Abstract
Atherosclerosis involves gradual arterial hardening secondary to the building up of lipid-laden plaques in the vessel wall, which may cause vascular stenosis, thromboembolism, or overgrowth across perforator arterial ostia.[1][1],[2][2] Despite common vascular risk factors and overlapping
Highlights
Recent technologic advances improving the clinical applicability of 3D high-resolution intracranial vessel wall imaging challenge these traditional assumptions.[5,6,7,9]
Because vascular remodeling in the form of compensatory dilation may occur secondary to plaque formation, traditional lumen-based approaches such as CT or MR angiography on which some historical epidemiologic or symptomatic stroke studies were based could underestimate the true prevalence of underlying intracranial atherosclerosis.[4,6,7,8,9,10]
Vessel wall imaging offers the opportunity to elucidate the pathophysiologic underpinnings of intracranial large-artery atherosclerosis, which may serve as potential targets for stroke prevention and treatment.[5,7]
Summary
Atherosclerosis involves gradual arterial hardening secondary to the building up of lipid-laden plaques in the vessel wall, which may cause vascular stenosis, thromboembolism, or overgrowth across perforator arterial ostia.[1,2] Despite common vascular risk factors and overlapping atherogenic molecular pathways, differential prevalence, onset, and progression of atherosclerosis exist across arterial beds and ethnic groups (eg, inordinate prevalence of intracranial atherosclerosis in Asians and Africans in epidemiologic data), suggesting multifactorial variation underlying the expression of this systemic disease.[2,3,4,5,6,7,8] Intracranial large-artery atherosclerosis is a known strong risk factor for ischemic stroke, associated with a high risk of recurrent ischemic stroke.[1].
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