Endocarditis and associated complications

Steven J. Lester, MD, FACC, FRCPC; Susan Wilansky, MD, FACC, FRCPC

Echocardiography is a most useful bedside tool to help in the
diagnosis and subsequent management of patients with infective
endocarditis. Transesophageal echocardiography provides comple-
mentary and often incremental information necessary in making a
diagnosis, and in identifying associated intracardiac complications.
This chapter will focus on the role of echocardiography in the
diagnosis and management of infective endocarditis. (Crit Care Med
2007; 35[Suppl.]:S384–S391)
KEY WORDS: endocarditis; transesophageal echocardiography;
transthoracic echocardiography; M-mode echocardiography; sur-
gical complications

A
n infection of the endocardium
or lining layer of the heart is
called infective endocarditis.
Although most commonly as-
sociated with a process involving the
valve leaflets, it also may affect the chor-
dae, chamber walls, paraprosthetic tissue,
implanted shunts, conduits, and fistulas.
This condition was first described by Sir
William Osler during his Gulstonian lec-
tures delivered at the Royal College of
Physicians in March of 1885 at a time
when it was considered universally fatal
(1). In 1906, Dr. Libman (2) addressed
the medical society of The Johns Hopkins
Hospital on his experience with a new
process of blood cultures: “The most in-
teresting condition connected with the
subject of bacteriemias is endocarditis.
The study of these cases by means of
blood cultures makes very definite
Leube’s view that the acute endocarditis
is secondary to infection.” The realization
that this condition is secondary to an
infectious process, the availability of di-
agnostic blood-culture techniques, the
discovery of antibiotics, the development
of surgical interventions for valvular and
perivalvular complications, and the ability
to characterize the anatomical and hemo-
dynamic manifestations of this disease with
echocardiography have significantly im-
proved treatment of this disease.
From the Mayo Clinic Arizona, Scottsdale, AZ.
For information regarding this article, E-mail:
lester.steven@mayo.edu
Dr. Wilansky has not disclosed any potential con-
flict of interest.
Copyright © 2007 by the Society of Critical Care
Medicine and Lippincott Williams & Wilkins
DOI: 10.1097/01.CCM.0000270275.89478.5F
There are two fundamental predispos-
ing factors for the development of infec-
tive endocarditis: a susceptible cardiac or
vascular substrate (endothelial injury)
and a microbiological source. Endothelial
injury is influenced by aberrant intracar-
diac flow, where either a high-velocity jet
directly impacts the endothelial surface
or there is increased shear stress second-
ary flow across a narrowed orifice or from
a high- to a low-pressure chamber. As a
consequence of the Venturi effect, micro-
biological deposits are maximal at the
low-pressure sink, immediately beyond
an orifice, or at the site where the jet
stream directly strikes the surface. Sur-
gery, dental procedures, or instruments
becoming involved with mucosal surfaces
or contaminated tissues may provide the
microbiological source that incites the
disease process of infective endocarditis.
It should be noted that 10% to 20% of
adults who develop endocarditis may
have no pre-existing heart disease (3).
Diagnosis
The clinical diagnosis requires the
physician to maintain an index of suspi-
cion, because the symptoms often are
only constitutional and many of the Os-
lerian manifestations (4) absent, except
for subacute or chronic forms of the dis-
ease. The diagnosis should be considered
in individuals with a fever and embolic
phenomenon, a predisposing endocardial
lesion, or bacteremia. Fever may be min-
imal or absent in the elderly or those with
congestive heart failure or chronic renal
failure; occasionally, fever also is minimal
or absent when associated with coagulase
negative staphylococci (5). The mere
presence of a fever in an individual with a
prosthetic heart valve or new dysfunction
in a prosthetic heart valve warrants an
evaluation for endocarditis.
In the absence of a “definite” patho-
logic diagnosis made at the time of open-
heart surgery or autopsy, the diagnosis of
infective endocarditis primarily involves
the integration of clinical, microbiologi-
cal, and echocardiographic data. In 1994,
Dr. Durack and colleagues (6) from Duke
University proposed a schema (The Duke
Criteria) with which to stratify patients
with suspected endocarditis into one of
three categories— definite, possible, and
rejected— using old (nonechocardio-
graphic) and new (echocardiographic)
criteria. The American Heart Association
scientific statement on infective endocar-
ditis supports minor modifications to the
Duke Criteria proposed by Li and col-
leagues (7, 8) (Table 1).
Blood Cultures
A detailed account of the microbiology
of endocarditis is beyond the scope of this
review; however, it is noted that staphy-
lococci and streptococci account for the
majority of the cases with notable trends
toward a rising prevalence of staphylo-
coccal skin flora caused by iatrogenic
nosocomial infection, Staphylococcus
aureus affecting intravenous drug users,
and Streptococcus bovis in the elderly
often associated with an underlying gas-
trointestinal neoplasm. Culture negative
infective endocarditis may be noted in up
to one-third of cases (9). This most com-
monly is a consequence of prior antibi-
otic use, but an increasingly common
scenario is infection by fastidious organ-
isms with limited proliferation under
conventional culture conditions (10).

S384 Crit Care Med 2007 Vol. 35, No. 8 (Suppl.)

Table 1A. Definition of infective endocarditis (IE) according to the modified Duke criteria blood culture for S. aureus, regardless of
whether community-acquired or not; a
Definite infective endocarditis
single positive blood culture for Coxiella
Pathological criteria
Microorganisms demonstrated by culture or histological examination of a vegetation, a burnetii; and a surrogate for positive
vegetation that has embolized, or an intracardiac abscess specimen; or blood cultures (antiphase 1 IgG antibody
Pathological lesions; vegetation or intracardiac abscess confirmed by histological examination titre ⬎1:800) helpful in establishing the
showing active endocarditis diagnosis when blood cultures may be
Clinical criteria negative (culture-negative endocarditis)
2 major criteria; or
1 major criterion and 3 minor criteria; or (7). If the clinical suspicion for the diag-
5 minor criteria nosis of infective endocarditis remains,
Possible IE despite sterile blood cultures after 48 hrs
1 major criterion and 1 minor criterion; or to 72 hrs of incubation, one may request
3 minor criteria
that the laboratory intensify efforts to re-
Rejected
Firm alternative diagnosis explaining evidence of IE; or cover fastidious organisms and initiate a
Resolution of IE syndrome with antibiotic therapy for ⬍4 days; or serologic assessment for possible cause.
No pathological evidence of IE at surgery or autopsy, with antibiotic therapy for ⬍4 days; or
Does not meet criteria for possible IE as above
Echocardiography
The ability to detect and characterize
Table 1B. Definition of terms used in the modified Duke criteria for the diagnosis of infective
the hemodynamic and pathologic conse-
endocarditis (IE) quences of infective endocarditis has es-
tablished the requirement of an echocar-
Major criteria diographic evaluation in individuals with
Blood culture positive for IE suspected disease. M-mode echocardiog-
Typical microorganisms consistent with IE from 2 separate blood cultures: Viridans raphy has relinquished its role to 2-di-
streptococci, Streptococcus bovis, HACEK group, Staphylococcus aureus; or community-
mensional transthoracic (TTE) and trans-
acquired enterococci in the absence of a primary focus; or
Microorganisms consistent with IE from persistently positive blood cultures defined as follows: esophageal (TEE) imaging techniques as
At least 2 positive cultures of blood samples drawn ⬎12 h apart; or all of 3 or a majority of the ultrasound-imaging modalities most
ⱖ4 separate cultures of blood (with first and last sample drawn at least 1 h apart) commonly employed in the evaluation of
Single positive blood culture for Coxiella burnetii or anti-phase 1 IgG antibody titer >1:800 individuals with suspected endocarditis.
Evidence of endocardial involvement Although limited, M-mode echocardiog-
Echocardiogram positive for IE (TEE recommended for patients with prosthetic valves, rated
raphy still has a role in the evaluation of
at least “possible IE” by clinical criteria, or complicated IE [paravalvular abscess]; TTE as
first test in other patients) defined as follows: oscillating intracardiac mass on valve or
patients with suspected endocarditis. Its
supporting structures, in the path of regurgitant jets, or on implanted material in the superior temporal resolution permits de-
absence of an alternative anatomic explanation; or abscess; or new partial dehiscence of tection of vibratory oscillations of a veg-
prosthetic valve; new valvular regurgitation (worsening or changing or preexisting murmur etation or associated disrupted cardiac
not sufficient) structures uncharacterized by standard
Minor criteria TTE- and TEE-imaging techniques. Dia-
Predisposition, predisposing heart condition, or IDU stolic vibrations of the aortic valve, or
Fever, temperature ⬎38°C
Vascular phenomena, major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, systolic vibrations noted during M-mode
intracranial hemorrhage, conjunctival hemorrhages, and Janeway’s lesions interrogation of the mitral valve, are not
Immunologic phenomena: glomerulonephritis, Osler’s nodes, Roth’s spots, and rheumatoid normal and represent a sensitive finding
factor for a vegetation, torn leaflet, or ruptured
Microbiological evidence: positive blood culture but does not meet a major criterion as noted chordae.
abovea or serological evidence of active infection with organism consistent with IE
Echocardiographic minor criteria eliminated
Transthoracic and
TEE, transesophageal echocardiography; TTE, transthoracic echocardiography; IDU, intravenous Transesophageal
drug user. Echocardiography
a
Excludes single positive cultures for coagulase-negative staphylococci and organisms that do not
cause endocarditis. Modifications are shown in boldface. Reprinted with permission from Li et al (7). Visualization of the endocardial lesion
is the central objective of the echocardio-
graphic examination in its role as a diag-
Such organisms include Coxiella, Bar- hrs. If obtained before antibiotic admin- nostic technique. Echocardiography
tonella, Legionella, Tropheryma whip- istration, the initial sets of blood cultures clearly does not provide histologic diag-
plea, fungi, and the HACEK group of bac- will generally be positive in individuals noses; however, there are image charac-
teria (Haemophilus, Actinobacillus, with bacterial endocarditis within a 48-hr teristics that support the designation of a
Cardiobacterium, Eikenella, and Kin- to 72-hr period, obviating the need to valve mass to a vegetation. These include
gella). continuously collect blood cultures be- a) location that is in the path of a high-
Three to five sets of blood cultures, yond this point (11). The “microbiologi- velocity jet or the upstream side of the
each from a separate venipuncture, incu- cal adaptations” to the Duke criteria sup- valve when it regurgitates; b) motion that
bated in both aerobic and anaerobic at- ported by the American Heart Association is chaotic and independent of the valve
mospheres, should be obtained over 24 include the mere presence of a positive with fine vibrations; c) shape that is

Crit Care Med 2007 Vol. 35, No. 8 (Suppl.) S385


Figure 1. Top, dehiscence of mitral-valve prosthesis; bottom, color Doppler illustrates perivalvular
regurgitation in the area of dehiscence.
amorphous; d) texture that is gray scale
and reflectance in relation to the myocar-
dium with calcification; and e) associated
abnormalities such as abscess, fistula,
new valve regurgitation for prosthetic
valves, dehiscence, perivalvular leaks, and
(rarely) obstruction (Fig. 1). Likely rep-
resenting a degenerative process, small
“stinglike” mobile strands with narrow
attachment often are noted on valves.
Similar finding are noted around the sew-
ing ring of valve prostheses, which too
may represent a degenerative process or
on occasion may represent a suture end.
Redundant chordae or a pronounced
Chiari’s network may too at times be mis-
taken for a pathologic finding. However,
these masses, by virtue of their shape and
high reflectance, can generally be differ-
entiated from pathologic vegetation.
The test characteristics of an echocar-
diographic evaluation for the detection of
S386
a vegetation are influenced by technical
factors, by the experience of the imager
and image interpreter, and by the pre-test
likelihood of either having or not having
the disease. With that said, the literature
generally reports a sensitivity of 60% to
65% for TTE and 85% to 95% for TEE.
The specificity for both imaging tech-
niques is very good at 90% to 98% (12–
17). Significant innovations to TTE im-
aging have occurred since many of the
studies with which the test characteris-
tics reported above were performed. In-
novations such as harmonic imaging,
faster scanning and higher line densities,
the use of higher-frequency transducers,
and higher-resolution monitors—although
having salutary effects on overall image
quality— have not significantly influenced
the sensitivity of TTE in the diagnostic eval-
uation for infective endocarditis (18). The
superior sensitivity of TEE over TTE is
even more pronounced in the evaluation
of individuals with valve prostheses. In
the setting of prosthetic-valve endocardi-
tis, the sensitivity of TTE is generally
reported to be below 50% while that of
TEE remains between 82% and 90% (15,
19, 20).
A negative TEE has a negative predic-
tive value of over 90%, but does not elim-
inate the possibility, requiring as always
interpretation to be integrated with good
clinical judgment (21, 22). A false-negative
echocardiographic evaluation may result
from vegetations that are smaller than
the image resolution, previous emboliza-
tion, or simply recognizing that there are
“blind spots” with TEE and TTE. If the
clinical suspicion for infective endocardi-
tis remains following an initial negative
TTE or TEE examination, serial echocar-
diographic evaluations may provide in-
cremental diagnostic value (23). In addi-
tion, integration of TTE with TEE images
may be necessary, because views ob-
structed in one imaging modality may
not be obstructed in the other.
Whether to begin the evaluation with
a TTE or directly proceed to a TEE is an
issue of considerable intellectual and eco-
nomic debate. Greaves and colleagues
(24) noted that in the absence of clinical
criteria that are significant independent
predictors for endocarditis (vasculitic/
embolic phenomena, central venous ac-
cess or pacing wire, recent injected drug
use, a prosthetic valve or a positive blood
culture) there was a zero probability that
a TTE would show any evidence of infec-
tive endocarditis. Bayer and colleagues
(25) propose a pragmatic approach to the
echocardiographic evaluation of patients
with suspected infective endocarditis,
which we also support (Fig. 2).
Individuals with a history of endocar-
ditis are at increased risk for future in-
fection. Following completion of therapy,
a TTE examination to establish a new
baseline for valvular and ventricular mor-
phology and function is very important.
In individuals with poor acoustic win-
dows or in whom there is complex anat-
omy, a TEE may be required to establish
a new baseline.
Cardiac Complications
Valvular Dysfunction. Valvular struc-
tural and functional integrity may be de-
stroyed by the proliferation of an infec-
tious organism within its tissue. The loss
of function primarily results in regurgi-
Crit Care Med 2007 Vol. 35, No. 8 (Suppl.)
Figure 2. Approach to diagnostic use of echocardiography. Reprinted with permission of Bayer et al (25). TTE, transthoracic echocardiography; TEE,
transesophageal echocardiography; IE, infective endocarditis.
tation; however, large bulk vegetations
may result in flow obstruction. Valve re-
gurgitation may progressively worsen
with ineffective medical management of
the underlying infectious organism, or
may present acutely as a result of leaflet
perforation or destruction of the valvular
supporting structures. Echocardiography
is the tool that best allows us to identify
such complications. Careful evaluation is
required when one is questioning the di-
agnosis of a prolapsing or flail-valve leaf-
let segment to ensure the appropriate dif-
ferentiation from highly mobile and
prolapsing vegetations, because each may
have similar visual tissue characteristics
and motion patterns (Fig. 3). Objective
quantification of the extent of either ste-
nosis or obstruction is required, with a
detailed description of such methods be-
yond the scope of this discussion.
Periannular Extension. Periannular
extension of the infection into the adja-
cent myocardium is a serious complica-
tion associated with increased patient
mortality (26 –28). Tissue necrosis and
pyogenesis may result in the formation of
an abscess cavity (Fig. 4). The weakened,
necrotic myocardial tissue— under in-
Crit Care Med 2007 Vol. 35, No. 8 (Suppl.)
creased pressure from an expanding space-
occupying lesion—may rupture, creating
fistulous communications commonly from
the aorta to left atrium or left ventricle to
right atrium. In individuals with aortic valve
endocarditis and associated aortic regurgi-
tation, the “infected” regurgitant jet may
cause local spread of infection as it strikes
subaortic structures. Such complications
can include aneurysm or perforation of
the anterior mitral-valve leaflet, or if the
jet impinges the mitral-aortic intervalvu-
lar fibrosa, an abscess or aneurysm may
form in that location (29 –31)(Fig. 5).
Periannular complications are more
commonly encountered in prosthetic
(56 –100%) than native (10 – 40%) valve
endocarditis, because in the latter the
annulus, rather than the leaflet, is gener-
ally the primary site of the infection (32–
35). There are a number clinical parameters
felt to be associated with an increased risk for
periannular extension, including those with a
fulminant presentation, persistent fever,
pericarditis, a history of intravenous drug
use, involvement of a prosthetic valve,
and (importantly) electrical-conduction
disturbance such as atrioventricular
block or new bundle-branch block (32,
33, 36 –39). The tendency is for the infec-
tion to extend into the weakest portion of
the paravalvular structure, and in the
case of the aortic valve this is the mem-
branous septal area, which contains the
conducting tissue and hence the associa-
tion with new conduction abnormalities
(40).
Although a number of proposed clini-
cal parameters associated with periannu-
lar extension are listed above, the pres-
ence of new atrioventricular block is
likely the most reliable (35). The finding
of atrioventricular block on the electrocar-
diogram has a reasonably positive predic-
tive valve (88%); however, the sensitivity of
this finding to detect a periannular ab-
scess is low (45%) (35). The increased
patient mortality associated with perian-
nular extension necessitates prompt eval-
uation of patients at risk. TEE is the mo-
dality of choice in the evaluation for
potential periannular extension. The re-
ported sensitivity, specificity, and positive
and negative predictive values are 76% to
100%, 95%, 87%, and 89%, respectively
(12, 31, 41, 42). Spectral and color Dopp-
ler is used to characterize the flow pat-
terns of fistulous communications.
S387

Figure 3. Top, patient with mitral valve prolapse, torn chordae, and flail segment; bottom, patient with
infective endocarditis and vegetation.
Extracardiac Complications
Embolization. Systemic embolization
adversely influences survival, and is a
complication occurring in approximately
one-third of patients with infective endo-
carditis, most commonly within the first
2 wks to 4 wks of antimicrobial therapy
(43– 47). The incidence of systemic em-
bolic complications is highest when there
is left-sided valve involvement and when
the microbial pathogen is S. aureus, Can-
dida, Abiotrophia, or a HACEK organism.
More than 50% of embolic events involve
the central nervous system, with ⬎90%
of central-nervous-system emboli affect-
ing the middle-cerebral-artery distribu-
tion (45). Vegetations on right-sided
heart valves are most frequently caused
by an S. aureus infection, and thus it’s
not surprising that embolization into the
pulmonary vascular distribution is com-
S388
mon and may been seen in approximately
50% of patients with right-sided vegeta-
tions (43, 44, 47).
Controversy exists as to the predictive
value of various echocardiographic char-
acteristics of a vegetation prone to embo-
lize. Vegetation size, consistency, extent,
and mobility all have to be considered
useful characteristics with which to pre-
dict risk for embolization (13, 43, 44,
48 –50). Less mired in controversy is the
fact that patients with large (⬎10 mm)
and highly mobile vegetations are at
highest risk (44). Continued growth or
failure of a vegetation to diminish in size
despite antimicrobial therapy also is pre-
dictive of embolic events.
Mycotic Aneurysm. Either intra- or ex-
tracranial, mycotic aneurysms are an un-
common but potentially lethal complica-
tion of infective endocarditis. They are
most frequently found at arterial branch
points and result from spread of infection
through the arterial wall (arteritis) as a re-
sult of septic embolization directly to the in-
traluminal surface or into the vasa vasorum.
A persistent focal headache, focal neu-
rologic findings, septic meningitis, or
neurologic deterioration raises the suspi-
cion for an intracranial mycotic aneu-
rysm before rupture and prompts further
evaluation (conventional, computed to-
mography, or magnetic-resonance an-
giography). The sensitivity and specificity
of either a computed-tomographic or
magnetic-resonance angiography to de-
tect an intracranial mycotic aneurysm is
90% to 95%. However, if suspicion re-
mains despite negative tests, then con-
ventional angiography is warranted (51,
52). Extracranial mycotic aneurysms
generally are detected only when they
begin to leak or rupture with associated
clinical findings depending on the loca-
tion of the involved vessel.
Whether or not the mere presence of a
mycotic aneurysm mandates surgical or
endovascular treatment is controversial
and influenced by individual patient char-
acteristics, because some may resolve
during antimicrobial therapy (25). My-
cotic aneurysms that leak, expand during
therapy, or persist after therapy require
intervention.
Splenic Abscess. A splenic abscess may
develop as a result of septic embolization
or direct seeding into a previously in-
farcted area. They are found in up to 5%
of patients with infective endocarditis
(53). The index of suspicion is increased
in the presence of abdominal pain, pleu-
ritic or shoulder pain as of diaphragmatic
irritation, or persistent fever. Although
detectable by abdominal ultrasound,
computed tomography and magnetic res-
onance imaging appear to be the imaging
modalities of choice, with sensitivities
and specificities of 90% to 95% (25, 54).
Imaging may not be able to differentiate
splenic infarction from abscess. Persis-
tent fever and enlargement of a noted
lesion suggest abscess, which can be con-
firmed by needle aspiration. The presence
of multiple abscesses or those not ame-
nable to percutaneous drainage are indi-
cations for splenectomy (25). If patient
management requires cardiac surgery,
splenic abscesses should be effectively
treated first and, if not, then splenectomy
should be performed as soon after cardiac
surgery as risk permits (25).
Aspirin and Anticoagulation. Neither
aspirin nor anticoagulation is indicated
Crit Care Med 2007 Vol. 35, No. 8 (Suppl.)
 as prophylactic therapy against potential
embolic complications. Such prophylaxis
is ineffective and likely associated with an
increased risk for bleeding (55, 56). In
general however, anticoagulation re-
quired for other proven indications such
as valve prostheses should be continued
unless neurologic complications occur,
in which case the anticoagulation should
be immediately reversed. Continuation
of anticoagulation should be with hep-
arin, and warfarin anticoagulation dis-
continued.

Indications for Cardiac Surgery

The cornerstone of management is to
sterilize the infected cardiac tissue with
antimicrobial therapy targeted to the in-
fectious etiology. A detailed account of
the antimicrobial treatment of organisms
commonly associated with endocarditis is
beyond the scope of this review. Often ap-
propriate antimicrobial therapy is all that is
Figure 4. Top, aortic-valve vegetation causing complete disruption of the valve leaflet; bottom left,
needed; however, in some instances surgi-
short-axis image of the vegetation; bottom right, periannular extension with abscess formation.
cal management is required too.
In general, the presence of severe con-
gestive heart failure resulting from valvu-
lar heart disease that is amenable to sur-
gery is an indication for immediate
surgical therapy (class 1, level of evidence
B) (57). This is a general recommenda-
tion, independent of the etiology of the
valve dysfunction. The presence of endo-
carditis should not result in a delay of
surgical therapy, because the risk of re-
infection of a newly implanted valve is far
less (⬃ 3%) than the quoted morbidity
and mortality (50%) associated with sur-
gical neglect (58, 59). Certainly these
comments are tempered when comor-
bidities preclude a reasonable chance for
recovery.
When the microbiological etiology of
the infection is either fungal or one
highly resistant to antibiotic therapy,
surgical intervention is indicated (class 1,
level of evidence B) (57). Periannular ex-
tensions of the infection (abscess, fistula,
dehiscence of valve prostheses) are indi-
cations for surgery (class 1, level of evi-
dence B) (57). Progressively more austere
valve dysfunction—whether regurgita-
tion or obstruction, the latter more com-
monly seen with valve prostheses—
resulting in hemodynamic evidence for
elevated left-ventricular end-diastolic or
Figure 5. Long-axis section of a necropsy heart showing the relations of the aortic valve (AV), annulus, left-atrial pressure generally indicates
and root (AO) to the subaortic structures, which include the mitral-aortic intervalvular fibrosa surgical disease (class 1, level of evidence
(MAIVF), anterior mitral leaflet (aml), chordae tendineae, and the left atrium (LA). The anterior leaflet B) (57). However, if the cardiac function
becomes contiguous with the posterior aortic root behind the left and posterior aortic cusps through is well compensated, surgery may be de-
the zone of MAIVF. LV, left ventricle; pml, posterior mitral leaflet; RV, right ventricle. layed until the completion of antimicro-

Crit Care Med 2007 Vol. 35, No. 8 (Suppl.) S389

bial therapy. If the infection is poorly
controlled, then delay in surgery is un-
warranted.
Surgery is reasonable in individuals
who have evidence of either recurrent
emboli or persistent bacteremia (class
IIa, level of evidence C) (57). However,
the timing of surgery in those that have
sustained a neurologic injury is conten-
tious. In general, if the patient is hemo-
dynamically stable and the response to
antimicrobial therapy adequate, then de-
laying cardiac surgery for 2 wks to 3 wks
following stroke and at least a month
following an intracerebral hemorrhage is
reasonable (60, 61).
The indication for surgery in an effort
to prevent embolic complications is
mired in debate. The American Heart As-
sociation/American College of Cardiology
2006 guidelines for the management of
patients with valvular heart disease state
“surgery of the native valve may be con-
sidered in patients with infective endo-
carditis who present with mobile vegeta-
tions in excess of 10 mm with or without
emboli” (class IIb, level of evidence C)
(57). The decision to proceed with sur-
gery for this indication must be consid-
ered carefully, and the morbidity and
mortality of potential embolic events
weighed against the short-term perioper-
ative morbidity and mortality and long-
term issues associated with a valve pros-
thesis if valve repair and removal of the
vegetation not possible.
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