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23 Normal Variants, Not-So-Normal Variants, andPitfalls ofFDG-PET inCardiovascular Imaging
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Right Ventricular Uptake
Abnormal myocardial glucose metabolism in
the right ventricle (RV) in the form of diffuse
tracer uptake within the ventricular wall has
been reported in multiple previous studies and is
often related to a shift in metabolism related to
increased RV pressures and/or hypertrophy
caused by pulmonary artery hypertension, either
idiopathic or secondary to underlying pulmonary disease [13, 14]. Compared to the LV, FDG
uptake in the RV walls is usually much less conspicuous [8] (Figs.23.5 and 23.6).
Some studies have shown a causal relationship
between FDG uptake in the RV and RV dysfunction, with increased RV uptake correlating with
a decrease in systolic function [15–17]. Mehmet
etal. conrmed that patients with higher RV glucose metabolic rate tend to have higher RV loads
and worse function [13]. Mielniczuk etal. have
shown a signicant relation between increased
uptake in the RV and a decrease in RV ejection
fraction, even after applying partial-volume correction owing to differences in wall thickness
[18]. In patients with idiopathic pulmonary artery
hypertension, the degree of RV uptake has been
shown to be elevated at baseline and decreased
after treatment [13, 19]. Studies have also shown
that the degree of FDG uptake within the RV wall
correlates with serum levels of N-terminal probrain natriuretic peptide (NT-proBNP) in patients
with idiopathic pulmonary arterial hypertension
[20, 21]. Furthermore, in a study examining
patients with coronary artery disease and ischemic cardiomyopathy, the degree of FDG uptake
in the RV was associated with RV pressure overload, with higher ventricular uptake (both left
and right) associated with poor outcomes [22].
Additional studies have conrmed the prognostic
signicance of increased RV uptake in patients
with pulmonary hypertension [23–25]. As such,
the presence of diffuse RV wall uptake should be
considered a “not-so-normal” variant; however,
the degree of clinical signicance of this nding
and its interpretation in routine clinical practice
requires additional study.
Fig. 23.6 Axial PET image of the chest of a 79-year-old
female patient with interstitial lung disease (arrows).
There is physiological FDG uptake in the right ventricular
wall (arrowhead), well above the blood pool activity.
There is also intense diffuse accumulation of the radiotracer in the left ventricular walls and papillary muscle
ab
Fig. 23.5 Axial PET images of the chest of a 54-year-old
woman with pulmonary hypertension demonstrating relatively intense but diffuse uptake through the right ven-
tricular wall (a, arrow). Note the dilation of the pulmonary
trunk (b, arrow), in keeping with elevated pulmonary arterial pressure
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I. Bloise et al.
Atrial Uptake
In the majority of patients, atria are devoid of
signicant FDG activity. Atrial activity has been
studied since the late 1990s when Fujii et al.
reported FDG uptake in the walls of the right
atrium in 10 of 2367 (0.4%) patients being
assessed for oncological indications [26]. These
authors found that patients with atrial uptake suffered from cardiac disorders, with atrial brillation particularly prevalent in their subjects. They
also noted that right atrial activity was much
more conspicuous than left atrial uptake. A
recent study showed that 30% of patients with
atrial brillation (AF) presented with diffuse
atrial FDG uptake involving at least the right
atrial wall (Fig. 23.7) and, of these, approximately one third also had activity in the left atrial
wall [27].
A predilection for right atrial uptake (when
compared to the left) in patients with AF was
also conrmed in the study by Xie et al. [28].
Interestingly, these authors compared the atrial
uptake to the activity seen in epicardial adipose
tissue (EAT). They found that atrial and atrial
appendage uptake was linearly correlated with
activity in the EAT.In a subsequent prospective
study, the same group demonstrated an association between atrial uptake and levels of
NT-proBNP, in addition to an association
between increased right atrial levels and successful termination of AF by radiofrequency
catheter ablation [29]. These ndings, together
with the known association between EAT activity and inammation, suggest that FDG PET
may provide a new lens by which to observe the
known relationship between inammation and
atrial brillation [30, 31].
A recent study by Sinigaglia etal. further conrmed the association between atrial uptake and
atrial brillation, while also nding an association with an increased risk of cardioembolic
stroke [27]. In fact, the authors report that, on
multivariate analysis, right atrial uptake had a
greater odds ratio for stroke than conventional
risk factors (including current smoking, hypertension, diabetes, and dyslipidemia).
In summary, atrial activity should be considered “not-so-normal” as it most likely
reects an element of underlying cardiovascular pathology; however, further research is
required before the implications of incidental
atrial activity on FDG PET translate to routine
clinical practice.
a b
Fig. 23.7 PET images showing intense diffuse right atrial uptake in this patient with atrial brillation on MIP (a) and
axial images (b). Left ventricular basal lateral uptake is nonspecic and represents incomplete myocardial suppression
23 Normal Variants, Not-So-Normal Variants, andPitfalls ofFDG-PET inCardiovascular Imaging
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349
Pitfalls
Knowledge of the physiological FDG distribution and glucose metabolism in every cardiac
chamber, as well as the normal variants, is imperative in order to avoid misinterpretation and misdiagnoses. Most pitfalls take the form of focal,
occasionally intense, uptake localizing within the
various cardiac chambers or walls. Such ndings
can be highly suggestive of pathology, particularly
masses, but frequently correspond to benign processes; however, with knowledge of the imaging
and clinical features, physiological distribution,
and a careful eye, these can be recognized and
misdiagnosis avoided.
Focal uptake in the left ventricular wall is a
common pattern of physiologic FDG uptake and
typically attributable to physiological uptake in
papillary muscles, although rarely displayed in isolation [32]. When not related to the papillary muscles (Figs.23.3 and 23.4), the patient history should
be carefully evaluated as focal uptake can also be
related to hibernating myocardium [2, 33–35], cardiac sarcoidosis, and increase stress on papillary
muscles (dilated cardiomyopathy, valvular insufciency, valvular stenosis, chordal failure, etc.).
A relatively common nding is increased
FDG accumulation associated with fatty deposition within the interatrial septum—a condition
typically referred to as lipomatous hypertrophy
of the interatrial septum (LHIAS)—seen in
approximately 3% of patients [36, 37]. In these
cases, image reconstruction with proper CT
fusion to ensure anatomical correlation is of
utmost importance. The CT ndings in LHIAS
typically consist of a “dumbbell” shape fat density lesion localizing to the interatrial septum—
this is due to fat accumulation cephalad and
caudal to the fossa ovalis, with the fossa itself
typically spared. While the mechanism of uptake
is generally considered to be the same as that of
brown fat, some authors have suggested that the
FDG uptake in LHIAS may represent inammation [38]. Irrespective of the mechanism of
uptake, LHIAS can be easily recognized due to a
pathognomonic appearance on CT (Fig. 23.8).
The presence of hypermetabolic brown adipose
tissue in the mediastinum, although uncommon,
ba
c
Fig. 23.8 Lipomatous hypertrophy of the interatrial septum (LHIAS) is a potential pitfall in cardiac imaging but
can be easily recognized by correlating with the CT images.
In this 52-year-old man, unusually avid focal cardiac uptake
can be seen on the MIP images (a, arrow), localizing to the
interatrial septum on axial fused images (b, arrow).
Comparison to the unenhanced CT images (c, arrow)
reveals corresponding fat density, diagnostic of LHIAS
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Fig. 23.9 Diffuse uptake can occasionally be seen in the
atrial appendage. The signicance of this nding remains
uncertain
is another potential pitfall, especially in patients
that do not present it in other usual regions such
as in the cervical and paravertebral soft tissues
[39].
Focal activity can also be seen within the atrial
appendages. Although often associated with cardiac disease, this nding can also be present in
patients without cardiac pathology [40, 41]. In
addition, focal activity has been reported within
the crista terminalis, which is the muscular band
at the junction of the right atrium and appendage,
and which contains the sinoatrial node [42]. The
reason for uptake in these structures remains
uncertain (Fig.23.9).
Conclusion
In order to condently identify pathological patterns of FDG uptake in the heart, one must rst
be cognizant of the normal patterns of myocardial activity, as well as of the potential pitfalls
that are frequently seen during cardiac imaging.
References
1. Davidson CQ, Phenix CP, Tai T, Khaper N, Lees
SJ. Searching for novel PET radiotracers: imaging
cardiac perfusion, metabolism and inammation. Am
J Nucl Med Mol Imaging. 2018;8(3):200–27.
I. Bloise et al.
2. Santos BS, Ferreira MJ. Positron emission tomography in ischemic heart disease. Rev Port Cardiol.
2021;38(8):599–608.
3. Tamaki N, Morita K, Kuge Y, Tsukamoto E. The
role of fatty acids in cardiac imaging. J Nucl Med.
2000;41(9):1525–34.
4. Yoshinaga K, Tamaki N.Imaging myocardial metabolism. Curr Opin Biotechnol. 2007;18:52–8.
5. Inglese E, Leva L, Matheoud R, Sacchetti G, Secco
C, Gandolfo P, et al. Spatial and temporal heterogeneity of regional myocardial uptake in patients
without heart disease under fasting conditions on
repeated whole-body 18F-FDG PET/CT.J Nucl Med.
2007;48(10):1662–9.
6. Gropler RJ, Siegel BA, Lee KJ, Moerlein SM,
Perry DJ, Bergmann SR, et al. Nonuniformity
in myocardial accumulation of uorine-18Fluorodeoxyglucose in normal fasted humans. J Nucl
Med. 1990;31(11):1749–56.
7. Maurer AH, Burshteyn M, Adler LP, Steiner
RM. How to differentiate benign versus malignant
cardiac and paracardiac 18F FDG uptake at oncologic
PET/CT.Radiographics. 2011;31(5):1287–305.
8. Lobert P, Brown RKJ, Dvorak RA, Corbett JR,
Kazerooni EA, Wong KK. Spectrum of physiological and pathological cardiac and pericardial
uptake of FDG in oncology PET-CT. Clin Radiol.
2013;68(1):e59–71.
9. Zanco P, Desideri A, Mobilia G, Cargnel S, Milan
E, Celegon L, et al. Effects of left bundle branch
block on myocardial FDG PET in patients without
signicant coronary artery stenoses. J Nucl Med.
2000;41(6):973–7.
10. Nowak B, Sinha AM, Schaefer WM, Koch K-C,
Kaiser H-J, Hanrath P, et al. Cardiac resynchronization therapyhomogenizes myocardial glucosemetabolism and perfusion in dilatedcardiomyopathy
and left bundle branch block. J Am Coll Cardiol.
2003;41(9):1523–8.
11. Nose H, Otsuka H, Otomi Y, Terazawa K, Takao
S, Iwamoto S, et al. The physiological uptake pattern of 18F-FDG in the left ventricular myocardium
of patients without heart disease. J Med Invest.
2014;61:55–8.
12. Israel O, Weiler-Sagie M, Rispler S, Bar-Shalom R,
Frenkel A, Keidar Z, etal. PET/CT quantitation of the
effect of patient-related factors on cardiac 18F-FDG
uptake. J Nucl Med. 2007;48(2):234–9.
13. Wang L, Li W, Yang Y, Wu W, Cai Q, Ma X, et al.
Quantitative assessment of right ventricular glucose
metabolism in idiopathic pulmonary arterial hypertension patients: a longitudinal study. Eur Heart J
Cardiovasc Imaging. 2016;17(10):1161–8.
14. Basu S, Alzeair S, Li G, Dadparvar S, Alavi
A. Etiopathologies associated with intercostal
muscle Hypermetabolism and prominent right
ventricle visualization on 2-Deoxy-2[F-18]uorod-glucose- positron emission tomography: signi-
23 Normal Variants, Not-So-Normal Variants, andPitfalls ofFDG-PET inCardiovascular Imaging
https://t.me/medicina_free
351
cance of an incidental nding and in the setting
of a known pulmonary disease. Mol Imaging Biol.
2007;9(6):333–9.
15. Ohira H, deKemp R, Pena E, Davies RA, Stewart DJ,
Chandy G, etal. Shifts in myocardial fatty acid and
glucose metabolism in pulmonary arterial hypertension: a potential mechanism for a maladaptive right
ventricular response. Eur Heart J Cardiovasc Imaging.
2016;17(12):1424–31.
16. Lundgrin EL, Park MM, Sharp J, Tang WHW,
Thomas JD, Asosingh K, etal. Fasting 2-Deoxy-2[18F]uoro--glucose positron emission tomography
to detect metabolic changes in pulmonary arterial
hypertension hearts over 1 year. Ann Am Thorac Soc.
2013;10(1):1–9.
17. Yang T, Wang L, Xiong C-M, He J-G, Zhang Y, Gu Q,
etal. The ratio of 18F-FDG activity uptake between
the right and left ventricle in patients with pulmonary hypertension correlates with the right ventricular
function. Clin Nucl Med. 2014;39(5):426–30.
18. Mielniczuk LM, Birnie D, Ziadi MC, deKemp RA,
DaSilva JN, Burwash I, et al. Relation between
right ventricular function and increased right ventricular [18F]Fluorodeoxyglucose accumulation in
patients with heart failure. Circ Cardiovasc Imaging.
2011;4(1):59–66.
19. Oikawa M, Kagaya Y, Otani H, Sakuma M,
Demachi J, Suzuki J, et al. Increased [18F]
Fluorodeoxyglucose accumulation in right ventricular free wall in patients with pulmonary hypertension
and the effect of Epoprostenol. J Am Coll Cardiol.
2005;45(11):1849–55.
20. Hagan G, Southwood M, Treacy C, Ross RM, Soon
E, Coulson J, etal. 18FDG PET imaging can quantify
increased cellular metabolism in pulmonary arterial
hypertension: a proof-of-principle study. Pulm Circ.
2011;1(4):448–55.
21. Can MM, Kaymaz C, Tanboga IH, Tokgoz HC,
Canpolat N, Turkyilmaz E, et al. Increased right
ventricular glucose metabolism in patients with
pulmonary arterial hypertension. Clin Nucl Med.
2011;36(9):743–8.
22. Tsai S-Y, Wu Y-W, Wang S-Y, Shiau Y-C, Chiu K-M,
Tsai H-Y, et al. Clinical signicance of quantitative
assessment of right ventricular glucose metabolism in patients with heart failure with reduced
ejection fraction. Eur J Nucl Med Mol Imaging.
2019;46(12):2601–9.
23. Kluge R, Barthel H, Pankau H, Seese A, Schauer J,
Wirtz H, etal. Different mechanisms for changes in
glucose uptake of the right and left ventricular myocardium in pulmonary hypertension. J Nucl Med.
2005;46(1):25–31.
24. Tatebe S, Fukumoto Y, Oikawa-Wakayama M,
Sugimura K, Satoh K, Miura Y, et al. Enhanced
[18F] uorodeoxyglucose accumulation in the right
ventricular free wall predicts long-term prognosis of
patients with pulmonary hypertension: a preliminary
observational study. Eur Heart J Cardiovasc Imaging.
2014;15(6):666–72.
25. Li W, Wang L, Xiong C-M, Yang T, Zhang Y, Gu Q,
etal. The prognostic value of 18F-FDG uptake ratio
between the right and left ventricles in idiopathic
pulmonary arterial hypertension. Clin Nucl Med.
2015;40(11):859–63.
26. Fujii H, Ide M, Yasuda S, Takahashi W, Shohtsu A,
Kubo A.Increased FDG uptake in the wall of the right
atrium in people who participated in a cancer screening program with whole-body PET.Ann Nucl Med.
1999;13(1):55–9.
27. Sinigaglia M, Mahida B, Piekarski E, Chequer R,
Mikail N, Benali K, etal. FDG atrial uptake is associated with an increased prevalence of stroke in patients
with atrial brillation. Eur J Nucl Med Mol Imaging.
2019;46(6):1268–75.
28. Xie B, Chen B-X, Wu J-Y, Liu X, Yang M-F.Factors
relevant to atrial 18F-uorodeoxyglucose uptake in
atrial brillation. J Nucl Cardiol. 2018;27(5):1501–12.
29. Xie B, Chen B-X, Nanna M, Wu J-Y, Zhou Y, Shi
L, et al. 18F-uorodeoxyglucose positron emission
tomography/computed tomography imaging in atrial
brillation: a pilot prospective study. Eur Heart J
Cardiovasc Imaging. 2022;23(1):102–12.
30. Mazurek T, Zhang L, Zalewski A, Mannion JD, Diehl
JT, Arafat H, et al. Human Epicardial adipose tissue
is a source of inammatory mediators. Circulation.
2003;108(20):2460–6.
31. Hu Y-F, Chen Y-J, Lin Y-J, Chen S-A. Inammation
and the pathogenesis of atrial brillation. Nat Rev
Cardiol. 2015;12(4):230–43.
32. Betancourt Cuellar SL, Palacio D, Benveniste MF,
Carter BW, Gladish G. Pitfalls and misinterpretations of cardiac ndings on PET/CT imaging: a careful look at the heart in oncology patients. Curr Probl
Diagn Radiol. 2019;48(2):172–83.
33. Haider A, Bengs S, Schade K, Wijnen WJ, Portmann
A, Etter D, etal. Myocardial 18F-FDG uptake pattern
for cardiovascular risk stratication in patients undergoing oncologic PET/CT.J Clin Med. 2020;9(7):2279.
34. Ando V, Koestner S, Pruvot E, Kamani C-H,
Ganiere V. Cardiac sarcoidosis involving the papillary muscle: a case report. Heart Rhythm Case Rep.
2021;7(12):801–5.
35. Duchenne J, Turco A, Bézy S, Ünlü S, Pagourelias ED,
Beela AS, etal. Papillary muscles contribute signicantly more to left ventricular work in dilated hearts.
Eur Heart J Cardiovasc Imaging. 2019;20(1):84–91.
36. Laura DM, Donnino R, Kim EE, Benenstein R,
Freedberg RS, Saric M. Lipomatous atrial septal
hypertrophy: a review of its anatomy, pathophysiology, multimodality imaging, and relevance to percutaneous interventions. J Am Soc Echocardiogr.
2016;29(8):717–23.
37. Kuester LB, Fischman AJ, Fan C-M, Halpern EF,
Aquino SL. Lipomatous hypertrophy of the interatrial septum: prevalence and features on fusion 18F
352
https://t.me/medicina_free
I. Bloise et al.
uorodeoxyglucose positron emission tomography/
CT.Chest. 2005;128(6):3888–93.
38. Zukotynski KA, Israel DA, Kim CK.FDG uptake in
lipomatous hypertrophy of the interatrial septum is
not likely related to brown adipose tissue. Clin Nucl
Med. 2011;36(9):767–9.
39. Truong MT, Erasmus JJ, Munden RF, Marom
EM, Sabloff BS, Gladish GW, et al. Focal FDG
uptake in mediastinal Brown fat mimicking malignancy: a potential pitfall resolved on PET/CT. Am J
Roentgenol. 2004;183(4):1127–32.
40. Nguyen BD.PET demonstration of left atrial appendage in chronic atrial brillation. Clin Nucl Med.
2005;30(3):177.
41. Okura K, Maeno K, Hirazawa M, Takemori H, Toya D,
Tanaka N, etal. Fluorodeoxyglucose accumulation in
the left atrial appendage of a patient with paroxysmal
atrial brillation. J Cardiol Cases. 2012;5(1):e32–5.
42. Minamimoto R. Series of myocardial FDG uptake
requiring considerations of myocardial abnormalities
in FDG-PET/CT.Jpn J Radiol. 2021;39(6):540–57.
Cardiovascular FDG-PET Atlas
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ofCases
YousifA.Lucinian, PatrickMartineau,
andMatthieuPelletier-Galarneau
24
Acronyms
AF Atrial brillation
AFB Acid-fast bacillus
AV block Atrioventricular block
CAD Coronary artery disease
CCTA Coronary computed tomography
angiography
CIED Cardiac implantable electronic
device
CIED-LI Cardiac implantable electronic device
lead infection
COPD Chronic obstructive pulmonary
CRP C-reactive protein
CS Cardiac sarcoidosis
CT Computed tomography
CTA Computed tomography angiography
CTPA Computed tomography pulmonary
angiography
DES Drug-eluting stent
DSWI Deep sternal wound infection
ECMO Extracorporeal membrane
oxygenation
Y. A. Lucinian M. Pelletier-Galarneau (*)
Montreal Heart Institute, Montréal, QC, Canada
e-mail: yousif.al-ali@umontreal.ca;
Matthieu.pelletier-galarneau@icm-mhi.org
P. Martineau
BC Cancer Agency, Vancouver, BC, Canada
e-mail: patrick.martineau@bccancer.bc.ca
ER Emergency room
FDG
GCA Giant-cell arteritis
GPI Generator pocket infection
HRS Heart and Rhythm Society
hs-cTnT High-sensitivity cardiac troponin T
ICD Implantable cardioverter-debrillator
IE Infective endocarditis
JCS Japan Circulation Society
LAD Left anterior descending coronary
LDCT Low-dose CT scan
LVEF Left ventricular ejection fraction
LVV Large-vessel
MPA Main pulmonary artery
MPI Myocardial perfusion imaging
MRI Magnetic resonance imaging
MSSA Methicillin-susceptible
NVE Native valve infective endocarditis
PAS Pulmonary artery sarcoma
PE Pulmonary emboli
PET Positron emission tomography
PICC Peripherally inserted central catheter
PVE Prosthetic valve infective
82Rb Rubidium-82
RCA Right coronary artery
RHS Right heart strain
RUL Right upper lobe
SSWI Supercial sternal wound infection
STEMI ST-elevation myocardial infarction
18
F-uorodeoxyglucose
artery
Staphylococcus aureus
endocarditis
© 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_24
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Y. A. Lucinian et al.
SUV Standardized uptake value
SWI Sternal wound infection
TAK Takayasu arteritis
TAVR Transcatheter aortic valve
replacement
TEE Transoesophageal echocardiogram
TTE Transthoracic echocardiogram
VG Vascular graft
VGI Vascular graft infection
VSD Ventricular septal defect
WBC White blood cell
Case 1
Initial Evaluation
An 85-year-old male had a history of type 2 diabetes mellitus, polycystic kidney disease, hypertension, atrial brillation (AF), and nonischemic
cardiomyopathy with a left ventricular ejection
fraction (LVEF) of 25% and a biventricular pacemaker (CRT-D) presented to the ER in septic
shock with an infection of unknown origin. He
reported coughing with worsening dyspnea and
new-onset back pain in the preceding weeks.
Blood cultures were positive for Salmonella
group D. Chest radiographs showed a left perihilar inltration. Transoesophageal echocardiogram (TEE) demonstrated thickening of the
right atrium lead with a mobile millimetric mass,
suggesting either a thrombus or a vegetation
(Fig.24.1).
Follow-Up
Despite clinical improvement under antibiotics,
bacteremia persisted. A chest radiograph was
repeated, showing regression of the previously
noted left lung opacities. A pacemaker lead infec-
a b
c
Fig. 24.1 PET 1 Interpretation. Whole-body FDG-PET/
CT (a) was performed following a myocardial suppression protocol consisting of a low-carbohydrate diet, 12h
fasting, and intravenous heparin in order to exclude endocarditis or pacemaker lead infection. Of note, the patient
had already undergone 7 days of treatment with large
spectrum antibiotics. Myocardial suppression was subop-
d
e
timal with diffuse left ventricular myocardial uptake (b).
No abnormal uptake was seen at the levels of the pacemaker generator pocket and leads, including the right
atrium lead (c, d). Slightly heterogeneous FDG distribution was noted at the thoracolumbar spine, but without
evidence of spondylodiscitis (e)
24 Cardiovascular FDG-PET Atlas ofCases
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355
a b
c
Fig. 24.2 PET 2 Interpretation. A second whole-body
FDG-PET/CT (a) was performed 17days following the
initial evaluation. Myocardial suppression was again suboptimal despite adherence to the preparation protocol,
limiting evaluation of valvular areas. However, there was
still no evidence of pacemaker-related infection. At the
level of the infrarenal aorta, a new intense hypermetabolic
d
e
lesion was noted on the left posterolateral side (b)
(SUV
=9.5). A probable saccular dilatation was dem-
max
onstrated on concomitant unenhanced CT (c). A diagnosis
of mycotic aneurysm was made. In retrospect, on the initial FDG-PET, a nonspecic slight increase in uptake (d)
(SUV
=2.9) was seen at approximately the same level
max
with an otherwise normal appearing aorta on CT (e)
tion was again suspected, prompting consideration of device removal (Fig.24.2).
Teaching Point
The patient’s initial clinical evaluation was
ambiguous, as no clear source of bacteremia was
evident. Both initial and follow-up FDG-PET/CT
accurately excluded a pacemaker-related infectious process, minimizing unnecessary interventions. The abdominal aorta appeared grossly
normal on initial FDG-PET/CT other than nonspecic FDG uptake, most likely a result of an
early disease process combined with ongoing
antibiotic treatment. A follow-up FDG-PET/CT
performed because of persistent bacteremia evidenced an aortic mycotic aneurysm, possibly
causing the patient’s back pain. As the great
majority of aortic mycotic aneurysms are metabolically active, the sensitivity of FDG-PET in
the detection of infected aortic aneurysms is very
high (>90%), while its specicity is lowered by
similar imaging ndings in inammatory aneurysms [1–3]. Contrast enhanced CT remains the
most commonly employed imaging modality to
assess aortic infections [4]. However, FDG-PET
has been shown to have higher diagnostic accuracy while also providing supplemental useful
information for reaching a conclusive diagnosis
in patients without infection [1].
Case 2
Initial Evaluation
An 81-year-old-male, known for AF, a permanent pacemaker (implanted 5 years prior)
and severe aortic stenosis, presented to the ER
6weeks after transcatheter aortic valve replacement (TAVR) with fever and chills. Multiple
blood cultures were positive for Staphylococcus
epidermidis. No clear source of infection was
evident. Gallium-67 scintigraphy was normal.
Both initial and repeat transoesophageal echocar-
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a b
Y. A. Lucinian et al.
c
Fig. 24.3 PET Interpretation. Whole-body FDG-PET/
CT (a) was performed following a myocardial suppression protocol consisting of a low-carbohydrate diet, 12h
fasting, and intravenous heparin. Myocardial suppression
was adequate. No abnormal uptake was seen at the levels
of the pacemaker generator pocket and leads. Intense, het-
diogram (TEE) were negative for endocarditis,
with a reported transprosthetic pressure gradient
of 10 mmHg. Pacemaker- related infection was
strongly suspected (Fig.24.3).
Teaching Point
The patient’s clinical presentation was strongly
suggestive of infective endocarditis after TAVR
(TAVR-IE). Because TEE was inconclusive, a
pacemaker-related infection was initially suspected. FDG-PET correctly identied TAVR-IE
and was crucial in guiding subsequent manage-
erogeneous, and asymmetric uptake (SUV
extending inferiorly was noted at the level of the TAVR
prosthesis (b, c, red arrows). Increased uptake was also
seen at the level of a left ventricle papillary muscle, a nonspecic nding (b, c, gray arrows). The remainder of the
study was unremarkable
= 10.8)
max
ment. FDG-PET’s usefulness in imaging prosthetic valve infective endocarditis (PVE) is well
established, making it a major criterion in the
European Society of Cardiology diagnostic criteria for PVE [5, 6]. FDG-PET/CT also offers
the possibility of treatment response monitoring
[7]. However, data about the diagnostic performance of FDG-PET in TAVR-IE remains limited
[8–10]. A recent retrospective analysis by
Wahadat et al. involving 30 patients showed
promising results, as FDG-PET/CT helped
reclassify 8 patients from the initial possible
TAVR-IE group to either the denite or the
rejected TAVR-IE groups [11].
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