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22 Prosthetic Valves
295
Fig. 22.22 Bileaet mechanical valve in the mitral position with noted thrombus (arrow) and xed lateral
mechanical occluder (panel A). Spectral Doppler shows
senting with cardiogenic shock following a
prolonged cessation of VKA anticoagulation
requiring emergent surgery. Intraoperative TEE
performed showed thrombosis of the mechanical
prosthetic valve (Fig.22.22 with corresponding
Video 22.23).
Bioprosthetic Valve Thrombosis
Bioprosthetic valve thrombosis, although less
common compared to mechanical valves, typically occurs in the rst 3 months postimplantation. However, cases of subclinical
bioprosthetic valve thrombosis occurring 1 year
or more post-intervention have been detected
with MDCT (multidetector cardiac computed
tomography) cardiac imaging and are characterized by the presence of hypoattenuating leaet
thickening and reduced leaet motion and may
represent a form of bioprosthetic dysfunction
[14–16].
By echo, valve thrombosis may present as an
abnormally elevated peak velocity and gradients
across the prosthesis. Additional ndings may
include either limited leaet motion, a xed
elevated gradient across MV prosthesis with mean gradient of 30mmHg at HR of 144bpm (panel B)
echogenic density on the valve leaet, or mobile
densities attached to the leaet.
Patients with bioprosthetic valves may require
anticoagulation with a VKA in the rst several
months after valve replacement to reduce the risk
of thromboembolism until the valve is endothelialized. Most patients do not require lifelong anticoagulation unless other reasons for
anticoagulation are present [15, 16].
Case 9
65 y.o. F with a history of bioprosthetic MV
replacement one year prior who presented with
dyspnea on exertion. TTE showed a signicant
increase in the MV mean gradient compared to
the TTE performed 9 months prior.
She underwent a TEE that showed thrombosis
of her mitral bioprosthetic valve resulting in stenosis (Fig. 22.23 with corresponding Videos
22.24 and 22.25). Pt was initiated on anticoagulation with a VKA and underwent a repeat TEE 3
months later with improvement in valve mobility
and gradient noted (Fig.22.24 with corresponding Video 22.26).
296
G. A. Ayuba and V. Rigolin
ab
Fig. 22.23 Bioprosthetic mitral valve thrombosis with valve thickening noted (arrow, panel A) with increased mean
gradient across the prosthesis measuring 11mmHg at HR of 66bpm (panel B)
Fig. 22.24 CW
Doppler of the mitral
valve showing
improvement of the
mean gradient from
11mmHg at HR of
66bpm to 5mmHg at
HR of 53bpm following
3 months of
anticoagulation
Summary Points
• Echocardiography plays a key role in the
assessment of prosthetic valve structure and
function.
• Detailed evaluation should include twodimentional Doppler evaluation and 3D imaging when available.
• It is important to understand the normal ow
dynamics of prosthetic valve types and recognize abnormalities when present.
• Evaluation of prosthetic valve dysfunction may
require transthoracic and transesophageal echo-
cardiography and potentially other imaging
modalities when ultrasound imaging is limited.
Questions
1. True or False?
Regarding prosthetic aortic valves, an ele-
vated gradient always represents pathologic
stenosis of the prosthesis.
Answer: False.
Elevated gradient across an aortic prosthe-
sis could represent prosthetic stenosis, patient
22 Prosthetic Valves
297
prosthesis mismatch, sub valvular narrowing,
high ow state or pressure recovery phenomenon. A careful and detailed evaluation should
be performed to assess the etiology and mechanism of elevated gradients.
2. Patient with 21mm bioprosthetic AV.
Echo shows: AV velocity 3.8 m/s, mean
gradient 35 mmHg, DI 0.26, triangular jet
contour, AVA 1.1cm2, AT 76ms, BSA 2.2m2,
trivial aortic regurgitation. This elevated
velocity likely represents what pathology?
A. Patient with high ow state.
B. Patient with severe prosthetic stenosis.
C. Patient with PPM.
D. Severe subvalvular stenosis.
Answer: C.
Given dimensionless index of 0.26 and
short acceleration time of 76 ms, this is not
consistent with severe prosthetic stenosis or
severe subvalvular stenosis.
The indexed EOA differentiates high ow
from PPM with a value <0.85cm2/m2 being
consistent with PPM.The above patient has a
calculated index EOA of 0.5cm2/m2 which is
consistent with severe PPM.
(See Table 22.1 and Fig. 22.13 for
reference)
3. True or False?
Anticoagulation with a factor 10a inhibitor
or VKA may be used for lifelong anticoagulation indicated for mechanical valves.
Answer: False.
Mechanical valves require the use of life-
long anticoagulation with a vitamin K antagonist (VKA).
Newer anticoagulants (such as antithrombin
or factor 10a inhibitors) have not been shown
to be effective or safe in preventing thromboembolism associated with mechanical prosthetic valves and are currently not approved for
use with mechanical prosthetic valves.
References
1. Otto CM, Nishimura RA, Bonow RO, et al.
Guideline for the management of patients with
Valvular Heart Disease: a report of the American
College of Cardiology/American Heart Association
Joint Committee on Clinical Practice Guidelines.
Circulation. 2021;143:72–227.
2. Zoghbi WA, Chambers JB, Dumesnil JG, et al.
Recommendations for evaluation of prosthetic
valves with echocardiography and Doppler ultrasound: a report from the American Society of
Echocardiography’s Guidelines and Standards
Committee and the Task Force on Prosthetic Valves. J
Am Soc Echocardiogr. 2009;22:975–1014.
3. Pibarot P, Dumesnil JG.Prosthetic heart valves selection of the optimal prosthesis and long-term management. Circulation. 2009;119:1034–48.
4. Graf T, Reul H, Detlefs C, etal. Causes of formation
of cavitation in mechanical heart valves. J Heart Valve
Dis. 1994;3(1):49–64.
5. Blais C, Dumesnil JG, Baillot R, et al. Impact of
valve prosthesis-patient mismatch on short-term
mortality after aortic valve replacement. Circulation.
2003;108:983–8.
6. Pibarot P, Dumesnil JG.Prosthesis-patient mismatch:
denition, clinical impact, and prevention. Heart.
2006;92:1022–9.
7. Zoghbi WA, Asch FM, Bruce C, etal. Guidelines for
the evaluation of valvular regurgitation after percutaneous valve repair or replacement: a report from the
American Society of Echocardiography. Developed
in collaboration with the Society for Cardiovascular
Angiography and Interventions, Japanese Society of
Echocardiography, and Society for Cardiovascular
Magnetic Resonance. J Am Soc Echocardiogr.
2019;32:431–75.
8. Kodali S, Pibarot P, Douglas PS, et al. Paravalvular
regurgitation after transcatheter aortic valve replacement with the Edwards sapien valve in the PARTNER
trial: characterizing patients and impact on outcome.
Eur Heart J. 2015;36(7):449–56.
9. Makkar RR, Thourani VH, Mack MJ, etal. Five-year
outcomes of transcatheter or surgical aortic-valve
replacement. N Engl J Med. 2020;382:799–809.
10. Wilson W, Taubert KA, Gewitz M, etal. Prevention of
Infective Endocarditis. Guidelines from the American
Heart Association: a guideline from the American
Heart Association Rheumatic Fever, Endocarditis,
and Kawasaki Disease Committee, Council on
Cardiovascular Disease in the Young, and the Council
on Clinical Cardiology, Council on Cardiovascular
Surgery and Anesthesia, and the Quality of Care and
Outcomes Research Interdisciplinary Working Group.
Circulation. 2007;116:1736–54.
11. Horstkotte D, Follath F, Gutschik F, etal. Guidelines
on prevention, diagnosis and treatment of infective
endocarditis executive summary: the Task Force on
Infective Endocarditis of the European Society of
Cardiology. Eur Heart J. 2004;3:267–76.
12. Li JS, Sexton DJ, Mick N, etal. Proposed modications to the duke criteria for the diagnosis of infective
endocarditis. Clin Infect Dis. 2000;30:633–8.
13. Piper C, Körfer R, Horstkotte D. Prosthetic valve
endocarditis. Heart. 2001;85:590–3.
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14. Horstkotte D, Scharf RE, Schultheiss HP.Intracardiac
thrombosis: patient-related and device-related factors.
J Heart Valve Dis. 1995;4:114–20.
15. Whitlock RP, Sun JC, Fremes SE, et al.
Antithrombotic and thrombolytic therapy for valvular disease: Antithrombotic Therapy and Prevention
of Thrombosis, 9th ed: American College of Chest
Physicians Evidence-Based Clinical Practice
Guidelines. Chest. 2012;141:e576S–600S.
16. Makkar RR, Blanke P, Leipsic J, et al. Subclinical
leaet thrombosis in transcatheter and surgical bioprosthetic valves: PARTNER 3 Cardiac Computed
Tomography Substudy. J Am Coll Cardiol.
2020;75:3003–15.
Infective Endocarditis
FloraLi andSaraNikravan
23
Learning Objectives
1. Discuss direct echocardiographic ndings
consistent with endocarditis, such as vegetations, abscesses, other perivalvular complications, and prosthetic valve dehiscence.
2. Identify normal anatomic variants on echocardiography that can be confused for vegetations.
3. Examine the indications for performing transesophageal echocardiography to aid in
diagnosis.
Introduction
Infective endocarditis is a rare but life- threatening
infection of the endocardial surface of the heart.
The causal organism is most often bacterial, with
80% of cases of native-valve endocarditis being
caused by gram-positive bacteria [1
hospital mortality for patients with endocarditis
is 15–20%, with one-year mortality near 40%.
Current treatments consist of a combination of
prolonged antibiotic therapy and surgical management, ideally with the involvement of a multi-
Supplementary Information The online version contains supplementary material available at https://doi.
org/10.1007/978- 3- 031- 80038- 2_23.
F. Li · S. Nikravan (*)
University of Washington, Seattle, WA, USA
e-mail: fmli@uw.edu; nikravan@uw.edu
]. The in-
disciplinary team including cardiology,
cardiothoracic surgery, and infectious disease
expertise [2]. The two main components of treatment are antibiotics and surgery. The timing and
indications of surgical intervention are still not
entirely clear, with some groups advocating for
early surgery (within 48 h of diagnosis) and others advocating for surgery after a “cool off”
period of antibiotic therapy [1–3]. Strong surgical indications include severe valvular dysfunction, heart failure, infection that is refractory to
antibiotic therapy, abscess formation, and large
lesions that are at high risk for embolism
(Table 23.1). Patients in cardiogenic shock or
with severe pulmonary edema should undergo
surgery urgently [2, 3].
Although endocarditis can occur in patients
with no prior cardiac issues, patients with preexisting structural abnormalities such as rheumatic
or sclerotic valvular disease, congenital cardiac
disease, or intracardiac prosthetic material are at
higher risk of developing endocarditis. The
source can be bacteremia from any source,
including transient bacteremia caused by everyday occurrences such as tooth brushing and
chewing. Bacteremia usually has little effect on
healthy, intact cardiac endothelium. However, in
the setting of endothelial damage, local inammation and thrombus formation can promote
bacterial adhesion and provide a site for bacterial
colonization. Bacterial colonization leads to
additional injury and inammation, eventually
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2025
M. J. Lanspa, A. T. Levinson (eds.), Echocardiography and Ultrasonography in the ICU,
Respiratory Medicine, https://doi.org/10.1007/978-3-031-80038-2_23
299
300
F. Li and S. Nikravan
forming a vegetation that is poorly penetrated by
host neutrophils and defense molecules [4]. If left
untreated, severe complications include sepsis,
Table 23.1 Indications for surgery
• Severe valvular dysfunction
• Heart failure
– Typically caused by severe valvular
regurgitation or obstruction by mass
• Perivalvular complications (e.g. abscess or stula)
• Embolic events despite appropriate antibiotic
therapy
– Cerebralvascular events, provided risk of
hemorrhagic conversion is low
– Other systemic embolic events: renal infarct,
splenic infarct, limb ischemia
– Pulmonary embolic events: pulmonary
embolism, pulmonary infarcts
• Large vegetation
– >10mm on aortic or mitral valves
– >15mm on tricuspid valves
• Persistent sepsis despite appropriate antibiotic
therapy
• Difcult organisms
– Examples include S. aureus, Brucella,
Staphylococcus lugdunesis, Pseudomonas
aeruginosa
• Nearly all cases of prosthetic valve endocarditis
valvular destruction and failure, spread of infection into paravalvular structures with abscess formation, left or right ventricular failure, and
emboli to systemic vessels and other organs with
abscess formation and tissue infarction. This can
ultimately lead to multiorgan failure and death.
Diagnosis
Diagnosis of endocarditis can be challenging due
to its variable presentation and requires utilization
of clinical ndings, laboratory examination using
blood cultures, and echocardiography. The modied Duke criteria for diagnosis of endocarditis
incorporate these ndings into one system that
categorizes each nding as a major or minor criterion. Under this system, the presence of two major
criteria, one major criterion and three minor criteria, or ve minor criteria is required for a denite
diagnosis of endocarditis (Table 23.2) [5].
Although the Duke criteria were initially created
for research use, subsequent studies have shown
that these criteria have a high sensitivity and specicity in the clinical setting, with sensitivity
reported to range from 62–76% [6–8].
Table 23.2 Modied Duke criteria
Major criteria Minor criteria
1. One of the following on blood cultures:
• Typical microorganisms (Staphylococcus aureus,
viridans streptococci, Streptococcus bovis,
HACEK (haemophilus, aggregatibacter,
cardiobacterium, Eikenella corrodens, kingella)
group, or community-acquired enterococci, in the
absence of a primary focus
• Microorganisms consistent with infective
endocarditis from persistently positive blood
cultures, dened as ≥2 positive cultures from
blood samples drawn >12 h apart or all of 3 or a
majority of ≥4 separate cultures of blood (with
rst and last sample drawn at least 1 h apart)
• Single positive blood culture for Coxiella burnetii
or phase I IgG antibody titer >1:800
2. Evidence of endocardial involvement
• Direct echocardiographic evidence of
endocarditis: vegetation, abscess, or new partial
dehiscence of a prosthetic valve
• New valvular regurgitation
Adapted from Li etal. [5]
1. Predisposing cardiac condition or intravenous drug
use
2. Temperature ≥38.0°C (100.4°F)
3. V ascular phenomena (major arterial emboli, septic
pulmonary infarcts, mycotic aneurysm,
intracranial hemorrhages, conjunctival
hemorrhages, Janeway lesions)
4. Immunologic phenomena (glomerulonephritis,
Osler nodes, Roth spots, or rheumatoid factor)
5. Positive blood cultures that do not meet major
criteria, or serologic evidence of active infection
with organism consistent with infective endocarditis
23 Infective Endocarditis
301
Echocardiographic Assessment
Echocardiographic assessment plays an important
role in the diagnosis of endocarditis. Of the two
major criteria of the modied Duke criteria, one
utilizes echocardiography heavily. The rst major
criterion is positive blood cultures, and the second
is evidence of endocardial involvement [5, 9].
There are three echocardiographic ndings
that are considered direct echocardiographic ndings of endocarditis: vegetations, abscesses and
related perivalvular complications such as pseudoaneurysms and stulas, and new dehiscence of
a prosthetic valve (Fig. 23.1). Valvular vegetations are the classic lesion of endocarditis and are
most frequently found on the low- pressure side of
the valve structure. They generally present as
oscillating masses that move with a motion independent of the valve. Although they are most
commonly found on the valvular or subvalvular
apparatus, they can also form on the endocardium,
especially along the path of a turbulent regurgitant
jet (Fig.23.1a, Video 23.1) [3, 10].
Abscesses and associated perivalvular complications are the second group of major echocardiographic ndings of endocarditis. Abscesses
are seen on echocardiography as thickened perivalvular tissue with a heterogeneous appearance
with echodense or echolucent uid-lled areas.
The uid cavity in an abscess is not in communication with the cardiovascular lumen. Although
abscesses can be associated with any location of
infection, they are most common in aortic valve
and prosthetic valve endocarditis (Fig.23.1a, b,
Videos 23.1 and 23.2). In contrast to abscesses,
pseudoaneurysms are perivalvular cavities that
do communicate with the cardiovascular lumen.
They have a similar appearance to abscesses but
have pulsatile ow that can be seen with color or
spectral Doppler. Fistulas are complications of
abscesses or pseudoaneurysms and are dened as
a communication between two neighboring cardiac chambers. Flow between the two chambers
should be visualized using color or spectral
Doppler in order to distinguish stulas from the
other perivalvular complications.
The last major direct echocardiographic
nding is new dehiscence of a prosthetic valve.
Even without the other two ndings, new perivalvular regurgitation in a prosthetic valve is
highly suspicious for endocarditis (Fig.23.1c,
Video 23.3). Valve dehiscence and abscess formation are seen in 60% of cases of prosthetic
valve endocarditis [3]. However, since perivalvular regurgitation can occur as a postoperative
complication of prosthetic valve implantation,
care must be taken to conrm that any regurgitation seen is new and has not been previously
documented [3, 10].
In the setting of a patient with high suspicion
for endocarditis, detection of new valvular regurgitation is also considered sufcient evidence for
endocardial involvement. This can be diagnosed
clinically (e.g., with a new murmur), but clinical
ndings should be conrmed with an echocardiogram. Care must be taken to ensure that any
regurgitation seen is indeed new and not worsening of previously seen regurgitation. New regurgitation due to endocarditis can occur from direct
destruction of the valve leaets or subvalvular
apparatus.
Echocardiographic imaging in patients
with high suspicion for endocarditis can be
performed using either transthoracic echocardiography (TTE) or transesophageal echocardiography (TEE) [5, 8]. TTE has a lower
sensitivity than TEE (72% for TTE compared to
over 90% for TEE) but is noninvasive and more
widely available [3, 5, 8]. It is recommended as
the initial imaging modality to use for evaluation of a suspected case of endocarditis. TEE
should be used as a supplemental imaging
modality to look for further cardiac complications in positive cases and as conrmation
in equivocal or complicated cases [10–12] as
depicted when comparing imaging from the
same patient in Video 23.4 (TTE) to Video 23.5
(TEE) (Fig. 23.2). 3D TEE is an additional
modality made possible by improvements in
transducer technology and can provide better
anatomic information than 2D TEE (Fig.23.3,
Video 23.6).
302
F. Li and S. Nikravan
a
b
c
Fig. 23.1 Examples of major echocardiographic ndings
of endocarditisThere are three major echocardiographic
ndings of endocarditis: vegetation (a), abscess (a and b),
and new valvular dehiscence (c). (a) (Video 23.1): TEE
short and long axis views of a large aortic valve vegetation.
Note the perivalvular thickening (yellow arrows) that is
suggestive of abscess. (b) (Video 23.2): TEE short and long
axis views of aortic valve endocarditis causing cusp
destruction and abscess (red arrows). (c) (Video 23.3):
mechanical prosthetic valve dehiscence in diastole and systole in TEE ME long axis view. Note that the lower edge of
the valve annulus moves into the aortic root during systole
23 Infective Endocarditis
ab
cd
303
Fig. 23.2 Comparison of TTE and TEE imagingThis is
a large mitral valve vegetation visualized using both
TTE and TEE.Although the mass and the valvular regurgitation jet are visible in the apical 4 chamber TTE
Patients who should have supplemental TEE
exams include those with prosthetic valves or
intracardiac devices, patients with non- diagnostic
TTE images, or patients with TTE exams that
were negative but with moderate to high clinical
suspicion for endocarditis. In these patient
groups, TEE has signicantly higher sensitivity
images (a and b), the analogous TEE mid-esophageal 4
chamber views (c and d) demonstrate both more clearly.
Videos 23.3 and 23.4 are the clips of (a) and (b),
respectively
for detecting vegetations. For example, in patients
with prosthetic valves, the sensitivity of TTE
decreases to 36–69% [10].
When performing echocardiographic evaluation, care must be taken to distinguish vegetations from normal anatomic variants that
resemble vegetations. In the right atrium, the
304
F. Li and S. Nikravan
Fig. 23.3 3D rendering of the aortic valve mass from
Fig.23.1a using multiplanar reconstruction. The red, blue,
and green planes show 2D cross sections at different angles.
In this example, the green plane at top left shows an aortic
valve short axis view, the red plane at top right shows a long
Eustachian valve, Chiari network, and crista terminalis are all normal structures that can be confused for vegetations. The Eustachian valve is an
embryonic remnant located near the inferior vena
cava that served to direct oxygen-rich blood from
the inferior vena cava to the foramen ovale in
fetuses. In adults, it is a thin structure that is
attached to the junction of the inferior vena cava
and the right atrium. The Chiari network is a
mobile net-like structure that may be continuous
with the Eustachian valve. It appears on echocardiograms as a thin, mobile structure that spans
the right atrium (Fig. 23.4a, Video 23.7). The
crista terminalis is a ridge of tissue running from
the superior vena cava to the inferior vena cava in
the right atrium.
axis view, and the blue plane at bottom shows a cut across
the non-coronary and left coronary cusps. The 3D in the
bottom right corner shows the mass at the coaptation
between the non and left coronary cusps. Video 23.6 is a
clip showing this view through the entire cardiac cycle
Lambl’s excrescences and broelastomas can
be found on any valve and can be difcult to differentiate from vegetations. Lambl’s excrescences are thin brous strands occurring at the
edges of the cusps and are most often seen on
the aortic valve. Unlike vegetations, they typically do not form masses and are not heterogeneous in appearance (Fig. 23.4b, Video 23.8).
Cardiac broelastomas are bulky, often pedunculated masses that can be found on the lowpressure side of valves and on endocardial
surfaces (Fig.23.4c, Video 23.9). They can be
especially difcult to distinguish from vegetations and require consideration of the whole
clinical picture to determine the likelihood of
endocarditis.