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Fig. 18.3 Tricuspid valve replacement with a bioprosthetic valve
patients with severe primary TR if symptomatic
or severe secondary TR which has responded
poorly to medical therapy [3]. Surgery is also
deemed reasonable in asymptomatic patients
with severe primary TR and progressive RV dilation or systolic dysfunction [3].
The timing of surgical intervention is preferrable before the onset of signicant RV dysfunction or end-organ damage. Once these are
present, surgery has a signicantly increased
risk with mortality rates of 8–20% and the additional risk of RV failure [3]. In specic cases
where patients develop acute severe primary
TR, TV surgery should be considered urgent
and completed prior to the onset of RV dysfunction [3]. Acute TR may develop from injury to
the valve apparatus, and survival is directly
related to RV function.
Preoperative Assessment
andSurgical Risk
A. Booke et al.
catheterization to assess for coronary artery disease. If cardiac disease is present, CABG should
be completed at the time of the valve surgery.
The STS does not include tricuspid valve
repair/replacement as part of their STS risk calculator. However, patient statistics and outcomes
may be viewed in the database to aid in the surgeon’s justication for risk assessment. In the
cases involving tricuspid valve surgery, a provider must account for physical assessment,
frailty, clinical judgment, and multidisciplinary
team discussions to determine if patient is an
appropriate surgical candidate.
Valve Selection
With tricuspid regurgitation, valve repair is the
preferred surgical approach. In tricuspid valve
repair, an annuloplasty ring is placed to correct
dilation, improve coaptation, and provide support
to the valvular apparatus. If repair is not feasible,
tricuspid valve replacement is warranted. The
surgical decision-making regarding valve selection is complex, multifactorial, and based on
patient age, life expectancy, medical compliance,
and ability to tolerate long-term anticoagulation.
Refer to the section on valve selection under surgical management of aortic insufciency in
Chap. 16 for further discussion.
Currently, there is no superiority between bioprosthetic and mechanical valves in TV replacement [5]. This may change as transcatheter TVR
modalities evolve and percutaneous valve-invalve replacements gain popularity.
Preoperative assessment for tricuspid valve surgery begins with a history, physical, and baseline
diagnostic testing. Dental evaluation is recommended preoperatively to decrease the risk of
endocarditis following the placement of a prosthetic valve. Refer to previous chapters regarding
preoperative assessment for further discussion
and Chap. 6: Tables 6.1 and 6.2.
Along with the standard preoperative testing
and transesophageal echo (TEE), all patient’s
undergoing cardiac surgery should have a cardiac
Tricuspid Stenosis
Tricuspid stenosis is most frequently rheumatic in
origin and often coexists with TR.Given that TS
is primarily rheumatic in origin, it is often associated with rheumatic MS.Rare causes of tricuspid
stenosis are congenital, carcinoid, drug induced,
endocarditis, and right atrial tumors. As diastolic
pressures rise, systemic venous congestion occurs,
resulting in right-sided heart failure. Cardiac output falls and fails to rise with exertion.
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Symptoms
Patients will experience exertional dyspnea that
is out of proportion to the hepatomegaly, ascites,
and edema they experience [6]. Severe TS is
associated with hepatic congestion resulting in
cirrhosis, jaundice, malnutrition, anasarca, and
ascites.
Evaluation
Often the murmur of TS is missed given that usually there is concomitant MS.If the provider can
auscultate the TS murmur, one might hear an
opening snap with a diastolic murmur along the
left lower sternal border that worsens with inspiration [6].
TTE will provide the most useful information,
although tricuspid stenosis is most often overlooked. One should evaluate valve anatomy and
assess the subvalvular apparatus. Stenosis is signicant when the mean transvalvular gradient is
≥5mmHg [2].
Management/Intervention
Patients with TS also often have TR and exhibit
marked systemic venous congestion. Diuretics
are the mainstay of management but have limited
long-term efcacy [6]. Intervention is usually
performed concomitantly with left-sided valve
disease in symptomatic patients despite optimal
medical therapy.
Percutaneous tricuspid balloon valvuloplasty
frequently induces signicant tricuspid insufciency and long-term results are lacking [2].
Surgical Management ofTricuspid
Stenosis
Tricuspid valve replacement is the surgical treatment of choice for tricuspid stenosis (TS). Given
the calcic nature of the leaets in stenotic disease, the native leaets are not amenable to repair.
Refer to the chapter on aortic stenosis for further
discussion on valve selection.
During tricuspid valve surgery, there are multiple areas to be mindful of during suture placement. The right coronary artery (RCA) lies in the
AV groove with close approximation to the posterior leaet of the tricuspid valve. Placement of
valve sutures may result in functional stenosis or
direct suturing of the coronary artery [5]. Care
should also be taken at the level of the AV node.
The AV node lies along the anteroseptal commissure at the base of the septal leaet. Injuring the
AV node during repair or replacement with valve
stitches may result in AV nodal blockade [5].
Indication and timing of surgical intervention
for TS is dependent on severity of disease and
timing of concomitant left-sided valve interventions. Isolated tricuspid valve disease is rare.
Rheumatic disease is the primary cause of TS and
occurs concurrent with rheumatic mitral valve
disease. Once surgical intervention of the mitral
valve is undertaken, the tricuspid valve is simultaneously addressed. Both the ACC/AHA guidelines and the European Society of Cardiology
(ESC) recommend tricuspid valve surgery on (1)
patients with severe TS at the time of operation
for left-sided valves and (2) on isolated TV with
symptomatic, severe TS [5].
Overall, tricuspid stenosis is rare in the given
population and is infrequently seen as an isolated
procedure in the operating room.
References
1. Zoghabi WA, etal. Recommendations for evaluation
of the severity of native valvular regurgitation with
two-dimensional and Doppler echocardiography. J
Am Soc Echocardiogr. 2003;16(7):777–802.
2. Vahanian A, Beyersdorf F, Praz F, Milojevic M,
Baldus S, Bauersachs J, Capodanno D, Conradi L,
De Bonis M, De Paulis R, Delgado V, Freemantle N,
Gilard M, Haugaa KH, Jeppsson A, Jüni P, Pierard
L, Prendergast BD, Sádaba JR, Tribouilloy C,
Wojakowski W, ESC/EACTS Scientic Document
Group, ESC National Cardiac Societies. 2021 ESC/
EACTS Guidelines for the management of valvular
heart disease: developed by the Task Force for the
management of valvular heart disease of the European
Society of Cardiology (ESC) and the European
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A. Booke et al.
Association for Cardio-Thoracic Surgery (EACTS).
Eur Heart J. 2022;43(7):561–632.
3. Otto CM, Nishimura RA, Bonow RO, Carabello BA,
Erwin JP III, Gentile F. 2020 ACC/AHA 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. J Am Coll Cardiol.
2021;77(4):e25–e197.
4. Taramassa M, etal. Tricuspid regurgitation, predicting the need for intervention, procedural success, and
recurrence of disease. JACC Cardiovasc Imaging.
2019;12(4):605–21. https://doi.org/10.1016/j.
jcmg.2018.11.034.
5. Cevasco M, Shekar PS. Surgical management
of tricuspid stenosis. Ann Cardiothorac Surg.
2017;6(3):275–82.
6. Loscalzo J, Fauci A, et al. Harrison’s principles of
internal medicine. 21st. ed, Volume 1 and Volume 2.
NewYork: McGraw Hill; 2022.
Infective Endocarditis
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AllenStephens, ToddMcVeigh, CaryWard,
ElisabethA.Powell, andLarryWatts
19
Symptoms
Symptoms of infective endocarditis are diverse
and often nonspecic. The most common presenting symptoms are fever, chills, weakness,
and malaise. Patients may also present with dyspnea which can be indicative of a severe lesion
causing onset of heart failure. See Table19.1 for
presenting symptoms [1].
The diagnosis of IE based upon physical
examination ndings alone can be difcult and is
often missed due to the variability of disease presentation [2]. Patients can present with nonspecic primary symptoms over a course of weeks to
months [3]. IE should be on the differential diagnosis in patients presenting with sepsis without
an obvious cause, as well as in patients who present with a fever of unknown origin and have IE
A. Stephens (*) · T. McVeigh · C. Ward
Duke University Health System, Durham, NC, USA
e-mail: Allen.stephens@duke.edu;
Todd.mcveigh@duke.edu; c.ward@duke.edu
E. A. Powell
Banner University Medical Center, Tucson, AZ, USA
e-mail: elisabeth.powell@bannerhealth.com
L. Watts
Atrium Health/Sanger Heart and Vascular Institute,
Charlotte, NC, USA
e-mail: Larry.Watts@atriumhealth.org
Table 19.1 Symptoms in infective endocarditis
Symptom Patients affected (%)
Fever 80–95
Chills 40–70
Weakness 40–50
Malaise 20–40
Sweats 20–40
Anorexia 20–40
Headache 20–40
Dyspnea 20–40
Cough 20–30
Weight loss 20–30
Myalgia/arthralgia 10–30
Stroke 10–20
Confusion/delirium 10–20
Nausea/vomiting 10–20
Edema 5–15
Chest pain 5–15
Abdominal pain 5–15
Hemoptysis 5–10
Back pain 5–10
Adapted from Braunwald’s Heart Disease Textbook (10th
Edition) Page 1527
risk factors (see Table19.3). Acute presentations
of IE can progress rapidly, as patients can present
with sudden onset of heart failure, stroke, systemic or pulmonary embolization, severe sepsis
with fevers, rigors, or septic shock.
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023
R. Musialowski, K. Allshouse (eds.), Cardiovascular Manual for the Advanced Practice Provider,
https://doi.org/10.1007/978-3-031-35819-7_19
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Physical Exam
The most common physical examination ndings
are shown in Table 19.2 with fever (present in
80–90% of patients) and a cardiac murmur (present in 75–85% of patients) being the two most
prevalent. Although IE is commonly associated
with a heart murmur (typically due to valvular
regurgitation), new murmurs are present in less
than 50% of cases [4]. A worsening of a preexisting heart murmur accounts for the remainder
of murmurs found on physical exam in IE.A central neurologic abnormality, such as focal decits
consistent with a cerebrovascular accident, can
be identied in 20–40% of IE patients [5]. An
abdominal exam can elicit nonspecic ndings
of tenderness, which can be suggestive of splenic
embolization and infarction when in the left
upper quadrant [1]. The spleen was found to be
the second-most common site of septic embolization after the brain in one study [1].
The classic diagnostic ndings of Janeway
lesions (painless hemorrhagic macules on the
soles and palms), Osler nodes (painful, erythematous nodular lesions on the pads of the ngers
and toes), and Roth spots (retinal hemorrhages)
are vascular and immunologic phenomena
(Fig.19.1). Acute IE can often evolve too quickly
for the development of these phenomena [6].
These classically described ndings are more
characteristic of later stages of subacute,
A. Stephens et al.
Fig. 19.1 Ischemic digit from emboli (red), Osler’s node
(black), and Janeway spots (yellow) in a patient with
MSSA endocarditis
untreated IE. Approximately 75% of patients
with IE are now diagnosed within 30days of the
onset of infection, so these long-term ndings are
less commonly seen [2].
The diagnosis of IE cannot be excluded on
history and physical exam ndings alone. Given
the variety of patient presentations and varying
physical exam ndings, misdiagnosis and delays
in diagnosis are common. These delays can postpone denitive management and contribute to
increased mortality due to progressive structural
heart damage that can eventually become irreparable [2].
Risk Factors
Table 19.2 Physical ndings in infective endocarditis
Physical Findings
Fever 80–90
Heart murmur 75–85
New murmur 10–50
Changing murmur 5–20
Central neurologic abnormality 20–40
Splenomegaly 10–40
Petechiae/conjunctival
hemorrhage
Splinter hemorrhages 5–15
Janeway lesions 5–10
Osler nodes 3–10
Retinal lesion or Roth spot 2–10
Patients affected
(%)
10–40
The incidence of IE is inuenced by a variety of
risk factors, both cardiac and non-cardiac
(Table 19.3). In less developed countries, rheumatic degenerative heart disease remains the
most common risk factor. In developed countries,
the most common risk factors include intrinsic
cardiac factors (history of prior infective endocarditis, congenital heart disease), followed by
pre-existing valve disease, such as mitral or aortic regurgitation, and the presence of implanted
devices. Non-cardiac risk factors include IV drug
use, immunocompromising conditions, such as
cancer or diabetes, and recent dental or surgical
procedures [7].
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Table 19.3 Endocarditis risk factors
Age >60years old
IV drug use
History of prior endocarditis
Poor dentition or recent dental procedure
Presence of intracardiac device or prosthetic valve
History of valvular heart disease (rheumatic disease,
congenital heart disease such as aortic stenosis or
bicuspid aortic valve)
Indwelling intravenous catheter
Immunosuppression
Hemodialysis patients
Pathology/Description
Infective endocarditis occurs when an underlying
valvular or nonvalvular structural abnormality
results in turbulent blood ow leading to endothelial injury [1]. This injury results in an inammatory response releasing cytokines and tissue
factors causing platelets and thrombin to adhere
to the sub endothelium. This ultimately forms a
microthrombotic lesion and bacteria in the blood
stream then adhere to the microthrombus. This
colonization leads to additional bacterial replication and formation of an infective vegetation.
These vegetations have high bacterial density and
are poorly inltrated by neutrophils, allowing
them to easily grow and fragment into the blood
stream [5].
Microbiology
Positive blood cultures are a hallmark of endocarditis. Gram positive bacteria account for 80%
of cases of native infective endocarditis. This
includes Staphylococcus aureus (35–40%), streptococci (30–40%), and enterococci (10%)
(Table 19.6). Coagulase negative staphylococci
are more common in prosthetic-valve infective
endocarditis [5]. The HACEK organisms (see
Table 19.4 HACEK organisms
Hemophilic parainuenzae
Aggregatibacter actinomycetemcomitans
Cardiobacterium hominis
Eikenella corrodens
Kingella kingae
Table 19.4) are fastidious gram-negative bacilli
that are difcult to grow in culture and are less
common causes of subacute IE. If these organisms are considered, discussion with the ID specialist and microbiology laboratory is important
for appropriate testing to be performed. Fungi are
extremely rare as cause of IE. Unfortunately,
some patients with endocarditis can have negative blood cultures, most commonly because of
recent antimicrobial exposure [1].
Imaging
Echocardiography is a key modality in the diagnosis of endocarditis and is a major component of
the Duke criteria (see below). Traditional transthoracic echocardiography (TTE) has a sensitivity for vegetation detection between 50–60%
while transesophageal echocardiography (TEE)
has a sensitivity close to 90%. Both modalities
have specicities close to 95% [5]. TEE has
increased sensitivity because it circumvents
impediments such as body habitus, pulmonary
disease, and other acoustic interference between
the chest wall and heart [1]. With improved spatial resolution in TTE technology, some newer
studies have shown sensitivity for TTE as high as
89% (Fig.19.6) [1]. Other imaging studies such
as cardiac CT (Fig.19.2) can also be useful in the
diagnosis of perivalvular extension and embolic
complications. Echocardiography demonstrates
the hemodynamic signicance of the leaet
destruction and regurgitant lesions in real time
(Figs.19.3 and 19.7.
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Fig. 19.2 Cardiac CT showing vegetation of infective
endocarditis of the native aortic valve (red arrow)
A. Stephens et al.
imity to the AV node and proximal intraventricular conduction system. Specically, a lesion
involving the right and non-coronary cusps is at
risk of impacting the conduction system. A less
common presentation is a perivalvular extension
or vegetation embolization which affects coronary artery patency resulting in ischemic ECG
changes (ST depression, T wave inversion, or ST
elevation) [1].
Diagnostic Criteria
The Duke Criteria for endocarditis were created
in 1994 to establish the denite or possible diagnosis of IE as well as reject the diagnosis.
Multiple clinical trials have reported sensitivity
of Duke Criteria to be around 80% with specicity and negative predictive value of approximately 90% [1]. The Duke criteria incorporate
clinical ndings, microbiologic analysis, and
imaging results. Criteria are weighted as major or
minor (see Table19.5).
Fig. 19.3 Destruction of the aortic valve leads to severe
eccentric insufciency (red arrow) seen on
echocardiography
EKG
12-lead EKG is less useful in diagnosis of IE and
is usually associated with nonspecic ndings.
Perivalvular extension of infection at the aortic
root can cause new atrioventricular block (AVB)
or bundle branch block (BBB) because of prox-
Table 19.5 Duke major and minor criteria for IE
Major criteria Minor criteria
Blood culture positivity
with an organism
associated with IE on
two separate blood
cultures sets (Tables
19.4 and 19.6)
Evidence of endocardial
involvement seen on
imaging to include
mobile vegetation,
abscess, and/or
dehiscence of a
prosthetic valve
Fever >38°C
Predisposing heart condition
(implanted prosthetic
material, recent or
unrepaired CHD, previous
IE), or IV drug use
Vascular phenomena and
evidence of embolic disease
(Janeway spots), Intercranial
hemorrhage
Microbiological evidence
not meeting major criteria
(organism not associated
with IE, single positive
blood culture)
Immunologic phenomena
Rheumatoid F, Osler’s
nodes, glomerulonephritis
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Denite diagnosis requires (a) two major criteria,
(b) one major with three minor, or (c) ve
minor criteria.
Possible diagnosis requires (a) one major and one
minor or (b) three minor criteria.
Diagnosis is rejected with (a) no clinical criteria
are met or (b) complete resolution of ID syndrome or absence of anatomic evidence for IE
on antibiotic therapy for no more than 4days
or (c) an alternative diagnosis explains the
patient presentation [8].
Management
In general, randomized controlled trials to guide
IE are minimal, and none of the recommendations in international guidelines on IE are
backed by Level A evidence [8]. The management of infective endocarditis (IE) includes
prompt diagnosis, treatment with antimicrobial
therapy, and in some cases of complicated IE,
surgical management [9]. Given its ability to
cause complications both at the cardiac site and
at extracardiac locations, management of IE
requires a team approach. In all cases, decisions
on intervention should be multifactorial and
include a discussion involving multidisciplinary
teams including cardiothoracic surgery, cardiology, and infectious disease. If a patient has
endured an embolic stroke from their IE, neurology should be consulted to make recommendations regarding the timing of surgery. Stroke is
an independent risk factor for postoperative
death, especially if the stroke is hemorrhagic.
Consultation with addiction medicine and discussion with an ethics team should also be considered in cases regarding IV drug abuse
associated IE, especially for recurrent IE.These
cases are complicated with longer hospital
stays, higher readmission rates, medical noncompliance, and re-infection from continued IV
drug abuse. Addiction medicine therapy has
shown to reduce mortality and morbidity rates
in this patient population postoperatively [10].
It is best practice for patients with IE to be managed in a medical center that offers these different specialists [5].
Antimicrobial Therapy
The American Heart Association, American
College of Cardiology, and American Association
for Thoracic Surgery have each published guidelines on the management of IE. While these
guidelines are generally concordant, there are
minor differences in their recommendations
about antimicrobial therapy [2]. Because there
are continuous changes in antimicrobial sensitivity over time, as well as regional and site-specic
differences in antimicrobial susceptibility proles, consultation with infectious disease is
imperative for treatment [2]. The infectious disease team is also essential as resistance to many
antibiotics is rising and has become one of the
greatest threats to modern health care [8].
The primary goal of antibiotic treatment is to
stabilize vegetations and eventually eradicate
infections [6]. The penetration of antibiotics is a
signicant challenge in the treatment of IE
because cardiac vegetations, which are composed
of brin and platelets, pose a considerable
mechanical barrier between the antibiotic and the
embedded targeted microorganisms [6]. These
vegetations create a protective micro- environment
that is poorly accessible to neutrophils and host
defense molecules. Vegetations are loaded with
bacteria at very high densities [5].
In treating IE, determination of the causative
pathogen is of prime importance, allowing clinicians to narrow and target therapy specically to
the pathogen (Table19.6) [4]. Empiric antibiotic
therapy should be initiated and continued after
blood cultures (ideally 3 sets) are obtained [2].
Table 19.6 Common organism and antibiotic regimens
for IE
Example of common
Common causes of IE
Staphylococcus aureus
35–40%
MRSA Daptomycin or vancomycin
MSSA Anti-staphylococcal PCN
Streptococci 30–40% Gentamicin plus penicillin or
Enterococci 10% Ampicillin plus gentamicin
antibiotic regimen
(ex: Nafcillin)
ceftriaxone
or ceftriaxone
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A. Stephens et al.
Once these cultures have been obtained, therapy
should be started very quickly [8]. The choice of
empiric therapy should take into consideration
the most likely pathogens. Gram positive bacteria
account for approximately 80% of cases of native
valve IE. These bacteria include methicillinsensitive Staphylococcus Aureus (MSSA) and
methicillin-resistant Staphylococcus Aureus
(MRSA) (35–40% of cases), streptococci (30–
40% of cases), and enterococci (10% of cases). S.
aureus is the leading cause of IE (both native and
prosthetic valve) in the United States. More rare
species include other gram-positive pathogens,
fungi, polymicrobial infection, and nally gramnegative bacilli [5]. Though fungal IE is rare, it
has well-recognized associated risk factors
including IV drug use, immunocompromised
state, and indwelling devices [6]. After initial
blood cultures have been obtained and empiric
antibiotic therapy started, adjustments in antimicrobial selection depend on the blood culture isolate and its antimicrobial susceptibility [5]. The
expectation is that this empirical therapy will be
revised once the susceptibility results are
obtained, as optimal treatment of IE is based on
antimicrobial therapy that is effective against the
specic infective organism identied [6].
Rarely, IE can occur without associated positive blood cultures. Most often this is caused by
recent administration of antibiotics prior to blood
culture collection or by organisms that grow
poorly or not at all in standard blood culture
media [5]. Empiric treatment of patients with culture negative IE should cover both gram positive
and gram-negative organisms, and infectious disease involvement is imperative in these cases.
PCR assays are now available for a variety of
these less-common microorganisms. Karius
Testing™ can also identify pathogen DNA in
plasma even when blood cultures are negative,
which can lead to more prompt antibiotic
therapy.
Because pathogen-specic recommendations
for antibiotics are often changing and vary geographically, organism-specic treatment regimens are outlined in consensus guidelines [9]. In
general, for patients with native valve IE, vanco-
mycin plus ceftriaxone is a reasonable choice for
empirical therapy to cover likely pathogens while
blood cultures are pending [5]. It should be noted
that recommendations for antimicrobial therapy
for IE are based almost entirely on observational
studies rather than on randomized controlled trials [5]. Common antibiotic regimens for specic
organisms are seen in Table19.6.
As mentioned, S. aureus is the most common
cause of IE (both native valve and prosthetic
valve). The rates of S. aureus IE have increased
over the years and are primarily a consequence of
healthcare contact (intravascular catheters, surgical wounds, indwelling prosthetic devices, and
hemodialysis) [6]. Antibiotic treatment decisions
for S. aureus IE hinge on the presence or absence
of antibiotic resistance [4]. Single antibiotic therapy is usually enough for native valve
IE. However, for S. aureus-infected prosthetic
valves, combination therapy from multiple antibiotic classes is recommended [4]. Daptomycin
or vancomycin monotherapy is recommended for
treatment of native-valve IE caused by MRSA.An
anti-staphylococcal penicillin (nafcillin) is the
drug of choice for IE caused by MSSA, as these
agents have shown higher cure rates for MSSA
than vancomycin [7]. Despite early diagnosis and
appropriate therapy, IE after S. aureus bacteremia
is frequently associated with disabling and lifethreatening sequelae [2].
For streptococcal IE, treatment regimens vary
widely based on the microorganism. Two common regimens for streptococcal IE are penicillin
and gentamicin or ceftriaxone and gentamicin.
Single antibiotic therapy (penicillin, ceftriaxone,
or vancomycin) alone is also a common treatment strategy for streptococcal IE.
For enterococcal IE, combination therapy is
recommended. Two common combination regimens involve ampicillin and ceftriaxone or ampicillin and gentamicin. The use of single-drug vs
combination drug therapy can vary according to
the specic pathogen, potential presence of antibiotic resistance, and whether the infection
involves a native or prosthetic valve [4].
Serial blood cultures should be obtained to
conrm clearance of bacteria with therapy. While
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undergoing treatment, these cultures are typically
obtained every 24–48h until bloodstream infection is cleared [6]. Antibiotics should generally
be continued for 4–6weeks after blood cultures
convert to negative [5]. Antimicrobial therapy
duration must be sufcient to ensure complete
eradication of microorganisms within vegetations [6]. The duration of antibiotics for nativevalve endocarditis typically ranges from
4–6 weeks. Factors that compel the extended
6-week antibiotic course include: left-sided vegetations (which tend to have higher bacterial densities), the presence of drug-resistant organisms,
and the use of slowly bactericidal antibiotics such
as vancomycin [9].
Most patients with IE become afebrile 3 to
5 days after initiation of appropriate antimicrobial therapy. Patients with S. aureus IE may
respond somewhat more slowly, remaining
febrile for up to 5–7days after initiation of therapy [11]. Patients with right-sided IE and septic
pulmonary emboli may remain febrile for an
even longer duration of time, given the recurrent
embolic events.
Careful serial examinations should be performed to evaluate for heart failure (new or worsening), emboli, or other complications. Patients
who develop new complications while on appropriate antimicrobial therapy should have an
urgent repeat echocardiogram [11].
The rst year after implantation is a vulnerable period for prosthetic valve endocarditis
because of a greater exposure to healthcare contact along with incomplete endothelialization of
the prosthetic valve early after implantation.
Mortality with antibiotics alone with the presence of a prosthetic valve is high (26–75%) [3].
There are some indications for antibiotic therapy
alone in prosthetic valve IE, including hemodynamically stable patients, improvement on antibiotic therapy, early diagnosis of prosthetic valve
IE, and right-sided endocarditis [3]. Treatment of
prosthetic valve IE is typically more difcult than
treatment of native-valve endocarditis and often
requires surgical replacement of the prosthesis in
addition to antibiotic therapy. The typical duration of therapy in prosthetic valve IE is the full
6weeks.
Surgical Management
In many patients with IE, despite antimicrobial
treatment, surgery is needed for effective treatment. Surgical treatment is typically undertaken
in 40–50% of patients with IE [12]. Infection
causes destructive mobile vegetations on the
valve leaets (Figs. 19.4, and 19.5). These vegetations prevent hemostatic coaptation of the leaflets and can produce detrimental tears or
perforations within the valve leaet (Figs.19.2,
19.3, 19.6, and 19.7). These changes can lead to
acute regurgitation requiring urgent surgical
intervention. Paravalvular infection may also
occur including annular or aortic abscesses which
are considered life threatening and has a ≥40%
mortality rate and increased risk of heart block
(Fig.19.8) [10]. The main goal of surgical inter-
Fig. 19.4 Mitral valve endocarditis with multiple
vegetations
Fig. 19.5 Mitral valve endocarditis with large vegetation
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