Identification of Suspected Ruptured
Atherosclerotic Plaque
in Acute Ischemic Stroke on
18
F-Sodium
Fluoride Positron
Emission Tomography-Computed
Tomography
Guang-Uei Hung, MD; Chao-Hsien Hung, MD; Tai-Yi Chen, MD; Woon-Man
Kung, MD;
Cheng-Yu Wei, MD; Chia-Hung Kao, MD; Shinichiro Uchiyama, MD, PhD
An 81-year-old woman, with a past history of type 2 diabetes and hypertension, was brought to the emergency
room with acute-onset decreased responsiveness
accompanying right-sided weakness. Neurological examination indicated motor aphasia, right central facial palsy, and right
hemiparesis. Computed tomography (CT) showed no evidence of intracranial hemorrhage, while laboratory data were unremarkable.
Magnetic resonance imaging showed acute ischemic
stroke in the left middle cerebral artery territory (Figure 1A). Carotid sonography showed non-obstructive atherosclerotic
plaque in the bilateral internal carotid arteries near the bifurcation,
with only 36% luminal stenosis for the left side (Figure 1B) and 15% stenosis for the right side (Figure 1C). Electrocardiography
in the emergency room showed normal sinus rhythm
at 62 beats/min; 24-h Holter monitoring during admission did not show any atrial fibrillation. Based on these clinical conditions and imaging features, the etiology of stroke subtype according to TOAST classification was large-artery atherosclerotic stroke. For assessing possible ruptured (or vulnerable) plaques in carotid or cerebral arteries, 18F-sodium fluoride positron emission
informed consent was obtained and approved by the institutional review board. An irregularly calcified plaque was found in the left internal carotid artery near the bifurcation, corresponding to the plaque shown on sonography, with nearby NaF avidity (maximum standardized uptake value [SUVmax], 2.3) on PETCT (Figure 2), highly suspected as the culprit lesion for this stroke. Using blood pool NaF activity in the superior vena cava as a reference, the target-to-background ratio (TBR) was also calculated. TBR was 3.54 for the suspected culprit plaque and 2.14 for the non-culprit plaque in the right internal carotid artery
(65% increase). Rupture of an atherosclerotic plaque is the major cause of acute myocardial infarction and ischemic stroke.1,2 Most of the
high-risk (also called vulnerable) plaques are non-obstructive and are not identified on routine stress testing or other noninvasive imaging, thus, ruptured plaque is difficult to predict.3
According to the literature, 18F-NaF PET-CT was found to be
the first non-invasive imaging method to identify ruptured or vulnerable coronary plaque.4 This is a major clinical advance
for the prevention and treatment of acute coronary syndrome.
Although some studies have shown the usefulness of 18F-fluorodeoxyglucose
as a surrogate for vascular inflammation and macrophage burden,5,6 18F-NaF activity seems to distinguish culprit
plaque and non-culprit plaques better.4 18F-NaF PET-CT is a
clinical, routine imaging modality used for the evaluation of primary and metastatic bone tumors, because it detects area of active calcification and region of remodeling in the skeleton. In addition, 18F-NaF PET-CT can detect vascular microcalcification,
a major feature of vulnerable atherosclerotic plaques
unable to be detected on standard CT.7 The accuracy of localization
on 18F-NaF PET-CT may be better than multi-slice CT to predict unstable plaque in
acute coronary syndrome.8 Here,
we report the first case of ruptured carotid plaque successfully identified on 18F-NaF PET-CT in an acute ischemic stroke
patient. Further studies are warranted to establish its clinical value in the prevention of ischemic stroke.
