Why the study?
Little data are available on the prevalence of calcified nodules in carotid arteries or their associations with cerebrovascular events.
This study evaluates the pathological prevalence and distribution of calcified nodules in carotid artery stenosis using endarterectomy specimens.
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Calcified nodules' role in carotid plaque vulnerability remains uncertain; leaves open whether they predict events or warrant targeted imaging.
Carotid artery stenosis is an important cause of cerebral ischemic events.Several studies have reported that this pathology is responsible for up to 25% of cerebral ischemic events. 1,2he significance of calcification in atherosclerosis remains controversial and the relationships between vascular calcification and plaque vulnerability or cerebral ischemic events are not fully understood.Calcified nodules (CNs) are eruptive calcified masses that protrude into the blood vessel lumen.In the field of cardiology, CNs are pathologically associated with acute coronary syndrome (ACS) 3 and other major cardiovascular events such as stent thrombosis and myocardial infarction after percutaneous coronary intervention. 4However, little data are available on associations with cerebrovascular events or prevalence in the carotid arteries.The purpose of this study was to evaluate the prevalence and distribution of CNs in carotid arteries using carotid endarterectomy (CEA) specimens in correlation with clinical symptoms.This study retrospectively analyzed 508 consecutive patients with carotid artery stenosis who underwent CEA at the National Cerebral and Cardiovascular Center in Osaka, Japan between April 2008 and March 2023.Prevalences of different degrees of stenosis were as follows: (1) none to mild stenosis (0-49%), n = 28 (6%); (2) moderate stenosis (50-69%), n = 97 (19%); and (3) severe stenosis (70-95%), n = 383 (75%) (see details in the Supplementary Materials).This study was approved by the institutional review board.CEA specimens were fixed overnight in 10% formalin neural-buffered solution, then decalcified.Specimens were subsequently cut into 5-mm sections from the bifurcation to the distal internal carotid artery (ICA) and embedded in paraffin.Serial 3-µm thick sections were stained with hematoxylin and eosin, Masson's trichrome, and Elastica van Gieson stains for histological evaluation.
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Yamada et al. (2025) studied this question.
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