboembolism".)
Specific considerations related to end-organ ischemia (kidney, gut, extremity) that may result from cholesterol crystal embolus are discussed in separate topic reviews.
ATHEROEMBOLISM VERSUS THROMBOEMBOLISM
Two types of emboli originate from atherosclerotic plaques: thromboemboli and atheroemboli (cholesterol crystal emboli). Although the underlying risk factors may be similar, the two can often be differentiated based upon associated conditions and clinical manifestations. This is an important distinction, since the prognosis and treatment differ. Thromboembolism from complex aortic plaques is common, particularly from thoracic aortic plaques. In comparison, cholesterol crystal embolism is fairly rare, but is probably under-recognized given its diverse presentations. (See 'Epidemiology and risk factors' below and "Embolism from aortic plaque: Thromboembolism".)