The dream of imaging coronary artery
inﬂammation with FDG PET/CT imaging
R. Glenn Wells, PhD, FCCPM,
and Terrence D. Ruddy, MD, FRCPC
Division of Cardiology, University of Ottawa Heart Institute, Ottawa, Canada
Received May 16, 2016; accepted May 17, 2016
‘‘Always dream and shoot higher than you know you can do.’’
Inﬂammation plays a major role in the development
of atherosclerotic plaque
and has been proposed as a
marker of plaque vulnerability to identify patients at risk
of vascular events.
Plaque inﬂammation is character-
ized by increased macrophage inﬁltration and FDG
uptake has been shown to correlate strongly with the
number of macrophages present in plaques.
Rudd et al
showed that FDG accumulated and could be measured
in vivo in carotid artery plaques associated with recent
transient ischemic attacks but that asymptomatic arteries
had less FDG accumulation.
Thus, FDG uptake can be
used to measure the degree of inﬂammation in tissues as
conﬁrmed with carotid endarterectomy specimens using
FDG uptake in carotid
arteries has also been shown to correlate with anatom-
ical and histological features of plaques that are at high
risk for rupturing.
Carotid inﬂammation measured with
FDG PET/CT has been shown to predict subsequent
ipsilateral cerebrovascular events in a prospective study
of 60 patients with recent stroke.
Much of the work investigating the use of PET/CT
to image vulnerable plaques with FDG has focused on
major vessels such as the aorta and carotids. Similar
studies with FDG PET/CT imaging of coronary plaques
are limited in number due to the difﬁculty of imaging the
See related article, pp. 1161–1170
smaller coronary vessels. Consequently, studies that
have explored plaque inﬂammation imaging in the
coronary arteries have tended to target plaques in the
left main artery and proximal major arteries.
are less conclusive with coronary imaging, with one
study showing FDG uptake in the appropriate culprit
lesion in patients with acute coronary syndromes as
compared to patients with stable coronary artery dis-
and another study
demonstrated that FDG uptake
was lowered in the left main artery following treatment
with pioglitazone which is suspected of having a plaque-
stabilizing effect. However, one conﬂicting study in 40
myocardial infarction patients
showed no differences
in FDG uptake between culprit and non-culprit plaques
and identiﬁable focal coronary FDG uptake in only 4 of
40 patients with stable angina. Robust identiﬁcation of
plaque inﬂammation with FDG in the coronary arteries,
while an attractive possibility, remains elusive, partic-
ularly in the more distal coronary arteries.
There are several challenges to measuring vulnerable
plaque in the coronary arteries using FDG.
Some of the
technical issues that need to be overcome are
Interference from the background signal of FDG uptake in
the myocardium. (2) The signal dilution from partial
volume effects. The voxel size typically used for PET
imaging is 4-6 mm and the best resolution achievable in
most PET scanners is similarly about 4-5 mm. The size of
the plaques being targeted is smaller than this as the
coronary arteries start at approximately 4 mm in diameter.
When the target being imaged is small, the signal from
that target is diluted into the volume of the voxel and the
signal intensity is correspondingly diminished. (3)
Finally, movement of the heart due to cardiac contraction
and respiratory motion which blurs out the signal over a
larger volume and thus also decreases signal intensity.
The presence of myocardial signal drowns out the
signal from the arterial plaque located immediately
Reprint requests: R. Glenn Wells, Cardiac Imaging Program, University
of Ottawa Heart Institute, Ottawa, Canada; email@example.com
J Nucl Cardiol 2017;24:1171–4.
Copyright Ó 2016 American Society of Nuclear Cardiology.