Abstract

Background18F-NaF positron emission tomography (PET) targets microcalcifications. We compared in vitro microPET assessed 18F-NaF uptake between culprit and non-culprit human carotid plaques. Furthermore, we compared 18F-NaF uptake with calcification visualized on microcomputed tomography (microCT). MethodsCarotid plaques from stroke patients undergoing surgery were incubated in 18F-NaF and scanned using a microPET and a microCT scan. The average PET assessed 18F-NaF uptake was expressed as percentage of the incubation dose per gram (%Inc/g). 18F-NaF PET volume of interest (VOI) was compared with CT calcification VOI. Results23 carotid plaques (17 culprit, 6 non-culprit) were included. The average 18F-NaF uptake in culprit carotid plaques was comparable with the uptake in non-culprit carotid plaques (median 2.32 %Inc/g [IQR 1.98 to 2.81] vs. median 2.35 %Inc/g [IQR 1.77 to 3.00], P = 0.916). Only a median of 10% (IQR 4 to 25) of CT calcification VOI showed increased 18F-NaF uptake, while merely a median of 35% (IQR 6 to 42) of 18F-NaF PET VOI showed calcification on CT. Conclusions18F-NaF PET represents a different stage in the calcification process than CT. We observed a similar PET assessed 18F-NaF uptake and pattern in culprit and non-culprit plaques of high-risk patients, indicating that this method may be of more value in early atherosclerotic stenosis development.

Highlights

  • Surgical removal of atherosclerotic plaques from the carotid artery highly reduces the risk of future stroke in symptomatic patients with ≥70% stenosis.[1]

  • Carotid plaques were collected from stroke patients who underwent carotid endarterectomy (CEA) at the Department of Surgery (Division of Vascular Surgery) of the University Medical Center Groningen (UMCG), between July 2015 and March 2016

  • The present study investigated in vitro microPET assessed 18F-NaF uptake, in culprit and non-culprit human carotid plaques

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Summary

Introduction

Surgical removal of atherosclerotic plaques from the carotid artery highly reduces the risk of future stroke in symptomatic patients with ≥70% stenosis.[1]. In order to improve risk stratification, research has been focused on the identification of plaques at risk for rupture, so-called vulnerable plaques.[6,7,8] Currently, plaque thickness and intraplaque processes, such as inflammation and microcalcification, are seen as important contributors to vulnerability. These processes have become targets of various molecular imaging techniques, as they potentially allow non-invasive risk stratification of individual patients with carotid artery stenosis.[9,10]. We compared 18F-NaF uptake with calcification visualized on microcomputed tomography (microCT)

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