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Native-Valve Endocarditis
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GadAbikhzer, JeremyY.Levett, IgalA.Sebag,
andMatthieuPelletier-Galarneau
13
Acronyms
IE Infective endocarditis
NVIE Native-valve infective endocarditis
PVE Prosthetic valve endocarditis
TEE Transesophageal echocardiogram
TTE Transthoracic echocardiogram
Introduction
Although relatively rare, infective endocarditis (IE)
is associated with signicant morbidity and mortality [1]. The diagnosis of IE is clinically challenging
due to diverse and variable clinical presentations,
G. Abikhzer (*)
Department of Radiology and Nuclear Medicine,
Jewish General Hospital, Montreal, QC, Canada
Faculty of Medicine and Health Sciences, McGill
University, Montreal, QC, Canada
e-mail: gad.abikhzer@mcgill.ca
J. Y. Levett
Faculty of Medicine and Health Sciences, McGill
University, Montreal, QC, Canada
I. A. Sebag
Faculty of Medicine and Health Sciences, McGill
University, Montreal, QC, Canada
Division of Cardiology, Jewish General Hospital,
Montreal, QC, Canada
M. Pelletier-Galarneau
Montreal Heart Institute, Montréal, QC, Canada
e-mail: Matthieu.pelletier-galarneau@icm-mhi.org
ranging from chronic, to subacute, to rapidly progressive disease. To circumvent these diagnostic
difculties, the Duke criteria were established. The
diagnosis of IE mostly relies on a modied version
of those criteria (the modied Duke criteria), consisting of major and minor criteria that are composed of clinical and paraclinical ndings including
blood cultures and echocardiographic ndings.
Studies have demonstrated that approximately one
third of patients investigated for IE are classied as
possible IE [2, 3]. In patients categorized as having
possible IE by the modied Duke criteria, 24–72%
of these patients are subsequently found to have IE
following additional investigations, such as repeat
TTE or TEE [4, 5]. This ultimately leads to delays
in diagnosis and initiation of treatment which is in
turn associated with poorer outcomes, including
increased rates of irreversible morphologic valvular damage, embolic events, surgery, and death [6,
7]. Advanced multimodality imaging has become
increasingly integrated in the diagnosis and evaluation of IE.Although the role of FDG-PET/CT in
native valve infective endocarditis (NVIE) is still
being dened, there is a growing body of evidence
supporting the role for FDG-PET/CT in the diagnosis and staging of this disease.
Pathophysiology
The healthy heart is naturally resistant to infection [8]. High pressures, constant hemodynamic
© 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_13
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G. Abikhzer et al.
ow, and poor adherence to endocardial surfaces
prevent infectious organisms from colonizing
endocardial structures [8, 9]. A predisposing
abnormality of the endocardium, massive bacteremia, or virulent microorganism is therefore
usually necessary to cause endocarditis of native
valves. The most common predisposing abnormalities of the endocardium are structural in
nature, typically involving the heart valves, and
include mitral valve prolapse, rheumatic valve
disease, calcic or bicuspid aortic valves,
congenital heart defects, hypertrophic cardiomyopathy, mural thrombi, ventricular septal defects,
or patent ductus arteriosus sites [8, 10–12]. As a
result of endothelial damage and activation of the
coagulation cascade, the nidus for infection is
typically a sterile brin-platelet vegetation [8].
Microorganisms colonize and proliferate the
endocardium in three stages [13]. First, they
begin by circulating in the bloodstream, causing
bacteremia. Second, a predisposing abnormality
of the endocardium promotes increased adherence and local stasis, enabling the pathogenic
agents to adhere to the abnormal or damaged
endothelium. Third, the nidus formed by the predisposing abnormality nurtures an environment
for microorganism proliferation and inammation of local structures, leading to the formation
of a mature vegetation. As a defensive mechanism from host innate and humoral immunity, as
well as from antibiotic penetration, many of the
causative endocarditis microorganisms produce a
protective matrix of polysaccharide biolms surrounding the mature vegetation [13].
NVIE is generally classied into two categories: left-sided NVIE (mitral or aortic valve),
which represents 80% of infections, or right- sided
NVIE (tricuspid or pulmonic valve) [13]. The
causative microorganisms vary by sites of infection, etiology of bacteremia, and host risk factors. Staphylococci and streptococci are the most
common causative microorganisms, accounting
for over 80% of NVIE cases [13]. The consequences of endocarditis can manifest locally
and systemically, depending on the progression
of disease [13]. Devastating local complications
can include valvular, myocardial, or aortic root
abscesses with tissue necrosis and conduction
system abnormalities, sudden and severe valvular regurgitation, or aortitis due to adjacent
spread of infection [8]. Systemic consequences
most commonly manifest as a result of embolization of vegetation material from the heart valve,
a devastating complication which can occur in
25–50% of patients [14], or immune- mediated
phenomena. Left-sided NVIE lesions can embolize to any tissue, particularly the central nervous
system, kidneys, or spleen, whereas right-sided
NVIE lesions can be complicated by septic pulmonary embolism, resulting in pulmonary infarction, pneumonia, or empyema [8]. As a result of
left-sided NVIE lesions, mycotic aneurysms of
major arteries can also form. Furthermore, cutaneous (Osler nodes and Janeway lesions) and
retinal emboli are specic features of left-sided
NVIE [13].
Epidemiology
While the precise estimate of NVIE incidence is
difcult to ascertain due to varying case denitions over time, it is estimated that the crude incidence for the global burden of IE ranges from 1.5
to 11.6 cases per 100,000 person-years [15].
NVIE is a fatal disease unless treated appropriately, with a mortality rate of approximately 25%
despite standard of care therapy [1]. Early diagnosis and management is essential to preventing
signicant morbidity and mortality. In highincome countries, the mean age of patients with
NVIE has signicantly increased over the past
century [1]. This is primarily attributable to the
changing etiology and predisposing cardiac risk
factors of patients with NVIE.Rheumatic heart
disease, primarily affecting the mitral valve, has
historically been the most frequent underlying
etiology of NVIE. However, in the past two
decades, its proportion has decreased to ≤5% in
developed countries [1]. Other risk factors including increasing age [16] structural heart disease
[11], poor dentition or dental infection [17],
injection drug use [18], and healthcare-associated
NVIE [19] have become prevalent in highincome countries and have changed the distribution of etiologies. At the time that endocarditis
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develops, approximately 75% of patients have a
preexisting structural cardiac abnormality [11].
In developing countries, rheumatic heart disease
remains the most common underlying heart condition [20].
Clinical Presentation andDiagnosis
Historically, the diagnosis of NVIE was made on
the clinical diagnosis of active valvulitis (such as
a cardiac murmur or chest pain), embolic sequela,
and immunological vascular phenomena in concurrence with positive blood cultures [13].
However, the latest advancements in developed
countries have resulted in a shift toward earlier
clinical presentations due to healthcareassociated NVIE with Staphylococcus aureus
infection. Accordingly, many of the classic
pathognomonic signs and symptoms associated
with NVIE do not manifest, with most patients
(approximately 90% of cases) presenting with
fever of unknown origin (FUO) [1, 21]. The
diverse and nonspecic nature of symptoms, as
well as the clinical variability in presentations,
complicates early diagnosis and identication of
patients who would be optimal candidates for
early effective antibiotic therapy or surgical inter-
vention. Therefore, the ability to accurately diagnose or exclude NVIE in a timely manner is of
utmost clinical importance in reducing morbidity
and mortality.
Currently, the diagnosis of NVIE requires a
combination of clinical manifestations, microbiological analysis, and imaging results. The modied Duke clinical diagnostic criteria integrate
these three spheres, weighing ndings as either
major or minor criteria, and allowing clinicians
and investigators to reach a denite, possible, or
rejected diagnosis of IE (Table 13.1) [22]. The
denite diagnosis of IE is established in the presence of pathologic criteria, two major clinical
criteria, one major clinical criterion, and three
minor clinical criteria, or ve minor clinical criteria (denite IE). In the presence of one major
criterion and one minor clinical criterion, three
minor criteria, IE is considered possible (possible
IE). IE is rejected if a rm alternate diagnosis is
made, clinical manifestations resolve with antibiotic therapy for less than or equal to 4days, there
is no pathologic evidence of IE at surgery or
autopsy with antibiotic therapy for less than or
equal to 4days, or clinical criteria for a denite
or possible diagnosis are not met (rejected IE).
While the modied Duke criteria remain the gold
standard for the diagnosis of IE, they are limited
Table 13.1 Modied Duke criteria for the diagnosis of IE
Denite IE
Pathological criteria
Pathologic lesions—Vegetation or intracardiac abscess demonstrating active endocarditis on histology, OR
Microorganisms—Demonstrated by culture or histology of a vegetation or intracardiac abscess
Clinical criteria
Using specic denitions listed below:
2 major clinical criteria, OR
1 major and 3 minor clinical criteria, OR
5 minor clinical criteria
Possible IE
Presence of 1 major and 1 minor clinical criteria OR presence of 3 minor clinical criteria
Rejected IE
A rm alternate diagnosis is made
Resolution of clinical manifestations with antibiotic therapy for ≤4days
No pathologic evidence of IE is found at surgery or autopsy with antibiotic therapy for ≤4days
Clinical criteria for denite or possible IE not met
(continued)
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Table 13.1 (continued)
Major clinical criteria
Blood culture positivity for either of the following:
1. Typical microorganism (viridans group streptococci, Streptococcus gallolyticus, HACEK organisms,
Staphylococcus aureus
separate blood cultures.
2. Persistent bacteremia (two positive cultures >12h apart, three positive cultures or a majority of four or more
culture-positive results >1h apart).
Evidence of endocardial involvement from either of the following:
1. Echocardiographic ndings of mobile mass attached to a valve or a valve apparatus, abscess, or new partial
dehiscence of a prosthetic valve.
2. New valvular regurgitation.
Serology:
Single positive blood culture for Coxiella burnetii or an antiphase 1 IgG antibody titer of ≥1/800
Minor clinical criteria
Predisposing condition:
Intravenous drug use
Predisposing cardiac condition
Vascular phenomena:
Arterial embolism
Septic pulmonary embolism
Mycotic aneurysm
Intracranial hemorrhage
Conjunctival hemorrhage
Janeway lesions
Description: Adapted from Li etal. Proposed modications to the Duke criteria for the diagnosis of infective endocarditis. Clin. Infect. Dis., 2000, 30, 4, 633–638 [22]
HACEK Haemophilus spp., Aggregatibacter spp., Cardiobacterium hominis, Eikenella corrodens, or Kingella spp.; IE
infective endocarditis, NVIE
, and community- acquired enterococci in the absence of a primary focus) from two
native- valve infective endocarditis
G. Abikhzer et al.
ab
Fig. 13.1 Representative echocardiographic ndings of
NVIE. Description: (a) Transthoracic echocardiogram
still image of a large, pedunculated, and prolapsing vegetation on the atrial surface of the noncoronary cusp of the
by their reliance on the presence of positive
microbiological criteria and typical echocardiographic ndings (Fig. 13.1), which remain the
cornerstone of an IE diagnosis.
Transthoracic echocardiography (TTE) is only
moderately sensitive (75%) for the detection of a
aortic valve. (b) Transesophageal echocardiogram still
image of a rounded, large, echo density on the atrial surface of the tricuspid valve leaet
vegetation in native valves [23], and blood cultures can be negative in up to 10% of cases [6].
Although the minority of cases (20%), the sensitivity of TTE is highest in right-sided IE due to
the tricuspid and pulmonic valves’ proximity to
the chest wall [13]. In patients with clinically
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suspected IE but equivocal or negative TTE,
transesophageal echocardiography (TEE) is the
gold standard and improves sensitivity and specicity to more than 90% with better detection of
the main cardiac complications (vegetation,
abscess, leaet perforation, and pseudoaneurysm) [6, 23]. However, its invasiveness and feasibility are important considerations, with major
complication rates ranging between 0.2% and
0.5% [24–26]. Furthermore, false positives can
occur with thrombi, brous strands on the aortic
valve, and cardiac tumors. The sequential and
indeterminate diagnostic evaluations can ultimately lead to delays in diagnosis and initiation
of treatment, which are in turn related to a poorer
outcome with increased rates of progressive and
potentially irreparable structural damage,
embolic events, surgery, and death [6, 7].
Management
The management of IE requires a multidisciplinary approach, including input from cardiologists, infectious disease specialists, and
cardiovascular surgeons [7]. The standard of care
is for all patients to receive antimicrobial therapy,
and a subset of patients may benet from cardiovascular surgical intervention [7, 13]. Antibiotics
can be started on an empirical basis as soon as
three blood cultures have been collected from
separate venipuncture sites [7, 13]. The empirical
antibiotic regimens for native valve endocarditis
are based on guidelines [27], although they can
be modied with the assistance of an infectious
disease consultant, according to blood culture
results, resistance patterns, and the clinical severity of infection [7]. In light of the primary purpose of antimicrobial therapy to completely
eradicate infection within cardiac vegetations, an
extended course of intravenous therapy is generally required (extending up to 6weeks in severe
cases) [13]. In addition to antimicrobial therapy,
surgical intervention is required in approximately
50% of cases [28]. In the only randomized trial
published to date on the effect of early surgical
intervention versus conventional treatment for
NVIE, early surgical intervention was found to
signicantly reduce the primary composite endpoint of in-hospital mortality and embolic events
by 90% [29]. The three most common indications
for surgery are heart failure caused by valvular
regurgitation or obstruction, uncontrolled or
complex infection involving valve leaet and
paravalvular tissue destruction, and prevention of
embolism [6, 7, 13].
FDG-PET/CT Imaging
Fluorodeoxyglucose-positron emission tomography/computed tomography (FDG-PET/CT)
has become extremely useful for infectious disease imaging such as FUO [30], sternal wound
infections [31], vascular graft infections [32],
spondylodiscitis [33], cardiovascular implantable electronic device (CIED) infections [34,
35], and prosthetic valve IE (PVE) [36, 37].
Activated granulocytes involved in the infectious and inammatory response have a high
expression of glucose transporters (GLUT1
and GLUT3) and increased hexokinase activity
[38]. Use of FDG- PET/CT for infection imaging
compared to SPECT radiotracers yields several
advantages including excellent image resolution, lack of blood manipulation, lower radiation exposure, and a shorter procedure for both
the patient and technical staff, allowing results
to be available in less than 2h after injection.
FDG-PET/CT is especially useful in patients
with renal failure or those who are allergic to
contrast media. FDG has, however, several limitations in the evaluation of cardiovascular infection. Physiological myocardial uptake can mask
or limit the distinction between physiological
uptake at the base of the myocardium and pathological valvular activity. Cardiac suppression
protocols consisting of fasting (12-18h), highfat-low-carbohydrate diet, and in some centers
IV heparin are recommended prior to imaging
(see Chap. 4) [39–41]. This preparation delays
the scheduling of an FDG- PET/CT by 20 h,
as well as being inconvenient for the patient.
Despite optimal preparation, partial or complete
failure of suppression of physiological myocardial activity may be present in 5–15% of scans
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[42]. Additionally, FDG is not an infection-spe-
cic radiotracer with uptake in inammation and
malignancy. The ongoing development of novel
infection-specic PET radiotracers yield promise to further improve on IE diagnosis, although
none are yet clinically available [43]. In the context of PVE, specicity of FDG may be affected
by uptake in post- operative inammation and
foreign body inammation surrounding prosthetic material or surgical adhesives [44]; in
the setting of suspected NVIE, these confounders are not present which explains the near perfect specicity of abnormal valvular uptake in
NVIE.Given the absence of physiological valvular activity in native valves, any focal valvular
activity above background or blood pool, after
excluding papillary muscle activity or residual
physiological myocardial activity at the base of
the myocardium, is considered positive for NVIE
on FDG- PET/CT (Fig.13.2). The added value of
standardized uptake values (SUV) in this context
has not yet been demonstrated [45]. In heavily
calcied native valves, very mild activity can
rarely be present, and it is also important to verify non-attenuation corrected images to ensure
over-correction artifacts.
The role of FDG-PET/CT in suspected PVE
has been well studied and introduced as a major
criterion for the diagnosis of PVE in the 2015
European Society of Cardiology (ESC) guidelines [36]. The role of FDG-PET/CT for NVIE is
less well dened and studied than for PVE,
mainly because of its higher false-negative rate
and the excellent diagnostic performance of TEE
in NVIE yielding less diagnostic dilemmas.
Initial PET/CT studies included small subgroups
of NVIE patients within larger subgroups of PVE
patients and resulted in very poor sensitivity [46,
47]. In a dedicated retrospective study of 88
patients with suspected NVIE, 20 patients had
NVIE according to multidisciplinary consensus.
Of these 20 patients, nine (45%) had abnormal
valvular FDG uptake [36]; however, septic
emboli were detected in 48 (55%) cases [48]. A
abc
Fig. 13.2 Representative examples of abnormal native
valve uptake in patients with IE.Description: (a) Aortic
valve endocarditis complicate by para-valvular abscess
and hemorrhagic pericardial effusion on CT. (b) Mitral
valve endocarditis with intense multifocal uptake in a
mitral valve with annular calcications, which can be a
predisposing factor for IE. (c) Tricuspid valve endocarditis with abnormal mild, focal uptake above background
(red arrow). Septic lung emboli are also present. FDG
PET/CT uorodeoxyglucose (18F)-positron emission
tomography/computed tomography
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dedicated retrospective study of 75 patients with
NVIE who underwent FDG-PET/CT demonstrated a sensitivity of 17.5% and specicity of
100%. Integration of PET/CT to the ESC in this
context increased sensitivity to 69.8% from
63.5% without affecting specicity [49]. In an
observational prospective study of patients
referred for suspicion of left-sided NVIE and
PVE, only 10/46 subjects with nal diagnosis of
NVIE had abnormal FDG uptake on consensus
interpretation, yielding a sensitivity of 22%,
while none of the 69 subjects without NVIE had
a positive FDG-PET/CT study [50]. The largest
contribution of FDG-PET/CT in this patient population was the appropriate reclassication of
11/26 (42%) patients from Possible IE to Denite
IE. Of note, imaging in this study was performed
with an older generation analog PET system. In
the European Infective Endocarditis Registry
(EURO-ENDO), a prospective observational
cohort including 156 centers from 40 countries, a
low sensitivity of 28% was observed. Further,
they reported that FDG-PET/CT is performed in
less than 10% of suspected NVIE cases [51]. In
the French registry study, although only 24% of
NVIE patients had abnormal valvular uptake,
51% had extracardiac ndings such as septic
emboli or identication of portal of entry. FDGPET/CT in this patient population changed management in 31% through modication of the
length of antibiotic therapy or surgery. PET/CT
modied classication or management mainly in
patients with non-contributory echocardiogram
or Possible IE [52]. These registry studies only
reported pooled sensitivity encompassing numerous centers using a variety of PET/CT scanners
with different technology. Poor reported sensitivity for NVIE can be improved through use of
more recent PET/CT devices. In a retrospective
study dedicated to NVIE using the best available
analog PET/CT, abnormal FDG uptake was identied in 21 of the 31 subjects with NVIE, yielding a sensitivity of 67.7% [5]. However, when
excluding subjects with suboptimal myocardial
suppression interfering with study interpretation,
the sensitivity rose to 77%. Incorporating FDGPET/CT uptake as a new major criterion, eight of
18 subjects (44.4%) with Possible IE and a nal
diagnosis of IE were appropriately reclassied as
Denite IE. A meta-analysis, with only four studies in the NVIE category, demonstrates a near
perfect specicity of FDG-PET/CT for NVIE at
98%, but low pooled sensitivity at 31%. However,
their results suggest that technological advances
have contributed to higher accuracy for all subtypes of IE, where pooled sensitivity and specicity were higher in studies published since 2015
than those between 2009 and 2014 [40]. In
another meta-analysis including seven NVIE
studies, pooled sensitivity was 36.3%, with
pooled specicity of 99.1%. Pooled positive likelihood ratio, negative likelihood ratio, and diagnostic odds ratio were 8.3, 0.6, and 15.3,
respectively [45].
The relatively low sensitivities of FDG-PET/
CT for NVIE can at least partly be accounted for
by physiological and technical factors. The more
frequent presence of isolated valve vegetations,
rare para-valvular involvement, lower predominance of polymorphonuclear cells, and increased
brosis in NVIE compared to PVE, result in
reduced inammatory response and subsequently
lower FDG uptake [50]. False-negative studies
have been associated with antibiotic use in some
studies, although duration of antibiotic therapy
before uptake normalization is unknown and
other studies show no diagnostic effect from the
use of antibiotics on FDG-PET/CT [45]. Poor
myocardial suppression is associated with a 4.8
odds ratio of having a false-negative study when
inadequate myocardial suppression is present [5].
Most importantly, the low reported sensitivity for
NVIE can be partly explained by the technical
properties of the PET systems used in these studies, with lower sensitivity and inferior spatial
resolution, limiting their ability to detect small
foci of uptake. Technological advances in PET/
CT camera design have considerably enhanced
resolution and contrast, with the possibility of
signicantly improving the detection of
NVIE.The development of digital PET/CT systems with silicon photodiodes, replacing photomultiplier tubes used in the analog PET devices
promises to further improve small lesion detection, as is present in NVIE, through improved
sensitivity, contrast, and resolution of these
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devices [53]. Vegetation size on echocardiography is on average smaller in false-negative PET
cases compared to true-positive cases
(9.6±5.9mm vs. 14.4±6.1, p=0.049) [5], but
within the resolution of digital PET/CT devices.
Additionally, new scanner technology allows
gated acquisition to account for both respiratory
and cardiac motions. Hence, the blurring of FDG
uptake related to the motion of the vegetations on
the valves, which limits the sensitivity of the test,
could be improved with ECG-gated and
respiratory- gated acquisitions which “freezes”
motion and subsequent blurring of uptake in the
infected valves [54]. The use of dual time point
imaging in patients with equivocal valvular activity can increase sensitivity by increased target to
background ratio on delayed images through
decreased blood pool activity or through the
reproduction of equivocal foci of valvular uptake
on two distinct acquisitions which raises the suspicion of true focal valvular uptake rather than
statistical noise or reconstruction artifacts [5].
The most useful role for FDG-PET/CT in the
evaluation of patients with suspected NVIE given
its limited sensitivity but near-perfect specicity
and the excellent performance of TEE appears to
be as additional major or minor criteria to the
modied Duke criteria which may help to
decrease the number of patients in the subgroup
classied as possible IE. This indication of FDGPET/CT for possible IE cases is in addition to its
role in the evaluation for septic emboli in cases
with denite IE as recommended by the ESC
guidelines [45, 55]. The ACC/AHA 2020 guidelines state that FDG-PET/CT is reasonable as
adjunct diagnostic imaging in some patients with
possible IE [7]. FDG-PET/CT may be particularly useful in patients with suspicion of IE who
cannot undergo the more invasive TEE.
Extracardiac Manifestations
ofInfective Endocarditis
There has been a paradigm shift in the evaluation
of IE, with increased awareness of the systemic
nature of the disease. Identication of extracardiac manifestations in patients with IE is critical
as they can signicantly impact patient management decisions and outcome. Extracardiac infectious ndings are present in 25–50% of patients
[14] and can include cerebral emboli, spondylodiscitis, septic arthritis, pneumonia, abscesses,
and mycotic aneurysm (Figs. 13.3 and 13.4).
Infectious manifestations can represent septic
emboli or an initial site of infection which seeded
the heart valve causing the IE.Gastrointestinal
polyps and cancers as well as various other
malignancies, which may represent the etiology
of IE in several cases, are detected by FDG-PET/
CT in approximately 10% of patients investigated for IE [56]. Extracardiac manifestations
identied on FDG-PET/CT are unknown or
unsuspected in the majority of cases and may
lead to change in management in about 10% of
patients [56].
In addition to infection and cancers, other
reactive changes can be observed on whole-body
FDG-PET/CT such as increased bone marrow
and splenic activity. In IE, increased marrow and
splenic activity, dened as uptake greater than
liver, has been attributed to hematological diffusion of bacteria and/or cytokines, indicating a
systemic inammatory response to the disease.
Increased marrow and splenic uptake is considered an indirect sign of IE and is correlated with
C-reactive protein levels as well as the major criterion of positive blood cultures [57]. Specically,
in NVIE, diffuse splenic uptake is present in
58.7% of NVIE cases and has been proposed as
a
f
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ad
b
c
Fig. 13.3 Examples of septic embolic disease in various
patients with IE.Description: (a) Left main coronary septic arteritis. (b) Septic splenic infarct. (c) Infected PICC
line. (d) Cervical spondylodiscitis. (e) Extensive septic
lung disease in a patient with tricuspid NVIE. FDG-PET/
CT uorodeoxyglucose (18F)-positron emission tomography/computed tomography, PICC=peripherally inserted
intravenous catheter
e
ei
b
g
c
j
d
Fig. 13.4 FDG-PET/CT images of a patient referred for
suspected lymphoma with night sweats and fever, diagnosed on FDG-PET/CT with native valve endocarditis and
extensive embolic disease. Description: Intense uptake is
present in the aortic valve (b, j). There is evidence of
h
embolic disease to the brain (a, arrow), lungs (c, d-arrow),
kidneys (f, g), prevertebral soft tissues (i) and bone (j).
FDG-PET/CT uorodeoxyglucose (18F)-positron emission tomography/computed tomography
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G. Abikhzer et al.
an additional minor criterion over ESC criteria
already including PET, to further increase sensitivity to 74.6% of the ESC criteria at 69.8%,
compared to 63.5% for modied Duke criteria
[49]. However, this nding is nonspecic and can
be medication related or present in a variety of
other inammatory, infectious, or malignant
conditions.
Prognostic Value
Early identication of patients with poorer prognosis is critical as more aggressive management
may improve their outcome [58, 59]. Several
well-established patient-related factors have been
associated with worse prognosis, including older
age, diabetes mellitus, and heart failure. Other histopathological and echocardiographic features,
including staphylococcus aureus as causative
organism, vegetation size, peri-annular complications, and severe valve regurgitation have also
been associated with worse prognosis [36, 60].
In a prospective study of 47 patients with IE who
underwent FDG-PET/CT imaging, the infectious
complications and relapse rate were signicantly
lower when compared to a matched control group
of 94 patients with IE who did not undergo FDGPET/CT imaging [61] In a multivariate model,
applying the best predictive model for major
adverse cardiac events, the four leading predictors of additional independent prognostic value
were as follows: C-reactive protein >100mg/L,
severe mitral regurgitation, positive FDG-PET/
CT scan, and FDG-PET/CT scan with moderateto-intense metabolic uptake. Unlike the PVE
subgroup in this study, FDG- PET/CT was not
predictive of a major adverse cardiac event in the
NVIE subgroup, but moderate- to-intense FDG
uptake was associated with a hazard ratio of 8.8
to predict new embolic events [62]. These data
suggest that FDG-PET/CT provides independent
prognostic information.
Conclusion
The role of FDG-PET/CT in NVIE is currently
evolving with technological advances promising to improve sensitivity for abnormal uptake
on native valves, while maintaining near-perfect specicity. Clinically, the greatest added
value of FDG-PET/CT appears to be in patients
classied as Possible IE, as well as in patients
with denite IE for the systemic staging of the
disease with potential prognostic signicance.
Declaration of Interests The authors have no
relevant conicts of interest to disclose.
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