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Table 16.4 (continued)
General wound
Possible=No surgical/
histology or purulent
discharge ± other
criteria
Surgical/histology Microbiology Clinical
•
Surgical debridement
not performed
•
No histology
•
Aseptic skin
culture positive or
negative and
patient not on
antibiotics or had
antiseptic used to
clean the wound
•
Local increase in
temperature
around the exit
site and.
•
Treated as
supercial
infection with
appearance
•
No discharge
•
Erythema
spreading
around the exit
a
site
clinical response
B.Deep VAD-specic percutaneous driveline infection
Proven=Surgical/
histology criteria ±
other criteria
•
Involves deep soft
tissue (e.g., fascial and
muscle layers) on
direct examination or
on direct examination
during reoperation
•
An abscess is found
•
Culture positive or
histology puncture
positive for
infection
•
Temperature
>38°C
•
Localized pain or
tenderness
•
A deep incision
spontaneous
dehiscence
•
Abscess deep to
the incision
around the
driveline
on direct examination
during reoperation
Probable=No surgical/
histology criteria with
spontaneous dehiscence
± other criteria
Possible=No surgical/
histology criteria with
positive ultrasound ±
other clinical criteria
•
No surgical
debridement
•
No histology
•
No surgical
debridement
•
No histology
•
Culture negative
but patients
already on
antibiotics or had
antiseptic used on
exit site
•
Cultures not
reserved
•
Temperature
>38°C or
•
Localized pain or
tenderness and
•
Treated as a deep
infection
•
Localized pain or
tenderness and
•
Treated as a deep
infection with
•
An incision
spontaneous
dehiscence
•
Positive
ultrasound
clinical response
VAD ventricular assist device
a
Erythema excluding stitch abscess (minimal inammation and discharge conned to the points of suture penetration).
Reprinted from The Journal of Heart and Lung Transplantation, Vol 30/Number 4, Hannan MM, Husain S, Mattner F,
Danziger-Isakov L, Drew RJ, Corey GR, etal. Working formulation for the standardization of denitions of infections
in patients using ventricular assist devices. Page 381. Copyright (2011) [8]
be secondary to direct inoculation at the time of
surgery, whereas infections acquired >30 days
postoperatively are typically secondary to extension from a driveline infection [26].
In addition to infection of the pump and/or
pocket, the inow cannula connecting the left
ventricle to the VAD pump and the outow cannula connecting the pump to the aorta may also
become infected. This relatively uncommon complication occurs in <1% of LVAD patients but is
associated with signicant morbidity and mortal-
ity. Analogous to driveline infections, pump,
pump pocket, and cannula infections are subcategorized into proven, probable, and possible.
Proven infection relies on isolation of organisms
intra-operatively directly from the pump, the
pocket, or the cannula or by identifying an abscess
on imaging. Probable and possible pump, pocket,
and cannula infections are diagnosed using major
and minor clinical criteria that were adapted by
the IHSLT from the Modied Duke Criteria [8,
28] (see Tables 16.1, 16.2, 16.3, and 16.4).
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VAD-Related Infections
VAD-related infections include infective endocarditis (in ~1% of patients), blood-stream infection, mediastinitis, and sternal wound infections
(in ~2% of patients) [8, 25, 31]. All cases of
endocarditis are considered VAD-related per the
ISHLT denitions. Bloodstream infections are
presumed VAD-related unless a clear alternative
source of infection can be identied. Similarly,
mediastinitis and sternal wound infections are
also considered VAD-related unless they are
denitively proven to have another cause.
Microbiology
Skin ora, primarily Gram-positive cocci, are the
most common microorganisms identied in all
types of VAD-specic and VAD-related infection
[25, 26]. Staphylococcus aureus, both methicillin-
susceptible and methicillin-resistant, and
coagulase- negative Staphylococci species are
isolated in 17–75% of driveline infections and
25–75% of pump pocket infections [25, 26, 32].
Additionally, enterococcus species are isolated in
5–29% of VAD-specic infections, followed by
Gram-negative rods including Pseudomonas
aeruginosa, Escherichia coli, and Klebsiella species which comprise 7–43% of VAD-specic
infections. Fungal pathogens, most notably
Candida species, while less common than bacterial organisms, account for 2–8% of VAD-specic
infections [25, 26]. Notably, the incidence of
LVAD infections has decreased in second- and
third-generation LVADs [33–35].
Treatment
A detailed review of the treatment of VADspecic and VAD-related infections is beyond the
scope of this chapter. However, there are certain
general considerations that are important in this
patient population. By denition, VAD-specic
infections involve the device hardware, and the
most common etiologic pathogens produce biolms which make their eradication from prosthetic material challenging. Given the potential
for ascending driveline infection resulting in the
highly morbid contamination of the pump or cannula, most VAD-specic infections as well as
VAD-related endocarditis or recurrent VADrelated bloodstream infections caused by the
same organism will require some duration of
intravenous antibiotic treatment in conjunction
with either denitive surgical debridement or
device explantation followed by long-term oral
antibiotic suppression until transplant. The notable exception to this approach is supercial driveline infections caused by non-Staphylococcus,
non-Pseudomonas, and non-fungal species for
which a shorter 2-week course of therapy without
long-term antibiotic suppression can be considered [25–27].
Diagnostic Strategies
Drawing from endocarditis literature, major and
minor criteria have been proposed to help determine the likelihood of LVAD infection (see
Tables 16.1 and 16.3). Using these clinical, pathological, and imaging criteria, suspected cases
can be classied as either proven, probable, possible, or unlikely for LVAD infection (see Tables
16.2 and 16.4) [36]. Proven infection requires
denitive microbiology, or histologic conrmation at explants, or two major clinical criteria [36,
37]. Infection is considered probable in the set-
ting of one major and three minor criteria, or four
minor criteria [36, 37]. Possible infection requires
one major and one minor criteria, or three minor
criteria [36, 37]. Infection is considered unlikely
in the presence of an alternative diagnosis or resolution after less than or equal to 4days of antibiotics, or no pathologic evidence at surgery after
less than or equal to 4days of antibiotics, or negative cultures from uid during surgery or aspiration, or not meeting the criteria above [36, 37].
LVAD infections are difcult to diagnose as
there are multiple external and internal compo-
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213
nents of the LVAD which can become infected. In
addition, many of these patients have other prosthetic devices, including pacemakers, debrillators, and valve replacements. These other devices
can also become infected and should be evaluated in LVAD patients in whom infection is
suspected.
Evaluation of all patients who are suspected of
having an LVAD infection should include the following: white blood cell count, C-reactive protein, erythrocyte sedimentation rate, sterile
aspirate for Gram stain, KOH preparation, routine bacterial and fungal culture of driveline at
exit site if pus is present, echocardiogram including TEE if TTE is without ndings consistent
with infection, at least three sets of blood cultures
drawn at different times over 24h (two sets from
peripheral sites), and chest radiograph [8].
Echocardiography is the rst-line screening
imaging modality for cardiac prosthetic device
infections as it is readily available, provides both
functional and anatomic information, does not
require radiation, and can detect valvular vegetations and other sequelae of infection including
paravalvular abscesses [38]. Transthoracic echocardiography (TTE) should be pursued rst as it
is noninvasive, and if it reveals ndings consistent with endocarditis, then in some instances can
obviate the need for further imaging. However,
TTE has limited sensitivity in detecting prosthetic valve endocarditis [39]. In cases where
TTE is inconclusive, then transesophageal echocardiography (TEE) should be pursued as it has
signicantly higher sensitivity in diagnosing
endocarditis, specically in patients with prosthetic devices. Limitations of echocardiography
include artifacts related to prosthetic material,
limited ability to detect perivalvular extension of
infection in the setting of prosthetic valves,
inability to detect peripheral complications of
infection or clinically important extracardiac
sequelae of infection, and, in some patients, contraindications that may make transesophageal
echocardiography difcult or impossible [38].
In addition, if there is concern for pocket
infection, then abdominal ultrasound and CT
with contrast of chest/abdomen may be helpful
[8]. Nonetheless, serum biomarkers of infection,
TEE, and CT have been found to be poor predictors of LVAD infection when used in isolation
[3]. Further, there is currently no gold standard
for the diagnosis of LVAD infections. Despite
this, a timely diagnosis is essential in the care of
LVAD patients who typically have multiple
comorbidities placing them at increased risk of
mortality [3].
FDG-PET/CT is useful in the evaluation of
patients suspected of having prosthetic device
infection. It has high sensitivity and specicity in
the evaluation of prosthetic valve endocarditis
(sensitivity of 86% and specicity of 84%) and
cardiac implantable electronic device (CIED)
endocarditis (sensitivity of 72% and specicity
of 83%) [40]. In addition, FDG-PET/CT can
detect perivalvular complications of infection
and characterize regional extent of infection [40].
Whole-body FDG-PET/CT imaging can identify
embolic phenomenon and other etiologies for the
source of infection [38]. Some of the limitations
of FDG-PET/CT include the inability to detect
small vegetations, false positives from postsurgical (sterile) inammation, false positives
from inammation induced by certain surgical
adhesives, and the reduced sensitivity to detect
infection in patients who have been on long-term
antimicrobial therapy prior to imaging.
Furthermore, the performance of FDG-PET/CT
is predicated on achieving adequate myocardial
suppression of endogenous glucose uptake with
metabolic preparation, necessitating a lowcarbohydrate, high-fat diet [41–43]. Interpretation
of FDG-PET/CT for cardiac infection requires
specialized training and knowledge of the aforementioned caveats and the ability to distinguish
normal versus pathological FDG uptake
patterns.
There is a nascent but growing body of literature which supports the use of FDG-PET/CT in
aiding the diagnosis of LVAD infection. A metaanalysis examined the utility of FDG-PET in the
evaluation of LVAD infections [3]. A total of 119
scans were included across four centers, and the
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Dell’Aquila et al., 2017
SENSITIVITY
SPECIFICITY
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C. Madamanchi et al.
authors found that when added to a comprehensive evaluation including biomarkers of infection and other imaging studies, FDG-PET had
a pooled sensitivity of 92% in the diagnosis of
LVAD infection [3] (see Fig.16.1). Specicity,
on the other hand, was only 83% with wide condence intervals [3]. Some of the limitations of
the study included the lack of a gold standard test
in diagnosing infections in cases where patients
did not undergo surgery, variations in protocols
and metabolic preparations for patients across
the four centers, and selection bias as not all
patients suspected of having LVAD infections
are referred to have FDG-PET/CTs [3]. Overall,
the use of FDG-PET/CT in the evaluation of
LVAD infections is promising with high sensitivity, but specicity is lacking and requires further
investigation.
FDG-PET/CT has been shown to be useful not
only in the diagnosis of LVAD infection but also
for prognosis of these patients based on the presence and site of infection [44]. In one study, FDGPET/CTs were obtained in 35 patients with LVAD
including 24 patients who were suspected of hav-
ing LVAD infections and 11 who were not suspected of being infected [44]. After a mean
follow-up of 23months, none of the patients without evidence of infection on FDG-PET died. In
contrast, 50% of patients with evidence of infection on FDG-PET/CT died [44]. Among those,
86% had evidence of infection involving central
components of the LVAD, whereas 14% had evidence of infection involving peripheral components of the LVAD [44]. This study highlights the
importance of detecting and treating LVAD infections early—before the infection spreads to involve
central components of the LVAD [44].
A diagnostic algorithm for the evaluation of
patients suspected of having an LVAD infection
is outlined in Fig. 16.2. Based on the criteria
listed above, if patients have proven infection,
they should be treated appropriately. If infection
is deemed unlikely, then alterative diagnoses can
be evaluated. In cases where a patient has probable or possible LVAD infection and is at high risk
for surgical intervention, then FDG-PET/CT
should be considered to aid in diagnosis and
treatment selection [3].
Fig. 16.1 Forest Plot. (Reprinted from JACC:
Cardiovascular Imaging, Vol 13/Number 5, Tam MC,
Patel VN, Weinberg RL, Hulten EA, Aaronson KD, Pagani
FD, Corbett JR, Murthy VL. Diagnostic Accuracy of
FDG-PET/CT in Suspected LVAD Infections: A Case
Series, Systematic Review, and Meta-Analysis. Page 1199.
Study Id Study IdSENSITIVITY (95% CI) SENSITIVITY (95% CI)
Ta m et al., 2020
Bernhardt et al., 2017
Akin et al., 2017
COMBINED
0.6 1.0
1.00 [0.72 - 1.00]
0.90 [0.76 - 0.97]
0.88 [0.62 - 0.98]
1.00 [0.63 - 1.00]
0.92 [0.82 - 0.97]
Q = 2.69, df = 3.00, p = 0.44
I2 = 0.00 [0.00 - 100.00]
Dell’Aquila et al., 2017
Bernhardt et al., 2017
Ta m et al., 2020
Akin et al., 2017
COMBINED
0.0 1.0
0.25 [0.03 - 0.65]
0.71 [0.48 - 0.89]
1.00 [0.75 - 1.00]
1.00 [0.16 - 1.00]
0.83 [0.24 - 0.99]
Q = 15.55, df = 3.00, p = 0.00
2
I
= 80.71 [62.08 - 99.33]
Copyright (2020)) [3]. The pooled sensitivity and specicity of individual studies assessing diagnostic accuracy
of uorine- 18 uorodeoxyglucose positron emission
tomography/computed tomography for left ventricular
assist device infections with measures of heterogeneity.
CI condence interval
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Suspected LVAD Infection
1. History & Physical
2. Lab Tests: WBC, ESR, CRP, 3 sets of Blood Cultures in 24h, Aspirate for gram stain, KOH, bacterial
3. Initial Imaging Studies: chest x-ray, TTE (TEE if TTE without evidence of infection), if concern for
Proven Probable Possible Unlike ly
Proceed with
appropriate
treatment
Fig. 16.2 Diagnostic approach for the evaluation of patients suspected of having an LVAD infection
pocket infection, abdominal U/S and/or CT Chest/Abdomen with contrast
If positive
& fungal culture of driveline
18F-FDG
PET/CT
If negative
215
Evaluate for
other
etiologies of
presentation
Factors That Aect Image Quality
andInterpretation
Preparation andImage Acquisition
One of the most important factors that affects
image quality and interpretation of FDG-PET/CT
for cardiac infection is the degree of suppression
of endogenous myocardial glucose uptake [41–
43]. Prior to undergoing FDG-PET/CT scanning,
metabolic preparation is necessary to shift the
energy source of the myocardium to free fatty
acids (i.e., to minimize the chance that FDG signal seen in the myocardium is due to normal cardiac myocytes metabolizing glucose for energy).
If proper suppression is not achieved, it can be
very difcult to distinguish between physiologic
and pathologic FDG uptake. In order to achieve
adequate myocardial suppression of glucose
uptake, it is imperative that patients adhere to a
high fat, no carbohydrate diet for 24h prior to the
test followed by fasting for several hours
including overnight prior to the day of the test
(see Chap. 4 for further details).
Whole-body FDG/PET CT imaging obtained
at the time of the cardiac PET/CT scan can identify embolic phenomenon that are sequelae of
infective endocarditis [38, 45]. It can also be useful in determining other causes of inammation
(see Case 16.1) including other infections or neoplasms [38]. This information is essential in the
evaluation of infective endocarditis as it can
modify treatment plans, including prolonging the
duration of antimicrobial therapy, lead to referral
for surgical procedures, and prevent unnecessary
device extraction [45].
CT attenuation correction images are used to
improve PET image quality and interpretation by
providing anatomic localization of radiotracer
uptake and attenuation correction of PET images.
In select cases, ECG-gated cardiac CTs can identify anatomic lesions including pseudoaneurysms, stulas, and thrombosis [46]. Pizzi etal.
demonstrated that fusing FDG images with ECGgated CTA images reduced the number of doubtful studies on PET/nonenhanced CT from 20 to
8%, primarily by reclassifying doubtful cases to
negative cases [46]. However, they did not nd
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signicant differences in the sensitivity and specicity of Duke Criteria + PET/CTA vs. Duke
Criteria + PET/Nonenhanced CT. In addition,
contrast-enhanced CT requires more radiation
[46]. Furthermore, iodinated contrast can create
artifacts on the CT attenuation images leading to
the appearance of false-positive FDG uptake on
the corrected PET images [47].
Interpretation andReporting
The qualitative approach to interpretation relies
on visual assessment of abnormal FDG activity
related to various components of the LVAD or
other prosthetic devices. This approach can be
bolstered by a semi-quantitative approach in
which increased FDG uptake involving any component of the LVAD is compared to background
LV blood pool FDG uptake using standardized
uptake value (SUV) to illustrate the intensity of
inammation.
The focality, intensity, and location of FDG
signal are important factors to report when interpreting FDG-PET/CT studies in the evaluation of
LVAD infection. FDG uptake that is very focal
and intense suggests signicant inammation,
more strongly suggesting infection. On the other
hand, FDG uptake that is diffuse and mild may
represent low-level inammation. This low-level
degree of inammation can be seen in the postsurgical state [48]. The location of FDG uptake is
important to report as it offers information on the
extent of infection including involvement of
driveline, inow cannula, outow graft, and any
other intracardiac prosthetic devices (e.g., ICDs).
It is important to recognize that FDG uptake
is non-specic and can be seen in infectious and
noninfectious inammatory conditions including sarcoidosis, myocarditis, postoperative state,
and malignancy [3, 49, 50]. In the postoperative
state, wound healing occurs via the formation of
granulation tissue (the action of broblasts and
inammatory cells) [49]. If FDG- PET imaging
is performed shortly following surgery, there
may be residual low-level inammation which
can appear as mild, diffuse FDG uptake surrounding the surgical site and any graft material.
In fact, low-grade FDG signal can be seen for up
to 1year following surgery [48]. Further investigation into additional metrics of normality is
required in these instances. This must be considered in the interpretation of FDG-PET/CT
images relative to the time of surgery. In addition, certain surgical adhesives can lead to falsepositive FDG scans [51]; thus, it is important to
take this information into account when interpreting studies. Furthermore, it is not uncommon
for LVAD patients to be treated with long courses
of antibiotics for various infections. Long-term
antimicrobial therapy prior to obtaining an FDGPET/CT can alter FDG uptake and lead to falsenegative studies, although the rate of false
negatives is thought to be low at approximately
5% [3].
Attenuation correction images are used to
improve PET image quality and interpretation as
mentioned above. However, CT attenuation correction in the presence of high-density metallic
implants can overcorrect for attenuation and lead
to overestimation of FDG activity in the vicinity
of an LVAD or other metallic objects [3, 52].
Thus, any FDG uptake noted on attenuation correction images should be compared with the nonattenuation corrected (uncorrected) images, with
the thought that FDG signal that is not due to artifact should be present on both the sets of images.
Acknowledgement of common imaging pitfalls as described above, combined with integration of the clinical presentation, is of key
importance when interpreting FDG-PET/CT
studies for suspected LVAD infection. In addition, collaborative reading involving nuclear cardiologists and nuclear medicine specialists is
benecial in cases of abnormal peripheral FDG
uptake. A comprehensive interpretation can accurately characterize LVAD infections and help
inuence treatment decisions.
Clinical Cases
Case 16.1
A 72-year-old man with ischemic cardiomyopathy, ICD, and HeartMate II Left Ventricular
Assist Device (LVAD) implantation presented
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with fevers, leukocytosis, hypotension, chest
pain, and elevated lactate dehydrogenase. Blood
cultures remained negative, chest X-ray did not
reveal any acute abnormalities, and transthoracic
echocardiogram did not reveal any vegetations.
FDG-PET/CT was obtained to evaluate for device
infection. It revealed no evidence of FDG uptake
in the myocardium, LVAD inow or outow cannulas (Fig. 16.3, red arrows), driveline, ICD
leads, or generator. There was no imaging evidence of LVAD infection. However, FDG-PET/
CT identied a rim of FDG uptake surrounding
the gallbladder (Fig.16.3, yellow arrows), indicating hypermetabolic activity which was suspicious for cholecystitis.
The patient was treated with antimicrobial
therapy for acute cholecystitis. This case helps
illustrate an important role of FDG-PET/CT in
suspected LVAD infection, namely that the
modality not only is useful in detecting devicerelated infection but also can reveal other etiologies for the patient’s presentation, including
infection or inammation located elsewhere in
the body [38, 45].
Case 16.2
A 64-year-old man with atrial brillation treated
with ablation and ultimately left atrial appendage
exclusion (left atrial appendage clip), nonischemic cardiomyopathy with ICD, and HeartMate
3 LVAD presented with nausea, vomiting, diarrhea, and generalized malaise. Blood cultures
revealed Streptococcus viridans bacteremia.
Chest X-ray did not reveal any acute abnormalities, and transthoracic echocardiogram did not
reveal any vegetations. Transesophageal echocardiogram revealed two small linear, mobile echodensities attached to the aortic valve which were
believed to represent Lambl’s excrescences or
atypical appearance of vegetations. FDG-PET/
CT was obtained to evaluate for LVAD infection.
It revealed focal, intense FDG uptake at the site
of the LVAD inow cannula (Fig.16.4a, yellow
arrows) with SUV
of 5.0, as well as FDG
max
uptake at the insertion of the outow graft to the
ascending aorta with SUV
of 3.3 (Fig.16.4b,
max
orange arrows). In addition, FDG uptake was
noted on the left atrial appendage clip with
SUV
of 4.5 (Fig.16.4b, yellow arrows), com-
max
pared to background FDG uptake of LV blood
pool with SUVmean of 2.0. These ndings were
concerning for infection of the LVAD inow and
outow cannulas, and left atrial appendage clip.
Although no FDG uptake was noted in generator pocket or ICD leads, the ICD was explanted
in setting of bacteremia and the patient was
Fig. 16.3 True-negative scan for LVAD infection. FDG
PET/CT images demonstrated no signicant FDG uptake
around the device pump, cannula, or driveline (red
arrows). There was intense uptake along the gallbladder
(yellow arrows), indicating high metabolic activity and
possible infection. There was no clinical evidence of
device infection, and the patient was treated for purulent
cholecystitis. (Adapted from JACC:Cardiovascular
Imaging, vol. 13, no. 5, 2020. Page 1195.)
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a
b
Fig. 16.4 Inammation of LVAD inow cannula (a, yellow arrows), outow graft (b, orange arrows), and left atrial
appendage clip (b, yellow arrows)
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treated with an extended course of antimicrobial
therapy for bacteremia and LVAD infection. This
case illustrates that FDG-PET/CT can detect
infection of various components of the LVAD
including inow cannulas, outow grafts, and
other prosthetic devices in the heart, such as the
left atrial appendage clip.
Case 16.3
A 73-year-old man with nonischemic cardiomyopathy and ventricular tachycardia with ICD and
Heartware LVAD presented with bilateral ank
pain, fevers, and rigors. On physical examination,
there was no drainage at the driveline site, but
there was mild erythema. Blood cultures revealed
Staphylococcus aureus bacteremia. Chest X-ray
and CTA chest/abdomen/pelvis did not reveal
any acute abnormalities. Transesophageal echocardiogram did not reveal any obvious vegetations. FDG-PET/CT was obtained to evaluate
for LVAD infection. It revealed intense FDG
uptake involving the inow cannula (Fig.16.5a,
yellow arrows) with SUV
graft (Fig.16.5b, yellow arrows) with SUV
of 3.4 and outow
max
max
of
3.6, compared to background FDG uptake of LV
blood pool of 1.7. These ndings were concerning for LVAD infection.
The patient was deemed a prohibitive risk for
reoperation and was treated with long-term antimicrobial therapy. This case illustrates that FDGPET/CT can help detect the extent of infection as
nearly the entire outow graft had intense, focal
FDG uptake concerning for infection. The
Standardized Uptake Value (SUV) units are a
semiquantitative assessment of intensity of FDG
uptake, which are reported along with a description of the focality and sites of involvement.
Together, this information can be helpful in clinical decision-making for patients who are at high
risk of surgical intervention.
Case 16.4
A 59-year-old man with ischemic cardiomyopathy with ICD and HeartMate II LVAD presented
with generalized fatigue, elevated lactate dehydrogenase, and itching and discharge from his
driveline site. Driveline cultures were positive for
Staphylococcus aureus. Peripheral blood cultures
remained negative. Transesophageal echocardiogram did not reveal any obvious vegetations.
FDG-PET/CT was obtained to evaluate for LVAD
infection. It revealed FDG uptake at the inow
cannula with SUV
of 2.4 compared to LV
max
blood pool of 1.1 (Fig.16.6a, yellow arrows). It
ab
Fig. 16.5 Inammation of LVAD inow cannula (a, yellow arrows) and entire outow graft (b, yellow arrows)
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a
c
b
Fig. 16.6 Inammation of LVAD inow cannula (a, yellow arrows), outow graft (a, orange arrows), driveline (b,
yellow arrows), and pacemaker leads (c, yellow arrows)
also revealed FDG uptake at the outow graft
with SUV
of 2.7 (Fig.16.6a, orange arrows).
max
In addition, there was FDG uptake along the
driveline just inside the insertion point into the
skin with SUV
of 3.1 (Fig. 16.6b, yellow
max
arrows). There was also FDG uptake involving
the pacemaker leads in the right atrium with
SUV
of 2.5 (Fig. 16.6c, yellow arrows).
max
Overall, these ndings are consistent with infection involving the LVAD inow cannula, outow
graft, driveline, and pacemaker leads.
The patient was treated with long-term antimicrobial therapy and underwent pump exchange as
he also had LVAD pump thrombosis. This case
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