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17 Sternal Wound Infection andMediastinitis
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CT (79% vs. 16%), with comparable specicity
(99% vs. 98%). Evidently, the sensitivity and
specicity reported in these studies is highly
dependent on the interpretation criteria used.
Nonetheless, it appears that identication of cartilage infection is more challenging with both CT
and PET, as infection can be present with mild or
minimal increased uptake [29, 33].
In a retrospective study of 40 subjects who
underwent FDG-PET/CT following open-heart surgery, Hariri etal. reported a sensitivity and specicity of 91% and 97%, respectively, for the diagnosis
of SWI [32]. They showed that uptake patterns
(e.g., heterogeneous vs. homogeneous) were superior to uptake intensity (SUV
) for differentiating
max
between SWI and inammation, especially in the
rst 6months following surgery (Fig.17.3).
Interestingly, Liu etal. reported that utilization of FDG-PET/CT was associated with fewer
recurrences following debridement surgery compared to CT alone (21% vs. 41%, p= 0.03) and
shorter hospital stays following surgery (18 vs.
29days, p<0.001) [33]. These results highlight
the ability of FDG-PET/CT to accurately delineate the areas of infection in various tissues,
which can guide surgeons for optimal debridement. In addition, 10 subjects underwent repeated
FDG-PET/CT to assess response to therapy. Of
these, six subjects showed progression of infection as evidenced by an increase in uptake intensity or more extensive uptake on follow-up scans
compared to the baseline study, all of which had
recurrent infection requiring additional surgery
(excluding one subject who died) while the
remaining four subjects without evidence of progression on FDG-PET/CT did not have recurrence. These results suggest that FDG-PET/CT
could be used to assess debridement success.
However, caution must be taken when interpreting studies following recent debridement as postsurgical inammation may mimic infection
progression.
Fig. 17.3 Sagittal and maximal intensity projection
FDG-PET/CT images of a 55 year-old female without
SWI who underwent medial sternotomy for a Ross procedure 6months prior to the study. Despite the intense linear
uptake (with an SUV
activity is relatively homogeneous and compatible with
sterile postsurgical changes
of 6.0) along the sternum, the
max
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M. Pelletier-Galarneau et al.
Imaging Protocol
Use of a myocardial suppression protocol is not
always necessary in cases of suspected SWI, as
physiological myocardial uptake should not
interfere with study interpretation. However, a
suppression protocol should be used whenever
possible in patients who underwent valve replacement surgery or ascending aorta repair for optimal assessment of these structures. Furthermore,
for patients with nonspecic presentations (e.g.,
fever of unknown origin) and in whom IE is not
excluded, suppression protocols should be used.
Approximately 185–370MBq of FDG is injected
intravenously. Whole-body PET/CT images are
acquired from the base of the skull to the midthigh 60–90min post tracer injection.
Image Interpretation
Distinction between benign postoperative
inammation and infection can be challenging,
especially early after surgery. Hariri et al.
showed that uptake intensity alone is not sufcient in order to accurately differentiate between
infection and inammation [32]. When PET
imaging was performed within 6months following surgery, sternal SUV
different between patients with sternal osteitis
was not signicantly
max
and those without infection (8.4 vs. 7.8 p=0.72).
On the other hand, in subjects with remote surgery (>6 months), sternal SUV
was signi-
max
cantly higher in patients with sternal osteitis
compared to noninfected subjects (8.5 vs. 1.3,
p< 0.0001) [32]. In noninfected sterna, uptake
intensity varied signicantly in the rst 6months
following sternotomy, with SUV
ranging from
max
3.2 to 18.6, highlighting the limited value of this
metric to distinguish infection from inammation [32].
For the evaluation of SWI, FDG-PET interpretation should integrate information on tracer
uptake pattern, especially in the early postoperative period, similar to evaluation of prosthetic
valves and vascular graft infections [31, 34, 35].
Diffuse uptake limited to the sternotomy site,
regardless of its intensity, is associated with sterile inammation in most cases (Fig.17.4). On the
other hand, focal uptake, uptake associated with
sternal wires, and heterogeneous uptake extending into the adjacent soft tissues is compatible
with infection (Figs.17.5, 17.6 and 17.7).
In some cases, focal uptake may be seen even
in the absence of infection. For instance, utilization of biological glue has been associated with
intense focal uptake which may persist for
months after surgery [34, 36]. In addition, focal
uptake may be seen around sternal wires, especially in the presence of mechanical strain [32].
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uptake
Diffuse low-grade
uptake
Diffuse high-grade
Focal uptake
MIP
PET CT PET/CT
uptake
Sternal wire
extension
Soft-tissue
Fig. 17.4 Anterior maximal intensity projection (MIP)
images, sagittal PET, CT, and fused PET/CT images of
the FDG sternotomy uptake patterns. Diffuse uptake is
associated with benign postsurgical changes while focal
uptake and soft tissue uptake are suggestive of infection.
Reproduced with permission from [32]
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M. Pelletier-Galarneau et al.
a
d
b
c
Fig. 17.5 A 78-year-old diabetic male, who underwent a
CABG and aortic valve replacement with medial sternotomy 3 weeks prior to imaging, was clinically suspected of
having mediastinitis. Sagittal (a) and axial (b, c) FDGPET/CT images as well as maximal projection images (d)
demonstrate intense uptake extending into the anterior
mediastinum and retro-sternal region, compatible with
mediastinitis. In addition, a pericardial uid collection
with circumferential FDG uptake (arrow) is compatible
with an abscess
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a
bc
de
Fig. 17.6 Sternal osteitis can also be seen in patients
without sternotomy. This 78-year-old male with mitral
valve endocarditis (a, white arrow) with septic emboli
causing spondylitis as seen on the sagittal CT (b) and
fused FDG-PET/CT (c) images (orange arrow). Axial CT
(d) and fused FDG-PET/CT images (e) also show extensive destruction of the manubrium (yellow arrow) associated with intense FDG uptake extending in the soft tissues
anteriorly, consistent with osteomyelitis
Fig. 17.7 Example of a patient with supercial sternal
wound infection with (left) a sagittal CT image demonstrating fat inltration and a soft tissue collection anterior
to the sternum and (right) a sagittal FDG-PET/CT image
demonstrating intense uptake limited to the soft tissue.
Manubrium uptake, although intense, is linear and contained within the sternal body, consistent with postoperative changes
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M. Pelletier-Galarneau et al.
Conclusion
SWIs are the most important cause of surgical
site infections following open-heart surgery. The
distinction between SSWI and DSWI is critical,
as the treatment and prognosis of these two entities differs signicantly. The role of FDG-PET
for the investigation of patients with suspected
SWI is growing, and this modality may provide
valuable information for the initial diagnosis of
SWI, differentiating between deep and supercial SWI, evaluating disease extent, aiding in surgical planning, as well as assessing response to
antibiotic therapy and the effects of surgical
debridement.
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Part IV
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Atherosclerotic Disease
Atherosclerosis Imaging
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AzarRadfar, ShadyAbohashem,
MichaelT.Osborne, andAhmedTawakol
18
Introduction
Cardiovascular disease (CVD) is the chief cause
of mortality worldwide [1]. Though previously
depicted as a monotonous process of subendothelial accumulation of gruel, atherosclerosis is now
understood to be a progressive inammatory process [2–4]. Inammation is the major pathological driver of several human maladies, including
CVD and malignancies. Notably, both acute and
chronic inammation play important roles in the
pathogenesis of numerous CVDs, of which atherosclerosis is of paramount importance [3].
Imaging atherosclerotic inammation and
other biological processes related to plaque formation and progression may provide important
insights that could facilitate the development of
A. Radfar
Cardiology Division, Massachusetts General
Hospital, Harvard Medical School, Boston, MA,
USA
S. Abohashem
Cardiovascular Imaging Research Center,
Massachusetts General Hospital, Harvard Medical
School, Boston, MA, USA
M. T. Osborne · A. Tawakol (*)
Cardiology Division, Massachusetts General
Hospital, Harvard Medical School, Boston, MA,
USA
Cardiovascular Imaging Research Center,
Massachusetts General Hospital, Harvard Medical
School, Boston, MA, USA
e-mail: atawakol@mgh.harvard.edu
new strategies to mitigate CVD. Further, it is
hoped that molecular imaging may potentially
improve current tools of risk stratication for atherosclerotic diseases, allowing more personalized disease management. In this chapter, we
focus on molecular imaging techniques used to
assess atherosclerotic plaque biology.
Atherosclerotic Plaque Biology
Atherosclerosis involves several distinct disease
pathways that collude to initiate and propagate
biologically active atheromatous plaques. The
disease is instigated by subendothelial accumulation of oxidized LDL, mostly in areas with disturbed laminar ow, which prompts a chronic
inammatory response in the affected arterial
wall. The local activated endothelial cells express
leukocyte adhesion molecules which help recruit
additional inammatory cells (i.e., monocytes
and T-lymphocytes). Monocytes then differentiate into resident lipid-laden foam cells.
Monocyte-derived macrophages, T cells, B cells,
dendritic cells, mast cells, and smooth muscle
cells with myobroblast characteristics constitute the main cellular components of atheroma.
The subsequent release of inammatory mediators and cytokines perpetuates the inammatory
cascade, leading to further accumulation of cellular and lipid material and plaque enlargement.
The apoptotic death of macrophages and smooth
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2022
M. Pelletier-Galarneau, P. Martineau (eds.), FDG-PET/CT and PET/MR in Cardiovascular
Diseases, https://doi.org/10.1007/978-3-031-09807-9_18
241
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A. Radfar et al.
Fig. 18.1 Molecular targets for imaging of atherosclerosis using PET. Macrophages, as critical cellular
constituents of atherosclerotic plaques, actively utilize
glucose. Accordingly, 18F-FDG and 18F-FDM, isomers
of glucose, are also taken up by macrophages. Several
other receptors are expressed on macrophages and act
as targets for PET tracers, including somatostatin receptors (68Ga-DOTATATE), translocator protein recep-
muscle cells further contribute to necrotic core
formation within advanced plaques. Subsequently,
thinning of the atheromatous brous cap is then
induced by the increased matrix metalloproteinases activity secreted by recruited inammatory
cells along with microcalcications (i.e., calcications <50μm in size) in the arterial intima. The
necrotic lipid core, thinning of the brous cap,
microcalcication, and heightened inammatory
state are all factors that predispose high-risk
vulnerable plaque to rupture resulting in atherothrombotic events [5]. Several of these biological
processes are attractive targets for molecular
imaging of atherosclerosis (Fig.18.1) [6].
Inammation inAtherosclerosis
Inammation is at the crossroads of the pathways that promote the progression of atherosclerotic CVD.In fact, basic science and human
autopsy studies of atherosclerotic diseases
tors (11C- PK11195), and macrophage cell membranes
(18F-FMCH). Additional radiotracers target other hallmarks of atherosclerotic inammation, such as microcalcication (18F-sodium uoride), neoangiogenesis
(68Ga-NOTA- RGD and 18F-Galacto-RGD), and cellular
hypoxia (18F-FMISO). FDG uorodeoxyglucose, FDM
uoro- deoxymannose, PET positron emission tomography. (Reprinted with permission [6])
have demonstrated that inammation plays an
important role in several phases of atherosclerosis, from plaque initiation to plaque progression and the potentiation of atherothrombotic
events [7].
This important role for inammation in atherosclerotic CVD has long been supported by the
well-established association between inammatory biomarkers and subsequent atherothrombotic events. Postmortem serum analysis of
patients with severe coronary artery disease and
sudden death revealed signicant elevation of
high-sensitivity C-reactive protein (hsCRP).
There was also a robust association between
hsCRP levels, supercial foam cells, expanded
necrotic cores, and thin cap atheromatous plaques
[8]. Moreover, inammatory biomarkers (e.g.,
hsCRP) have been independently associated with
CVD risk, which can be particularly useful for
rening risk among individuals with intermediate
risk by traditional criteria [9].
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