Infections of Intracardiac Devices: Treatment Complexities

Infect Dis Clin N Am 16 (2002) 477505
Infections of intracardiac devices

Adolf W. Karchmer, MDa,b,*,
David L. Longworth, MDc,d,e
a
Division of Infectious Diseases, Beth Israel Deaconess Medical Center,

330 Brookline Avenue, Kennedy-6, Boston, MA 02215, USA
b
Harvard Medical School, 25 Shattuck Street, Boston, MA 02115, USA
c
Department of Infectious Diseases, The Cleveland Clinic Foundation,
Infectious Diseases Section, 9500 Euclid Avenue, Cleveland, OH 44106, USA
d
Cleveland Clinic Foundation Health Sciences Center, The Ohio State University
School of Medicine, Cleveland, OH, USA
e
School of Medicine, Pennsylvania State University, PA, USA
Prosthetic cardiac valves, pacemakers, and implanted debrillators are

essential to maintain the hemodynamic capacity or electrical integrity of the
heart in several cardiac disease states. Severe morbidity and mortality results
when these devices become infected. Treatment of infected cardiac devices is
particularly complex. Eradication of infection involving an implanted foreign device often requires removal of the foreign material in conjunction
with antimicrobial therapy. If the device is not essential and if removal does
not entail signicant risks, treatment may be simple. Prosthetic valves and
electrophysiologic devices, however, are usually essential for life. Furthermore, removal requires replacement with a functioning device, a procedure
that is associated with morbidity and potential mortality. This article will
address infection of these devices and their treatment.
Prosthetic valve endocarditis

Frequency and risk
The frequency of prosthetic valve endocarditis (PVE) after cardiac surgery is not uniform. The rate is highest during the initial three months after
surgery, remains high through the sixth month, then declines gradually to a
relatively constant rate of 0.3% to 0.6% at 12 months and thereafter [13].
* Corresponding author.
E-mail address: akarchme@caregroup.harvard.edu (A.W. Karchmer).
0891-5520/02/$ - see front matter 2002, Elsevier Science (USA). All rights reserved.
PII: S 0 8 9 1 - 5 5 2 0 ( 0 1 ) 0 0 0 0 5 - 8
478
A.W. Karchmer, D.L. Longworth / Infect Dis Clin N Am 16 (2002) 477505
When valve recipients are followed actively after surgery, the actuarial estimate of the cumulative rate of PVE ranges from 1.0% to 1.4% at 12 months
and from 3.0% to 5.7% at 60 months [16] (Table 1). Although conicting
data have been reported, recent studies have suggested that infection occurs
with similar frequency on valves implanted at the mitral or aortic site [1,3,6].
Additionally, at the end of the initial postoperative year, the rates of infection involving mechanical valves and bioprosthetic valves (tissue leaets) are
similar [69]. Alternatively, other studies have indicated that the risk of
infection is greater for mechanical valves compared with bioprosthetic
valves during the initial year after valve replacement, but that over time the
risk of infection for bioprosthetic valves increases so that rates are comparable for the two valve types 5 years after valve surgery [1,3,5,8].
Pathogenesis
The pathogenesis of infective endocarditis is complex. Anatomic and
hemodynamic abnormalities alter endothelial surfaces resulting in the
deposition of plateletbrin thrombi. These plateletbrin aggregates are
sites at which organisms with unique surface components acting as adhesins
can attach. Some organisms, most notably Staphylococcus aureus, which
uses surface proteins that recognize and bind to adhesive matrix molecules,
can also adhere to apparently normal or minimally traumatized endothelial
surfaces in the absence of preparatory plateletbrin thrombi. Adherent
organisms that survive and proliferate in spite of host defenses give rise to
infective endocarditis. The presence of a foreign body (e.g., a prosthetic
heart valve) at the site of infection introduces other major variables. Initially, the annulusprosthesis interface is not endothelialized and acts as a formation site for plateletbrin thrombi. Exposed sutures anchoring the
prosthesis provide pathways whereby organisms can invade cardiac tissue.
Table 1
Estimated cumulative rate of PVE after valve replacement
% patients with PVE
Months after surgery
Study (years valves

implanted)
Initial number valve

recipients
12
24
48
60
Rutledge et al. (195681) [6]

Ivert et al. (197579) [3]
Calderwood et al. (197582) [1]
Arvay and Lengyel (198185) [5]
Agnihotri et al. (197092) [4]
Glower et al. (197595) [2]
1598
1465
2608
912
2413a
1119b
1.4
3.0
3.1
1.0
1.5
4.1
5.4
3.2
5.7
4.9
3.0
3.0
Aortic position only.

Carpentier-Edwards bioprosthesis only.
Adapted from Karchmer AW. Infections of prosthetic valves and intravascular devices. In:
Mandell GL, Bennett JE, Dolin R, editors. Principles and practice of infectious diseases, 5th
edition. Philadelphia: Churchill Livingstone; 2000. p. 90317; with permission.
b
479
After several years in place, the stress of repetitive motion may alter the surface of leaets in bioprostheses and allow the deposition of infection-prone
plateletbrin thrombi. The foreign material also impairs host defenses in its
immediate microenvironment and alters the behavior of adherent infecting
microorganisms, rendering them more dicult to eradicate with antimicrobial agents. Organisms can reach the prosthesis site either by the hematogeneous route (from a remote site) or by direct introduction at the time of
surgery. This grossly oversimplied scenario has been reviewed in detail
[1012].
The clinical events that contribute to the development of PVE markedly
inuence the microbiology, time of symptomatic onset, and, potentially, the
pathology of PVE. Accordingly, understanding and recognizing these events
is relevant to the management of infected patients. Based on the types
of organisms causing PVE that develop during the rst two months after
valve surgery, it appears that many of these episodes are nosocomial. Epidemiologic and microbiologic studies have linked PVE caused by coagulasenegative staphylococcithe cause of 31% of PVE cases during the initial
postoperative monthsto intra-operative contamination [1316]. Most
cases of PVE occurring in these clusters became symptomatic within 60 days
after surgery; however, occasional patients presented clinically between 3
and 13 months postoperatively. The cases with delayed onset illustrate the
potential for slow evolution from early infection to symptomatic PVE.
Early-onset PVE has been linked to bacteremia arising from invasive monitoring and support devices and surgical wound infections. The frequency of
these events engenders the high rates of PVE noted through the initial six
months after surgery. Furthermore, during these early months after valve
surgery, infection of the prosthesis is more likely to be associated with paravalvular invasion and hemodynamically signicant valve dysfunction
[17,18].
While not universally indicative of endocarditis, nosocomial bacteremia
or fungemia occurring in a patient with a prosthetic valve constitutes a risk
for subsequent PVE. Fang et al. noted PVE in 18 of 115 patients (16%) with
nosocomial bacteremia. Of the bacteremias associated with subsequent
PVE, 61% arose from intravascular catheters or skin and wound infections
[19]. Bacteremia due to staphylococci and gram-negative bacilli resulted in
55% and 33% of subsequent PVE, respectively. Although the experience is
small, PVE developed in 6 of 19 patients (31%) with bacteremia due to Staphylococcus epidermidis, 4 of 23 (17%) with S. aureus bacteremia, and 6 of 58
(10%) with gram-negative rod bacteremia. In 12 of the 18 patients with PVE,
the inciting bacteremia occurred within 60 days of surgery; however, the
published data do not allow assessment of risk for PVE following bacteremia in the early months after surgery versus later bacteremia [19]. Nasser et
al. examined the consequences of nosocomial candidemia in 44 patients with
prosthetic heart valves [20]. Eleven patients (25%) developed PVE. In 7
patients (16%) with a mean of 8.1 days of fungemia, coincident PVE was
480
evident at the time of presentation (median 149 days, range 81240 days
after surgery; only 3 within 60 days postoperatively). These patients generally lacked an identiable portal of entry for fungemia, and in retrospect had
not experienced a complicated recovery after surgery. Among the 37
patients without evident PVE at the time of candidemia, 4 (11%) developed
PVE. Blood cultures had been obtained in these 4 patients between days 4
and 36 postoperatively, but PVE was not noted until days 26, 101, 112, and
690. In contrast to those with PVE on presentation, these 37 patients had
denable portals of entry and had experienced long, complicated recoveries
after surgery. Among these 37 patients, the 4 with subsequent PVE had
more sustained fungemia than those who did not develop endocarditis
(mean 14.3 days versus 4.3 days). Patients with prosthetic valves who experience fungemia are at signicant risk of either having (those without an identiable portal of entry) or developing PVE. In spite of aggressive antifungal
therapy, patients with nosocomial fungemia remain at risk for the development of PVE months or years later.
Microbiology
Many and varied organisms, including Coxiella burnetii, Mycoplasma
hominis, many species of bacteria, Tropheryma whippelii, atypical mycobacteria, Legionella dumoi and Legionella pneumophila, and an array of yeasts
and molds have infected prosthetic heart valves. The vast majority of episodes, however, are caused by a relatively small number of organisms
(Table 2). From a microbiological perspective, PVE can be divided into
three periods. The origin of infection among those who become symptomatic within 60 days of valve surgery (i.e., those with early PVE) is predominantly nosocomial. Accordingly, the major causes of these infections
are organisms commonly associated with intraoperative contamination and
nosocomial infection. With the exception of an increased frequency of cases
caused by S. epidermidis and other species of coagulase-negative staphylococci, the organisms causing PVE that presents more than 12 months after
cardiac surgery in generally healthy community-residing patients resemble
the causes of native valve endocarditis; the major pathogens are viridans
streptococci, S. aureus, and enterococci. The HACEK group of organisms
(Haemophilus aphrophilus, Actinobacillus actinomycetemcomitans, Cardiobacterium hominis, Eikenella spp, and Kingella spp) cause a small but signicant number of these late PVE cases. During the period from 2 months to 12
months after surgery the organisms causing PVE are a blend of those
encountered in early and late PVE cases.
The coagulase-negative staphylococci causing PVE vary signicantly in
relation to the time of onset of infection after cardiac surgery. Those causing
infection during the initial year after valve surgery are S. epidermidis, and
almost 85% are methicillin-resistant. The coagulase-negative staphylococci
are roughly equally divided between S. epidermidis and non-epidermidis
481
Table 2
Organisms causing prosthetic valve endocarditis
Number of cases (%)
Time of onset after valve surgery
Organism
Streptococcia
Pneumococci
Enterococci
Staphylococcus aureus
Coagulase-negative staphylococci
Fastidious gram-negative
coccobacilli (HACEK group)b
Gram-negative bacilli
Fungi, Candida species
Polymicrobial/miscellaneous
Diphtheroids
Culture negative
2 mo
N 161
>212 mo
N 31
>12 mo
N 194
13
36
51
4
4
11
61
22
34
22
11
(11)
(18)
(11)
(6)
11
3
9
5
16
(6)
(1)
(5)
(3)
(8)
19
12
4
9
7
(3)
(8)
(22)
(32)
(11)
(7)
(2)
(5)
(7)
1
4
2
(9)
(12)
(12)
(32)
(3)
(12)
(6)
(6)
(31)
Includes viridans streptococci, Streptococcus bovis, other non-group A, groupable streptococci, and Abiotrophia species (nutritionally variant streptococci).
b
Includes Haemophilus species, Actinobacillus actinomycetemcomitans, Cardiobacterium
hominis, Eikenella species, and Kingella kingae.
Data from Karchmer AW. Infections of prosthetic valves and intravascular devices. In:
Mandell GL, Bennett JE, Dolin R, editors. Principles and practice of infectious diseases, 5th
edition. Philadelphia: Churchill Livingstone; 2000. p. 90317; and Karchmer AW. Infective
endocarditis. In: Braunwald E, editor. A textbook of cardiovascular medicine. Philadelphia:
W.B. Saunders Company; 2000.
species after 12 months have elapsed; additionally, only 30% or less of these
isolates are methicillin resistant [1,17,21]. Although the mechanism of methicillin resistance is the same as that in methicillin-resistant (MR) S. aureus,
coagulase-negative staphylococci commonly exhibit heteroresistance, which
makes detection of the MR phenotype more dicult. When initiating
therapy for coagulase-negative staphylococcal PVE, the organism should
be assumed to be MR until the microbiology laboratory denitively excludes MR.
Various diphtheroids or Corynebacterium spp, including isolates consistent with the antibiotic-resistant C. jekiem, have caused PVE. Many
diphtheroids are fastidious and dicult to grow and test for antibiotic susceptibility; however, most isolates are highly susceptible to vancomycin.
Additionally, strains not resistant to gentamicin are killed synergistically
by the combination of penicillin and gentamicin [22].
Among 270 cases of fungal endocarditis reported from 1965 through
1995, 135 (50%) occurred on prosthetic valves [23]. Candida albicans, followed by non-albicans Candida spp and Aspergillus spp, are the most
common fungi that cause PVE [17,24,25]. Occasional cases have been caused by Cryptococcus neoformans, Histoplasma capsulatum, and a variety of
molds that are uncommon human pathogens. Blood cultures are commonly
482
positive in patients with PVE caused by Candida spp or C. neoformans,

whereas blood cultures are often negative when PVE is caused by other
fungi. In the latter circumstance, cultures and microscopic examination of
vegetation recovered at cardiac surgery or embolized peripherally may be
needed to establish a microbiologic diagnosis.
Although a rare cause of endocarditis in the United States, C. burnetii is
an important cause of PVE in regions where Q fever is endemic. Among 229
episodes of C. burnetii endocarditis diagnosed between 1985 and 1998, 157
(69%) involved prosthetic valves [26].
Pathology
Infection involving prosthetic valves commonly invades paravalvular tissue, resulting in abscess formation or valve dehiscence, and occasionally
aects the valve orice directly, resulting in either regurgitation or stenosis
[17,2731]. Extension of infection through the aortic valve annulus may
cause pericarditis, and invasion of the membranous portion of the interventricular septum may disrupt the conduction system and cause various forms
of heart block [27,28,31,32]. Annulus invasion and myocardial abscess were
noted at surgery or autopsy in 42% and 14%, respectively, of 85 patients
with mechanical valve endocarditis [15,30]. Ismail et al. noted annulus invasion and valve dehiscence in 82% of 41 patients with mechanical valve infection [29]. With bioprosthetic valve infection, especially that occurring within
the initial postoperative year, invasion into and beyond the annulus has
been reported in 36% to 54% of cases [17,33,34]. Among patients with PVE
treated surgically, Lytle et al. noted that infection invaded paravalvular tissue in 43 of 54 (79%) mechanical valves and 37 of 90 (41%) bioprosthetic
valve infections [18]. In addition, Lytle et al. reported that invasion was
common among patients with mechanical valve endocarditis regardless of
time of onset, whereas among patients with bioprosthetic valve infection
invasive disease was more common among those with onset during the initial year after valve replacement (15 of 18, 83%) versus those with later onset
infection (22 of 71, 31%) [18]. Infection involving the leaets of bioprosthetic
valves can result in perforation and tears with regurgitation, bulky vegetations can cause stenosis, and after infection has been cured, delayed leaet
stiening also can result in stenosis [34,35].
Clinical and laboratory manifestations
The clinical and laboratory features of PVE are similar to those encountered in patients with native valve endocarditis [36]. When PVE presents during the early postoperative period, the subtle and time-dependent signs of
endocarditis may be absent or masked by complications of surgery. The high
frequency of paravalvular invasion infection in patients with PVE, especially
in those with aortic valve infection during the initial postoperative year,
results in a higher frequency of new or changing regurgitant murmurs,
483
congestive heart failure, persistent fever in spite of optimal antimicrobial

therapy, and new electrocardiographic conduction disturbances than is
encountered with native valve endocarditis [17,37]. Almost 40% of patients
experience clinically apparent systemic emboli; 20% to 40% experience stroke,
central nervous system hemorrhage, or neurologic complications [29,38,39].
Unless antibiotics have been administered recently, blood cultures will be
positive in 90% of patients with PVE, and multiple cultures obtained independently over time will be positive (persistent bacteremia). When dealing
with blood cultures yielding coagulase-negative staphylococci or diphtheroids (organisms that often contaminate cultures), persistent bacteremia
helps to distinguish patients with PVE. Although polyclonal coagulasenegative staphylococcal endocarditis has been reported, this is unusual, and
using molecular techniques to demonstrate clonality among sporadic coagulase-negative staphylococci in blood cultures obtained from patients with
prosthetic valves is also suggestive of PVE rather than contamination [40,41].
Occasionally, patients with PVE who have not received antibiotics recently will have persistently negative blood cultures. These cases are caused by fastidious microorganisms, for example, Legionella spp, C. burnetii,
M. hominis, Bartonella spp, atypical mycobacteria, and fungi other than
Candida spp (particularly molds). Special blood culture, techniques, serologic
tests (antigen or antibody detection), and, when possible, culture, microscopic, and molecular analysis of vegetation may facilitate making a diagnosis
in these cases [42].
Transthoracic echocardiography (TTE) and transesophageal echocardiography (TEE) using biplane or multiplanar transducers that allow continuous wave, pulse-wave Doppler, and color-ow imaging are essential for the
diagnosis and management of PVE [43,44]. Together the two approaches
provide optimal imaging of prostheses in the aortic, mitral, and tricuspid
positions. TEE is superior to TTE when imaging a mitral valve prosthesis.
Although TTE and TEE are complimentary, TEE is more sensitive without
loss of specicity for the diagnosis of PVE than is TTE (82% to 96% versus
17% to 36%) regardless of prosthesis type or anatomic position (Table 3)
[4347]. Additionally, TEE is also superior to TTE for detecting paravalvular abscesses, stulae, and paraprosthetic leaksintracardiac complications
that have a major impact on management strategy [48]. The negative predictive value of a single TEE in a patient with suspected PVE is 86% to 94%
[46,49]. However, if PVE is strongly suspected in a patient with negative
TEE, the study should be repeated. Although a repeat TEE may provide
diagnostic evidence of PVE, a second negative study does not exclude PVE
in the face of strong clinical evidence [49].
Diagnosis
The diagnosis of PVE requires a high index of suspicion, knowledge of
the subtle signs of endocarditis, obtaining 3 or 4 blood cultures prior to the
484
Table 3
Echocardiography in the diagnosis of PVEa
Number of valves (%)
Transthoracic
Transesophageal
Prosthesis type and position

(number studied)
Non-diagnostic
Diagnostic
Non-diagnostic
Diagnostic
Aortic position (34)

Bioprosthesis (12)
Mechanical valve (22)
Mitral position (37)
Bioprosthesis (10)
Mechanical valve (27)
16
6
10
32
8
24
18
6
12
5
2
3
5
1
4
4
2
2
29
11
18
33
8
25
(53)
(50)
(55)
(14)
(25)
(11)
(85)
(92)
(82)
(89)
(80)
(93)
Patients had pathoanatomic or clinically conrmed (Von Reyn criteria) PVE.

Data from Refs. [36,45,46].
administration of antibiotics, and full echocardiographic assessment. The

Duke criteria for the diagnosis of endocarditis provide a systematic
approach to evaluating patients with suspected PVE [50]. In three studies
of pathologically conrmed PVE, retrospective application of the Duke criteria classied 76% to 79% of patients as denite and 21% to 24% as possible
endocarditis [5153]. Although a signicant number of patients were not
assessed by TEE, the diagnosis of PVE was erroneously rejected in only 1
of 118 patients. The importance of TEE evaluation in the diagnosis of PVE
was examined by Roe et al. [54]. Among 34 patients with prosthetic heart
valves and suspected endocarditis, the classication of 13 (38%) was changed
when the assessment included TEE data versus when only TTE ndings were
used; 11 were reclassied from possible to denite and 2 from rejected to
possible. The positive predictive value of a TEE for PVE was 89%. The TEE
can be negative in patients with PVE; in the diagnosis of PVE a negative
TEE should never override strong clinical evidence of endocarditis [49,54].
Antimicrobial treatment
Eective therapy for PVE requires identication of the microbial cause,
determination of a bactericidal regimen of proven ecacy, an understanding
of the intracardiac pathology of PVE and its implications for valve replacement, and eective management of extracardiac complications. The complexity of evaluation and treatment suggests that patients should be
hospitalized in centers with experience in treating PVE. It is essential to isolate the causative organism. When evaluating patients who present with
indolent disease and are hemodynamically stable, antibiotic therapy should
be delayed for 2 or 3 days awaiting the results of blood cultures. This is particularly important if antibiotics have been administered recently, because if
initial cultures are negative, it allows one to obtain additional cultures without further confounding. Patients who present with fulminant PVE or who
are hemodynamically unstable and may require urgent replacement of the
485
infected prosthetic valve should be treated empirically immediately after

obtaining blood cultures.
Although administered for a longer duration, the antimicrobial therapy
recommended for the treatment of PVE caused by specic organisms, with
the exception of staphylococci, is similar to that used to treat native valve
endocarditis (Table 4). Detailed comments regarding these regimens can
be found elsewhere [17,36,55]. If streptomycin or gentamicin is to be combined with a cell wall active antibiotic to achieve synergistic killing of streptococci or enterococci, the organism must not exhibit high-level resistance to
the selected aminoglycoside (i.e., unable to grow in the presence of 500 lg/
mL of gentamicin or 1000 lg/mL of streptomycin). The presence of highlevel resistance precludes a synergistic eect from the respective aminoglycoside. Gentamicin high-level resistance also generally precludes a synergistic
eect from netilmicin, kanamycin, tobramycin, and amikacin. Optimal therapy for PVE caused by vancomycin-resistant Enterococcus faecium (VREF)
that are also resistant to penicillin and ampicillin and highly resistant to
streptomycin and gentamicin has not been established. Although linezolid
and quinupristindalfopristin are often active against VREF, these agents
have not been proven to be eective therapy for PVE. Surgical intervention
during suppressive antimicrobial therapy should be considered for these
patients.
For optimal treatment of staphylococcal PVE, a multi-drug regimen is
recommended. In vitro data, evidence from animal models, and clinical
experience indicate that rifampin has a unique ability to kill staphylococci
adherent to foreign material and is an important component of regimens
used to treat staphylococcal PVE [17,21,5660]. Staphylococci have a relatively high intrinsic mutation rate for the gene controlling the site of rifampin action; thus when relatively large populations of staphylococci are
exposed to rifampin, selection of rifampin-resistant organisms is common.
To prevent the emergence of rifampin-resistant organisms, the regimens
selected for the treatment of staphylococcal PVE should contain two antibiotics that are known to be active against the staphylococcal isolate in
addition to rifampin. All three antimicrobials can be started at the same
time. If two additional anti-staphylococcal agents have not been identied,
treatment with a single anti-staphylococcal agent should be administered for
3 to 5 days before beginning rifampin. This approach may reduce the total
number of staphylococci and thus diminish the probability that a rifampinresistant subpopulation will emerge.
The regimens recommended for the treatment of staphylococcal PVE are
not based on the species of the isolateS. aureus or coagulase-negative
staphylococcibut rather upon susceptibility of the isolate to methicillin.
For isolates that are susceptible to gentamicin, it is an eective second
anti-staphylococcal antimicrobial. For strains resistant to gentamicin and
other aminoglycosides, a uoroquinolone to which the strain is highly susceptible should be considered [57,60].
2 g IV or IM daily
as single dose
1 mg/kg IM or IV q 8 h
15 mg/kg IV q 12 h
B. Ceftriaxone plus
C. Vancomycinb
3. Enterococci (in vitro

evaluation for MIC
to penicillin and vancomycin,
b-lactamase production,
and high-level resistance
to gentamicin and
streptomycin required)
2. Relatively penicillin-resistant
streptococci (penicillin MIC
>0.2 lg/mL)
1824 million units IV

daily in divided
doses q 4 h
A. Penicillin G plus
1. Penicillin-susceptible
viridans streptococci,
Streptococcus bovis,
and other streptococci
(penicillin MIC 0.1 lg/mL)

daily in divided
doses q 4 h
1 mg/kg IV or IM q 8 h
gentamicin
gentamicin

daily in divided
doses q 4 h
gentamicin
gentamicin
Dose and routea
Antibiotic
Infecting organism
Table 4
Recommended antibiotic therapy for patients with PVE
Duration
(wk)
Streptomycin can be used instead

of gentamicin if streptomycin high-level
resistance is not present. If high-level
resistance to gentamicin but not to
streptomycin is detected, streptomycin
is preferred.
Preferred for nutritionally variant

(pridoxal- or cysteine-requiring)
streptococci (Abiotrophia spp).
Can be used in patients

with non-immediate penicillin allergy.
Intramuscular ceftriaxone is painful.
Cephapirin 2 g IV q 4 h can be
substituted for ceftriaxone.
Use for patients with immediate
or severe penicillin or cephalosporin allergy.
Infuse doses over 1 hour to avoid
histamine release reaction (redman syndrome).
May omit aminoglycoside

when potential for nephrotoxicity
is increased
Comments
486
15 mg/kg IV q 12 h
300 mg po q 8 h
2 g IV or IM daily
as a single dose
2 g IV daily in divided
doses q 4 h
A. Vancomycinb plus
gentamicin
plus rifampinc
A. Ceftriaxone
B. Ampicillin plus
5. Staphylococci
methicillin-resistant
6. HACEK organismsd
gentamicin
2 g IV q 4 h
300 mg po q 8 h
A. Nafcillin or oxacillin
plus gentamicin
plus rifampinc
2 g IV q 4 h
Same dose as noted above
15 mg/kg IV q 12 h
Same dose as noted above
4. Staphylococci
methicillin-susceptible
(assume penicillin resistance)
B. Ampicillin plus
gentamicin
C. Vancomycinb plus
gentamicin
68
2
68
68
2
68
6
6
6
6
(continued on next page)
Cefotaxime or other third generation

cephalosporin in comparable doses
may be used.
Test organism for b-lactamase production.
Do not use this regimen
if b-lactamase is produced.
Use gentamicin during the initial two

weeks of therapy. See text for alternatives
to gentamicin. Do not substitute
a cephalosporin or imipenem for vancomycin.
Penicillin 1824 million units daily in divided

doses q 4 h can be used instead of nafcillin
or oxacillin if strains do not produce
b-lactamase and penicillin MIC is 0.1 lg/mL.
Cephapirin 2 gm IV q 4 h can be used
in lieu of nafcillin/oxacillin for patients
with non-immediate allergy to penicillins.
Use gentamicin during initial two weeks.
See text for alternates for gentamicin.
For patients with immediate penicillin allergy,
use regimen 5.
Use for patients with penicillin allergy.

Do not use cephalosporins.

487
7. Diphtheroids

daily in divided
doses q 4 h
15 mg/kg IV q 12 h
Dose and Routea
6
6
Duration
(wk)
Use if organism resistant

to gentamicin,
highly resistant to penicillin,
or patient is allergic
to penicillin.
Bactericidal synergy results if isolate

is not resistant to gentamicin
(MIC 4 lg/mL).
Comments
a
Recommended doses are for adults with normal renal and hepatic function. Doses of gentamicin, streptomycin, and vancomycin must be adjusted in
patients with renal dysfunction. Use ideal body weight to calculate doses (men 50 kg + 2.3 kg per in over 5 ft; women 45.5 kg plus 2.3 kg per in over 5 ft).
Do not use aminoglycosides as single daily doses.
b
Peak levels obtained 1 hour after completion of the infusion should be 3045 lg/mL trough level 1020 lg/mL.
c
Rifampin increases the dose of warfarin or dicumarol required for eective anticoagulation.
d
HACEK organisms include Haemophilus parainuenzae, Haemophilus aphrophilus, Actinobacillus actinomycetemcomitans, Cardiobacterium hominis,
Eikenella corrodens, and Kingella kingii.
Adapted from Karchmer AW. Infections of prosthetic valves and intravascular devices. In: Mandell GL, Bennett JE, Dolin R, editors. Principles and
practice of infectious diseases, 5th edition. Philadelphia: Churchill Livingstone; 2000. p. 90317; with permission.
gentamicin
B. Vancomycin
Antibiotic
Infecting Organism
Table 4
(continued )
488
489
For fungal PVE, amphotericin B (0.7 to 1.0 mg/kg/d) is recommended;

larger doses (1.0 to 1.5 mg/kg/d) are recommended for treatment of PVE
caused by molds (e.g., Aspergillus spp). A synergistic eect is often sought
by combining amphotericin B with 5-uorocytosine (150 mg/kg/d divided
into 4 doses with adjustments for renal dysfunction). The role of liposomal
formulations of amphotericin B or caspofugin in the treatment of PVE has
not been established. Early surgical intervention is considered a standard
element of treating fungal PVE [2325]. As a result of the high rate of
relapse of candida PVE, initial therapy is often followed by long-term or
indenite suppressive therapy with uconazole (200 to 400 mg orally per
day) [24,25,61].
Surgical management
Murmurs suggesting valve dysfunction, moderate to severe congestive
heart failure due to valve dysfunction, fever for 10 or more days in spite
of appropriate antibiotic therapy, new onset electrocardiographic conduction abnormalities, or selected ndings on echocardiogram identies complicated PVE with extension of infection into paravalvular tissue or valve
dysfunction. PVE with one or more of these features is not likely to respond
to antibiotic therapy alone [37,62,63]. Complicated PVE is more common
with infection of aortic valve prostheses and with infection during the initial
year after valve surgery [37]. Antibiotic therapy combined with valve replacement and cardiac reconstruction results in higher survival rates and fewer
relapses, rehospitalizations for valve surgery, and late endocarditis-related
mortality than does treatment with antibiotics alone in patients with complicated PVE [37,6365].
Indications for surgical treatment of PVE have been developed step-wise
as the pathology of PVE was dened, surgical techniques were rened, and
the presumed inevitability of recurrent PVE involving the newly implanted
prosthesis was disproven. The indications (see box on following page) are
not absolute and must be implemented with a careful riskbenet analysis.
Notably, patients with late-onset PVE caused by viridans streptococci,
HACEK, or enterococci and without evidence of paravalvular invasion or
valve dysfunction can be treated successfully with antibiotics alone [17].
Survival rates among PVE patients with moderate to severe congestive
heart failure due to valve dysfunction are dramatically improved if these
patients are treated surgically. Only occasional patients in this group will
survive if treated with antibiotics alone. In contrast, 44% to 64% survive
when treated with antimicrobials plus valve replacement [17,63,66]. If outcome is to be optimal, surgical intervention to correct valve dysfunction
must be performed before intractable heart failure ensures. There is no
evidence that delaying surgery in the face of progressive hemodynamic
deterioration in order to administer additional antibiotics improves outcome or reduces the frequency of recurrent endocarditis [33,67]. In fact,
490
Indications for cardiac surgery in patients with PVEa

Moderate to severe congestive heart failure due to valve
dysfunction (regurgitant or stenotic)
Unstable prosthesis
Paravalvular extension of infection, especially with abscess
formation or fistula
Uncontrolled infection (persistent bacteremia) on optimal
antimicrobial therapy
PVE caused by selected microorganisms
fungi
P. aeruginosa
S. aureus
enterococci in the absence of available bactericidal
therapy
other gram-negative bacilli and microorganisms that
usually require surgery when infecting native valves
(e.g., Brucella spp, Coxiella burnetii)
Relapse after optimal therapy
Large (>10 mm) hypermobile vegetations
Culture negative PVE with unexplained persistent (10 days)
fever
a
Not all indications are absolute (see text)
Adapted from Karchmer AW. Infections of prosthetic valves and intravascular
devices. In: Mandell GL, Bennett JE, Dolin R, editors. Principles and practice of
infectious diseases. New York: Churchill Livingstone; in press.
postoperative mortality is proportional to the severity of hemodynamic

impairment at the time of surgery [33,68]. Occasionally, patients with PVE
who have responded to antibiotics develop valve dysfunction but remain
hemodynamically compensated. Surgery can be delayed until late in the
course of antimicrobial therapy in these patients.
Even in the absence of heart failure, mortality rates are high for patients
with paravalvular invasion when they are treated with antibiotics alone. In
contrast, complex reconstructive surgery in these patients has been associated with survival rates of 80% [64,69,70]. Relapse of PVE after optimal antimicrobial therapy commonly reects unrecognized invasive disease. These
patients should be treated with antibiotics plus surgery [37,62].
The outcome of S. aureus PVE is improved by aggressive surgical intervention. When treated with antibiotics alone, 70% of patients with S. aureus
PVE die [7173]. Intracardiac complications in patients with S. aureus PVE
are associated with a 13.7-fold increase in mortality; however, mortality is
reduced 20-fold (OR 0.05, 95% CI: 0.0050.42; P 0.004) by surgical intervention during antimicrobial therapy [51]. In fact, improved survival with
491
antibiotics plus surgical treatment versus antibiotics alone was noted among
both those with and without intracardiac complication. Multiple studies
have suggested that PVE caused by S. aureus is treated most eectively with
antibiotics plus aggressive cardiac surgery [63,7274].
The role of surgical intervention to prevent systemic emboli is unclear.
Patients with native valve endocarditis who have vegetations >10 mm in diameter experience a higher rate of embolic complications than do patients
with smaller vegetations [75]. Although data are not available correlating
vegetation size with arterial emboli in patients with PVE, the overall rates
of embolic events are similar in patients with infection of native and prosthetic heart valves. Furthermore, these rates decrease rapidly with eective antibiotic therapy. While it is desirable to prevent emboli to vital organs, it is
not clear that mortality and morbidity are reduced by cardiac surgery in
PVE patients simply because vegetations >10 mm in diameter are detected.
The decision to operate in this situation must be made in the context of an
overall clinical evaluation and integrated plan for therapy rather than on
vegetation size alone.
An optimal outcome for patients with PVE often requires complex reconstruction of the aortic or mitral valve and the supporting or adjacent tissue.
With appropriate antibiotic therapy and surgical intervention by experienced cardiac surgeons, survival rates for patients with complicated PVE
range from 70% to 90% [18,64,69,70,7679]. These remarkable results support the concept thatwhen possiblepatients with PVE complicated by
extensive invasion and tissue disruption should undergo surgery in centers
with extensive experience.
The long-term results of surgical treatment of PVE are also encouraging.
Recurrent PVE is noted in only 6% to 15% of patients, and repeat cardiac
surgery for either recrudescent PVE or dysfunction of the newly implanted
valve is required in 18% to 26% [18,33,37,64,70,77,79]. Survival rates 5 years
after surgery for PVE have ranged from 54% to 87% [18,33,70,76,77].
Anticoagulant therapy
The use and specic type (heparin versus warfarin) of anticoagulant therapy in patients with active PVE is controversial [8084]. Cerebrovascular
accidents were reported in 16 of 133 patients (12%) with mechanical valve
infection who were eectively anticoagulated versus 32 of 76 patients (42%)
who were not anticoagulated. Additionally, hemorrhagic complications
were not increased among those who were anticoagulated [80]. Accordingly,
carefully monitored anticoagulant therapy is recommended for patients with
infected mechanical or bioprosthetic valves when this therapy would be used
routinely in the absence of infection. The authors prefer warfarin and
suggest the International Normalized Ratio (INR) be maintained between
2.5 and 3.0. If intracerebral hemorrhage or another contraindication to
anticoagulant therapy is noted, anticoagulation should be reversed. Because
492
rifampin accelerates the hepatic clearance of warfarin, patients being treated

for PVE with rifampin require major adjustments in daily warfarin doses
during and following rifampin therapy.
Infections involving implantable electrophysiologic cardiac devices

Cardiac pacemakers and implantable cardioverter debrillators have
revolutionized the treatment of patients with rhythm disorders, and their use
has become increasingly common in clinical practice. It is estimated that, as
of April 1999, there are approximately 180,000 functioning implantable cardiac debrillators and 3.25 million permanent pacemakers presently in use
worldwide [85]. The rates of infectious complications involving these devices
have decreased in recent years with improvements in surgical techniques and
with the development of transvenous devices. Nevertheless, infection rates
remain in the range of 1% to 7% [8589]. With the burgeoning number of
devices implanted, infections involving them are increasingly encountered
in clinical practice.
Anatomy, pathogenesis, and classication
Most permanent pacemakers and cardiac debrillator devices presently
in use are transvenous devices. They consist of a generator or debrillator
implanted in the subcutaneous tissue of the chest wall or abdomen, and electrodes which traverse the soft tissue, enter the subclavian vein, pass through
the right heart, and terminate in the right atrial and ventricular endocardium. Depending on the type of device, some patients with transvenous cardiac debrillators may have a mesh debrillator patch positioned in the
subcutaneous tissue in the left mid or posterior axilllary area. In over 98%
of patients, the current cardioverterdebrillator systems are completely
transvenous. In the early years of cardiac pacing and cardiodebrillator
technology, electrodes and mesh debrillator patches were placed by way
of thoractomy or sternotomy directly onto the epicardial surface of the
heart. Some patients still have these devices in place. The development of
transvenous devicesespecially cardioverter debrillators and combination
devices that serve both pacing and debrillating functionsrepresents an
important advance in the eld, given the reduced morbidity associated with
their implantation.
Infections involving these devices have traditionally been classied anatomically and by time of onset following implantation. Infection may
involve the generator or debrillator pocket (Fig. 1), the electrodes as they
traverse the soft tissue and venous system or track to the epicardium in older
devices, mesh patches in the subcutaneous tissue or on the surface of the
heart, and valvular or nonvalvular endocardium. Deep endovascular infection may involve the tricuspid valve, the insertion site of the lead tip in the
right atrium or ventricle and, on occasion, thrombi that form around the
493
Fig. 1. Pocket infection: Erythematous discoloration of the skin overlying an infected pocket
in a patients left chest wall, containing an implantable cardioverterdebrillator. (Courtesy of
Bruce Wilko, MD.)
electrodes in the venous system or right atrium (Fig. 2) [90]. Myocardial

abscesses are rare but have been described [90]. Early infection is classied
as infection developing in the rst month following implantation; late infection presents beyond the rst month [85,91]. Some studies have further classied this latter group into those presenting from months 1 to 12 after
implantation (late infection) versus those presenting beyond one year
(delayed infection) [85].
Several pathogenetic mechanisms contribute to the development of infection involving these devices. Early infection most often arises from intraoperative contamination at the time of device implantation or generator
exchange and is attributable to direct microbial seeding of the device or
pocket. Late infection occasionally develops from primary mechanical erosion of the generator or debrillator through the skin, with resultant seeding
of the pocket. In other cases, chronic smoldering infection in the pocket produces a thinning of the overlying tissue and ultimately device erosion.
Whichever mechanism occurs, infection may spread from the pocket to
involve the electrodes and ultimately the endocardial surfaces of the heart.
Hematogenous seeding of the device from distant sites of infection has been
reported, but with the exception of S. aureus bacteremia appears to be relatively rare [90,92,93]. In one study of 21 patients with S. aureus bacteremia
occurring a year or more after device placement, 29% developed a subsequent device infection [94].
494
Fig. 2. Implantable cardioverterdebrillator lead with a large, attached, infected vegetation.

Adjacent to the lead is a large, infected embolus that was removed from the pulmonary artery of
the patient from whom this infected device was extracted. (Courtesy of Bruce Wilko, MD.)
Epidemiology and risk factors

A number of studies have examined risk factors associated with the development of infections involving these devices. Underlying conditions that
predispose patients to pacemaker-related infections include malnutrition,
malignancy, diabetes mellitus, skin disorders, and the use of corticosteroids,
other immunosuppressive agents, or anticoagulants [92,95,96]. Prolonged
operation, re-operation, generator replacement, catheter-related bacteremia,
sternal wound infections, and diabetes mellitus are risk factors associated
with the development of cardiodebrillator-associated infections [97,98].
In the largest recent review of infections associated with these devices in
123 patients treated at the Cleveland Clinic Foundation, comorbid conditions were common and included coronary artery disease in 64%, coronary
artery bypass surgery in 32%, diabetes mellitus in 26%, anticoagulation
in 19%, atrial brillation in 19%, malignancy in 6%, corticosteroid use in
5%, and hemodialysis in 2% [85].
The timing, route, and location of implantable cardiodebrillator placement have been associated with the risk of subsequent infection. In one
recent study, infectious complications fell from 16.7% to zero coincident
with an increase in transvenous device placement and with the elimination
of two staged procedures in which electrophysiologic studies performed in
the cardiac catheterization laboratories were followed within hours to days
by the placement of debrillator devices in the operating room by cardiac
495
surgeons [88]. In recent years, electrophysiologic studies have been followed

immediately by pacemaker or debrillator placement in the cardiac catheterization laboratory or in the operating room for patients requiring these
devices.
Microbiology
Numerous studies have examined the microbiology of these infections
[85,87,89,91,93,99105]. In nearly all series, the majority of infections are
caused by staphylococci, including S. aureus and coagulase-negative staphylococci. Some studies have suggested that infections occurring within the
rst month following implantation are more likely due to S. aureus, and late
infections are more commonly caused by coagulase-negative staphylococci.
This is likely attributable to the fact that many late infections arise from
mechanical erosion of the device through the skin, resulting in contamination of the pocket with skin ora. Less common isolates include enterococci,
Peptostreptococcus spp, Propionibacterium acnes, micrococcus, and gramnegative bacilli such as E. coli, and Enterobacter, Serratia, Pseudomonas,
and Klebsiella species. Mycobacterium avium-intracellulare and fungal
pathogens such as Candida spp, Torulopsis glabrata and Aspergillus spp have
been implicated on rare occasion [106108].
In the most recent series from the Cleveland Clinic, which evaluated 123
patients with infected pacemakers (87) or cardioverter debrillators (36), the
most common pathogens were coagulase-negative staphylococci (68%),
S. aureus (24%), and enteric gram-negative bacilli (17%). Thirteen percent
of infections were polymicrobial. The distribution of pathogens was similar
between infected pacemakers and cardioverterdebrillators.
Clinical presentation
The clinical presentation of these infections is highly variable, both with
regard to time of onset and clinical severity. In the series by Chua et al., 25%
of infections occurred within the rst month, 33% presented late (days
29364), and 42% were delayed, presenting beyond 1 year [28]. Clinical manifestations in patients from this series are summarized in Table 5 in descending order of frequency and are consistent with earlier reports [87,98].
Several points merit emphasis. Eighty-ve patients (69%) presented with
symptoms localized to the device pocket, including erythema (55%), pain
(55%), a draining sinus (42%), erosion (32%), and warmth (23%). Twentyve patients (20%) presented with a combination of local and systemic
symptoms, and thirteen (11%) presented with systemic complaints alone.
Overall, a history of fever was present in only 29%, and was documented
in only 19%. The frequent absence of fever in patients with these infections
has been emphasized by other researchers [98]. Despite the absence of
documented fever in over 80% of patients in the Cleveland Clinic series, bacteremia was surprisingly common and occurred in one-third of patients.
496
Table 5
Clinical manifestations in 123 patients with infections involving implantable electrophysiologic
cardiac devicesa
Manifestation
Number
Percent
Pocket pain
Pocket erythema
Draining sinus from pocket
Pocket swelling
Bacteremia
Pocket erosion
History of fever
Pocket warmth
Purulent drainage from pocket to sinus
Chills
Malaise
Bacteremia accompanied by systemic symptoms
Fever on examination
Anorexia
Sepsis (fever and tachycardia)
Tachycardia (>100 beats/min)
Nausea
68
68
52
44
40
39
35
28
28
27
26
24
23
14
14
10
10
55
55
42
36
33
32
29
23
23
22
21
20
19
12
12
8
8
Includes pacemakers (87) and cardioverter debrillators (36).

Modied from Chua JD, Wilko BL, Lee I, Juratli N, Longworth DL, Gordon SM.
Diagnosis and management of infections involving implantable electrophysiologic cardiac
devices. Ann Int Med 2000;133:6048, with permission.
Among the 40 patients with bacteremia, fever and systemic symptoms were
absent in 16 (40%). Clinicians must therefore have a high index of suspicion
for bacteremia, even in patients who lack fever and systemic signs of infection. Blood cultures are indicated in all patients with suspected or proven
infections of these devices. The possibility of cryptic device infection, including infection limited to the generator pocket, must be considered in patients
with staphylococcal bacteremia. Additionally, occurrence of pulmonary
emboli (Fig. 2) can provide a clue that an intracardiac lead has become
infected, especially if a chest radiography shows multiple focal inltrates,
indicating the likelihood of septic emboli.
Some studies conned to the analysis of patients with pacemaker endocarditis have reported fever in up to 86% to 91% of patients and chills in
up to 75% [99,101]. In a review of 44 cases from Israel, a new or changing
murmur was present in 13%, leukocytosis exceeding 10 109/L in 66%, splenomegaly in 11%, anemia in 39%, and microscopic hematuria in 59% [99].
Several studies have examined the role of echocardiography in the diagnosis of implantable cardiac device infections. In the Cleveland Clinic study,
64 of 123 patients had transthoracic (45), transesophageal (8), or both (11)
echocardiographic procedures performed. Vegetations involving the device
leads or a valve were present in 13 patients, 12 with a pacemaker, and 1 with
a cardioverterdebrillator. In three other studies conned to patients with
proven pacemaker endocarditis, the sensitivity of transthoracic echocardio-
497
graphy in demonstrating valvular or lead vegetations was 23% to 30%, compared with 91% to 96% with transesophageal echocardiography [100,101,
105]. The authors believe that echocardiography is indicated in all patients
with bacteremic implantable device-related infections and in those whose
clinical ndings that suggest the possibility of endovascular infection. Transesophageal echocardiography is superior in sensitivity to the transthoracic
approach.
Management
The optimal management of implantable device-related infections has
been debated in the literature, especially regarding the necessity for device
removal. Some authors have advocated a conservative approach consisting
of antibiotic therapy with hardware in place. Pursuit of this strategy has been
motivated by the desire to avoid invasive surgical procedures, especially in
debilitated individuals and in those with epicardial devices. Turkisher et al.
described a single patient in whom a cardiodebrillator infection was successfully managed with a 3-month course of oral fusidic acid and rifampin
[109]. Lee et al. reported successful treatment of 4 patients with implantable
cardiodebrillator infections with wide debridement of the device pocket
followed by placement of a closed irrigation system and continuous irrigation with polymyxin, bacitracin, and neomycin solution, along with culturedirected antimicrobial therapy [110]. In general, reports of success without
removing the entire device have been based on small numbers of patients
or patients with infections limited to the generator pocket [102].
Other authors have recommended complete explantation of infected
devices, but have commented that in rare cases patients may be successfully
treated with partial device removal [91,98,102]. Partial removal is likely to
be sucient only when infection is clearly limited to the removed component, usually the generator unit and immediately adjacent leads. In the
recent large study involving 123 patients at the Cleveland Clinic, complete
removal of the device and all lead material was successful in 117 patients
(95%) [85]. One hundred nineteen received antimicrobial therapy after hardware removal; specic therapy was guided by culture results but was not
standardized with regard to route or duration. Seventy-one patients received
intravenous therapy for a median of 28 days. Forty-three received intravenous antibiotics (median 7 days) followed by oral therapy (median 16 days).
Five patients received oral therapy alone for a median of 24 days. Among
the 117 patients who had complete device removal, relapse occurred in only
one. By contrast, among the remaining six patients in whom device removal
was incomplete, relapse occurred in three. Chua et al. concluded that complete explantation of all hardware combined with antibiotic therapy is the
optimal method of management of implantable device-related infections.
Data from several recent studies of pacemaker endocarditis strongly support
removal of the entire system as the preferred therapy [93,99,100102].
498
Among 190 patients with pacemaker endocarditis, 12 of 29 patients (41%)

treated with antibiotics alone died as contrasted with 30 of the 161 patients
(19%) treated with antibiotics plus removal of the entire system [100].
Older studies have emphasized the morbidity and potential mortality
associated with device removal, especially in those requiring sternotomy
or thoracotomy [99]. Older traction techniques to remove transvenous
devices were sometimes associated with complications such as tricuspid
valve tear, rupture of the right atrial or ventricular wall, tearing of the
cephalic or subclavian veins, or rupture of the chordae tendineae [86]. In
recent years, the availability of laser sheath technology for extraction of
pacing leads has facilitated nonoperative removal of transvenous devices
[111]. In one recent study, use of the Excimer laser sheath to extract pacing
leads was successful in 94% of cases versus 64% using standard non-laser
technology; in patients who failed non-laser standard extractions, 88% were
successfully treated utilizing the laser tool. Life-threatening complications
occurred in 3% of patients treated with standard non-laser extraction, compared with 0% in those treated with the laser Excimer sheath [111]. Patients
with suspected infection of an implanted debrillator with epicardial patches
are particularly vexing because removal of the entire device requires a thoracotomy. Bacteremia, fever, and signs of septic pericarditis are clues that
point to epicardial lead infection. Additionally, computed tomography and
a gallium or labeled white blood cell scan can be used to evaluate for infection involving the deep leads and patches. If infection appears limited to the
generator pocket (i.e., there are neither clinical clues or patch abnormalities
by computed tomography or isotope scan) removal of only the generator
and adjacent lead wires, in combination with antibiotic therapy, mayon
occasionbe sucient to eradicate infection [102]. Success rates with partial
device removal are low because the entire device is typically infected.
Few studies have examined the optimal route or duration of antibiotic
treatment for infected electrophysiologic devices. Experience suggests that
those patients with bacteremia and denite or probable endocarditis or pericarditis will require long courses of parenteral therapy as advocated for
endocarditis. Patients with infection limited to the generator unit pocket and
no bacteremia can be treated with less intensive regimens (parenteral therapy followed by oral therapy) and wound care for the pocket from which
the device has been explanted [36].
At the Cleveland Clinic, all patients with suspected infections involving
cardiac devices have at least 2 sets of blood cultures collected. At the time
of device removal, cultures are obtained from the device pocket and from
all lead tips and mesh. Patients with endocarditis receive at least 4 weeks
of culture-directed intravenous antibiotic therapy. Those with infection conned to the device pocket are treated with parenteral therapy with or without subsequent oral therapy; the duration of therapy depends on the
presence or absence of bacteremia and on the clinical response. The optimal
duration of therapy remains controversial and has not been well dened for
499
those individuals who lack bacteremia, fever, and echocardiographic evidence of endocarditis but who nevertheless have positive lead tip cultures.
Because of the concern about focal infection at the right atrial or ventricular
lead tip site in those with positive lead tip cultures, most patients receive 4
weeks of parenteral therapy. The optimal antibiotic management of patients
with these infections requires further study.
The timing of device reimplanation has been an area of ongoing controversy. Some authors have recommended reimplanation as early as 36 hours
following explantation in those with infection conned to the device pocket
[112]. Because blood cultures may take longer than 36 hours to become
positive, others have advocated waiting at least several days [85]. In the
Cleveland Clinic study, the median interval from device explantation to reimplantation was 5 days (range 068 days). Among the thirteen patients
with endocarditis, reimplantation was successfully performed in those who
required it at a median of 7 days following explantation (range 525 days).
Before replacing an intracardiac device in a patient with device-associated
endocarditis, it is prudent to provide sucient antibiotic therapy to eradicate bacteremia and to suciently suppress or eradicate endothelial infection so that the probability of reinfection of the new device is minimized.
It is important to emphasize that not all patients with electrophysiologic cardiac device-related infections require new devices. In the Cleveland
Clinic study, 18% of patients did not require further device therapy after
re-evaluation of their cardiac status.
Infections of left ventricular assist devices and articial hearts

As an increasing number of left ventricular assist devices (LVAD) are
implanted, it has become clear that they are subject to serious risk of infection. In a controlled study of 68 patients followed for up to 2.5 years after
implantation of LVADs for severe heart failure, approximately one-third of
the devices became infected within three months [113]. Infections of the
drive-line tract or pocket occurred at a rate of 0.41 per patient year, and
infection of the pumps interior or inow/outow tracts at a rate of 0.23 per
patient year. This resulted in an overall sepsis rate of 0.6 per patient year.
Moreover, sepsis was the most common cause of death. Sepsis caused
41% of the 41 deaths in the LVAD group, but only one (2%) of 54 deaths
among the controls [113]. It is evident that until more eective means to
reduce the high rate and high mortality of infections of LVADs and similar
devices such as articial hearts are found, their long-term value will be
limited.
As to treatment, removal of the device oers the best chance for cure. De
Jonge et al. [114] reported recently an apparent cure of a case of endocarditis in an LVAD by valve replacementthat is, removal and replacement of the mechanical inow and outow valves of the device. For various
500
reasons, removal of the device may not be practicable, so many of these

patients have been treated empirically with antibiotics. Data are so far inadequate to assess the likelihood of successful long-term suppressionor even
possibly cureof such infections by means of antibiotic treatment alone.
However, extensive previous experience with infections of other prosthetic
devices indicates that cure with antibiotics alone is unlikely. Thus, a more productive strategy may be suppression of infection and early cardiac transplantation with eradicative therapy administered after heart transplantation.
References
[1] Calderwood SB, Swinski LA, Waternaux CM, Karchmer AW, Buckley MJ. Risk factors
for the development of prosthetic valve endocarditis. Circulation 1985;72:317.
[2] Glower DD, Landolfo KP, Cheruvu S, et al. Determinants of 15-year outcome with 1,119
standard Carpentier-Edwards porcine valves. Ann Thorac Surg 1998;66:S448.
[3] Ivert TSA, Dismukes WE, Cobbs CG, Blackstone EH, Kirklin JW, Bergdahl LAL.
Prosthetic valve endocarditis. Circulation 1984;69:22332.
[4] Agnihotri AK, McGin DC, Galbraith AJ, OBrien MF. Surgery for acquired heart
disease. J Thorac Cardiovasc Surg 1995;110:170824.
[5] Arvay A, Lengyel M. Incidence and risk factors of prosthetic valve endocarditis. Eur
J Cardio-Thorac 1988;2:3406.
[6] Rutledge R, Kim J, Applebaum RE. Actuarial analysis of the risk of prosthetic valve
endocarditis in 1,598 patients with mechanical and bioprosthetic valves. Arch Surg
1985;120:46972.
[7] Bloomeld P, Wheatley DJ, Prescott RJ. Twelve-year comparison of a Bjork-Shiley
mechanical heart valve with procine bioprostheses. N Engl J Med 1991;324:5739.
[8] Grover FL, Cohen DJ, Oprian C, et al. Determinants of the occurrence of and survival
from prosthetic valve endocarditis. J Thorac Cardiovasc Surg 1994;108:20714.
[9] Hammermeister KE, Sethi GK, Henderson WG. A comparison of outcomes eleven years
after heart valve replacement with a mechanical valve or prosthesis. N Engl J Med
1993;328:128996.
[10] Bayer AS, Scheld WM. Endocarditis and intravascular infections. In: Mandell GL,
Bennett JE, Dolin R, editors. Principles and practice of infectious diseases. Philadelphia:
Churchill Livingstone; 2000. p. 857902.
[11] Karchmer AW. Infective endocarditis. In: Braunwald E, editor. A textbook of cardiovascular medicine, 6th edition. Philadelphia: W.B. Saunders Company; 2000. p. 172348.
[12] Lowy FD. Medical progress: Staphylococcus aureus infections. N Engl J Med 1998;339:
52032.
[13] Alloway JA, Evangelisti SM, Sartin JS. Mycobacterium marinum arthritis. Sem Arthr
Rheumat 1995;24:38290.
[14] Boyce JM, Potter-Bynoe G, Opal SM, Dziobek L, Medeiros AA. A common-source
outbreak of Staphylococcus epidermidis infections among patients undergoing cardiac
surgery. J Infect Dis 1990;161:4939.
[15] Dismukes WE, Karchmer AW, Buckley MJ, Austen WG, Swartz MN. Prosthetic valve
endocarditis: analysis of 38 cases. Circulation 1973;XLVIII:36577.
[16] van den Broek PJ, Lampe AS, Berbee GAM, Thompson J, Mouton RP. Epidemic
of prosthetic valve endocarditis caused by Staphylococcus epidermidis. BMJ 1985;291:
94950.
[17] Karchmer AW. Infections of prosthetic heart valves. In: Waldvogel F, Bisno AL, editors.
Infections associated with indwelling medical devices. Washington, DC: American Society
for Microbiology; 2000. p. 14572.
501
[18] Lytle BW, Priest BP, Taylor PC, et al. Surgery for acquired heart disease: surgical
treatment of prosthetic valve endocarditis. J Thorac Cardiovasc Surg 1996;111:198210.
[19] Fang G, Keys TF, Gentry LO, et al. Prosthetic valve endocarditis resulting from
nosocomial bacteremia: a prospective, multicenter study. Ann Int Med 1993;119:5607.
[20] Nasser RM, Melgar GR, Longworth DL, Gordon SM. Incidence and risk of developing
fungal prosthetic valve endocarditis after nosocomial candidemia. Am J Med 1997;103:
2532.
[21] Karchmer AW, Archer GL, Dismukes WE. Staphylococcus epidermidis causing prosthetic
valve endocarditis: microbiologic and clinical observations as guides to therapy. Ann Int
Med 1983;98:44755.
[22] Murray BE, Karchmer AW, Moellering RC Jr. Diphtheroid prosthetic valve endocarditis:
a study of clinical features and infecting organisms. Am J Med 1980;69:83848.
[23] Ellis ME, Al-Abdely H, Sandridge A, Greer W, Ventura W. Fungal endocarditis: evidence
in the world literature, 19651995. Clin Infect Dis 2001;32:5062.
[24] Gilbert HM, Peters ED, Lang SJ, Hartman BJ. Successful treatment of fungal prosthetic
valve endocarditis: case report and review. Clin Infect Dis 1996;22:34854.
[25] Melgar GR, Nasser RM, Gordon SM, Lytle BW, Keys TF, Longworth DL. Fungal
prosthetic valve endocarditis in 16 patients. An 11 year experience in a tertiary care
hospital. Medicine (Baltimore) 1997;76:94103.
[26] Raoult D, Tissot-Dupont H, Foucault C, et al. Q fever 19851998: clinical and epidemiologic features of 1,383 infections. Medicine (Baltimore) 2000;79:10923.
[27] Anderson DJ, Bulkley BH, Hutchins GM. A clinicopathologic study of prosthetic valve
endocarditis in 22 patients: morphologic basis for diagnosis and therapy. Am Heart J
1977;94:32532.
[28] Arnett EN, Roberts WC. Prosthetic valve endocarditis: clinicopathologic analysis of 22
necropsy patients with comparison of observations in 74 necropsy patients with active
infective endocarditis involving natural left-sided cardiac valves. Am J Cardiol 1976;38:
28191.
[29] Ismail MB, Hannachi N, Abid F, Kaabar Z, Rouge JF. Prosthetic valve endocarditis: a
survey. Br Heart J 1987;58:727.
[30] Richardson JV, Karp RB, Kirklin JW, Dismukes WE. Treatment of infective endocarditis: a 10-year comparative analysis. Circulation 1978;58:58997.
[31] Rose AG. Prosthetic valve endocarditis: a clinicopathological study of 31 cases. S Afr
Med J 1986;69:4415.
[32] Madison J, Wang K, Gobel FL. Prosthetic aortic valve endocarditis. Circulation 1975;51:
9409.
[33] Baumgartner WA, Miller DC, Reitz BA, et al. Surgical treatment of prosthetic valve
endocarditis. Ann Thorac Surg 1983;35:87102.
[34] Fernicola DJ, Roberts WC. Frequency of ring abscess and cuspal infection in active
infective endocarditis involving bioprosthetic valves. Am J Cardiol 1993;72:31423.
[35] Magilligan DJ Jr, Quinn EL, Davila JC. Bacteremia, endocarditis, and the Hancock valve.
Ann Thorac Surg 1977;24:50818.
[36] Karchmer AW. Infections of prosthetic valves and intravascular devices. In: Mandell GL,
Bennett JE, Dolin R, editors. Principles and practice of infectious diseases, 5th edition.
Philadelphia: Churchill Livingstone; 2000. p. 90317.
[37] Calderwood SB, Swinski LA, Karchmer AW, Waternaux CM, Buckley MJ. Prosthetic
valve endocarditis: analysis of factors aecting outcome of therapy. J Thorac Cardiovasc
Surg 1986;92:77683.
[38] Dworkin RJ, Sande MA, Lee BL, Chambers HF. Treatment of right-sided Staphylococcus
aureus endocarditis in intravenous drug users with ciprooxacin and rifampin. Lancet
1989;ii:10713.
[39] Tornos P, Sanz E, Permanyer-Miralda G, Almirante B, Planes AM, Soler-Soler J. Late
prosthetic valve endocarditis: immediate and long-term prognosis. Chest 1992;101:3741.
502
[40] Archer GL, Karchmer AW, Vishniavsky N, Johnston JL. Plasmid-pattern analysis for the
dierentiation of infecting from noninfecting Staphylococcus epidermidis. J Infect Dis
1984;149:91320.
[41] Van Wijngaerden E, Peetermans WE, Van Lierde S, Van Eldere J. Polyclonal staphylococcus endocarditis. Clin Infect Dis 1997;25:6971.
[42] Bayer AS, Bolger AF, Taubert KA, et al. Diagnosis and management of infective endocarditis and its complications. Circulation 1998;98:293648.
[43] Khandheria BK. Transesophageal echocardiography in the evaluation of prosthetic
valves. Am J Cardiac Imag 1995;9:10614.
[44] Stewart WJ, Shan K. The diagnosis of prosthetic valve endocarditis by echocardiography.
Sem Thorac Cardiovasc Surg 1995;7:712.
[45] Daniel WG, Mugge A, Grote J, et al. Comparison of transthoracic and transesophageal
echocardiography for detection of abnormalities of prosthetic and bioprosthetic valves in
the mitral and aortic positions. Am J Cardiol 1993;71:2105.
[46] Morguet AJ, Werner GS, Andreas S, Kreuzer H. Diagnostic value of transesophageal
compared with transthoracic echocardiography in suspected prosthetic valve endocarditis.
Herz 1995;20:3908.
[47] Vered Z, Mossinson D, Peleg E, Kaplinsky E, Motro M, Beker B. Echocardiographic
assessment of prosthetic valve endocarditis. Eur Heart J 1995;16(Suppl B):637.
[48] Daniel WG, Mugge A, Martin RP, et al. Improvement in the diagnosis of abscesses associated with endocarditis by transesophageal echocardiography. N Engl J Med 1991;324:
795800.
[49] Sochowski RA, Chan KL. Implication of negative results on a monoplane transesophageal echocardiographic study in patients with suspected infective endocarditis. J Am Coll
Cardiol 1993;21:21621.
[50] Durack DT, Lukes AS, Bright DK. New criteria for diagnosis of infective endocarditis:
utilization of specic echocardiographic ndings. Am J Med 1994;96:2009.
[51] John MVD, Hibberd PL, Karchmer AW, Sleeper LA, Calderwood SB. Staphylococcus
aureus prosthetic valve endocarditis: optimal management and risk factors for death. Clin
Infect Dis 1998;26:13029.
[52] Nettles RE, McCarty DE, Corey RG, Li J, Sexton DJ. An evaluation of the Duke criteria
in 25 pathologically conrmed cases of prosthetic valve endocarditis. Clin Infect Dis
1997;25:14013.
[53] Perez-Vazquez A, Farinas MC, Garcia-Palomo JD, Bernal JM, Revuelta JM, GonzalezMacias J. Evaluation of the Duke criteria in 93 episodes of prosthetic valve endocarditis:
could sensitivity be improved? Arch Intern Med 2000;160:118591.
[54] Roe MT, Abramson MA, Li J, et al. Clinical information determines the impact of
transesophageal echocardiography on the diagnosis of infective endocarditis by the Duke
criteria. Am Heart J 2000;139:94551.
[55] Wilson WR, Karchmer AW, Bisno AL, et al. Antibiotic treatment of adults with infective
endocarditis due to viridans streptococci, enterococci, other streptococci, staphylococci,
and HACEK microorganisms. JAMA 1995;274:170613.
[56] Archer GL, Johnston JL, Vazquez GJ, Haywood Iii HB. Ecacy of antibiotic
combinations including rifampin against methicillin-resistant Staphylococcus epidermidis:
in vitro and in vivo studies. Rev Infect Dis 1983;5(Suppl 3):S53842.
[57] Chuard C, Herrmann M, Vaudaux P, Waldvogel FA, Lew DP. Successful therapy of
experimental chronic foreign-body infection due to methicillin-resistant Staphylococcus
aureus by antimicrobial combinations. Antimicrob Agents Chemother 1991;35:26116.
[58] Kobasa WD, Kaye KL, Shapiro T, Kaye D. Therapy for experimental endocarditis due to
Staphylococcus epidermidis. Rev Infect Dis. 1983;5(Suppl 3):S5337.
[59] Lucet JC, Herrmann M, Rohner P, Auckenthaler R, Waldvogel FA, Lew DP. Treatment
of experimental foreign body infection caused by methicillin-resistant Staphylococcus
aureus. Antimicrob Agents Chemother 1990;34:23127.
503
[60] Rouse MS, Wilcox RM, Henry NK, Steckelberg JM, Wilson WR. Ciprooxacin therapy
of experimental endocarditis caused by methicillin-resistant Staphylococcus epidermidis.
Antimicrob Agents Chemother 1990;34:2736.
[61] Nguyen MH, Nguyen ML, Yu VL, McMahon D, Keys TF, Amidi M. Candida prosthetic
valve endocarditis: prospective study of six cases and review of the literature. Clin Infect
Dis 1996;22:2627.
[62] Karchmer AW, Dismukes WE, Buckley MJ, Austen WG. Late prosthetic valve endocarditis: clinical features inuencing therapy. Am J Med 1978;64:199206.
[63] Yu VL, Fang GD, Keys TF, et al. Prosthetic valve endocarditis: superiority of surgical
valve replacement versus medical therapy only. Ann Thorac Surg 1994;58:10737.
[64] Sae JR, Gardner P, Schoenbaum SC, Wild W. Prosthetic valve endocarditis: the case for
prompt valve replacement. J Thorac Cardiovasc Surg 1977;73:41620.
[65] Tornos P, Almirante B, Olona M, et al. Clinical outcome and long-term prognosis of late
prosthetic valve endocarditis: a 20-year experience. Clin Infect Dis 1997;24:3816.
[66] Horstkotte D, Bircks W, Loogen F. Infective endocarditis of native and prosthetic
valvesthe case for prompt surgical intervention? A retrospective analysis of factors
aecting survival. Z Kardiol 1986;75(Suppl 2):16882.
[67] Boyd AD, Spencer FC, Isom OW, et al. Infective endocarditis: an analysis of 54 surgically
treated patients. J Thorac Cardiovasc Surg 1977;73:2330.
[68] Reinhartz O, Herrmann M, Redling F, Zerkowski HR. Timing of surgery in patients with
acute infective endocarditis. J Cardiovasc Surg 1996;37:397400.
[69] dUdekem Y, David TE, Feindel CM, Armstrong S, Sun Z. Long-term results of operation for paravalvular abscess. Ann Thorac Surg 1996;62:4853.
[70] Jault F, Gandjbakheh I, Chastre JC, et al. Prosthetic valve endocarditis with ring
abscesses: surgical management and long-term results. J Thorac Cardiovasc Surg 1993;
105:110613.
[71] Anwar H, Strap JL, Costerton JW. Establishment of aging biolms: possible mechanism
of bacterial resistance to antimicrobial therapy. Antimicrob Agents Chemother 1992;36:
134751.
[72] Roder BL, Wandall DA, Espersen F, Frimodt-Moller N, Skinhoj P, Rosdahl VT. A study
of 47 bacteremic Staphylococcus aureus endocarditis cases: 23 with native valves treated
surgically and 24 with prosthetic valves. Scand Cardiovasc J 1997;31:3059.
[73] Wol M, Witchitz S, Chastang C, Regnier B, Vachon F. Prosthetic valve endocarditis in
the ICU: prognostic factors of overall survival in a series of 122 cases and consequences
for treatment decision. Chest 1995;108:68894.
[74] Sett SS, Hudon MPJ, Jamieson WRE, Chow AW. Prosthetic valve endocarditis:
experience with porcine bioprostheses. J Thorac Cardiovasc Surg 1993;105:42834.
[75] Aragam JR, Weyman AE. Echocardiographic ndings in infective endocarditis. In:
Weyman AE, editor. Principles and practice of echocardiography. Philadelphia (PA): Lea
& Febiger; 1994. p. 117897.
[76] David TE. The surgical treatment of patients with prosthetic valve endocarditis. Sem
Thorac Cardiovasc Surg. 1995;7:4753.
[77] Dossche KM, Defauw JJ, Ernst SM, Craenen TW, DeJongh BM, de la Riviere AB.
Allograft aortic root replacement in prosthetic aortic valve endocarditis: a review of 32
patients. Ann Thorac Surg 1997;63:16449.
[78] Glazier JJ, Verwilghen J, Donaldson RM, Ross DN. Treatment of complicated prosthetic
aortic valve endocarditis with annular abscess formation by homograft aortic root
replacement. J Am Coll Cardiol 1991;17:117782.
[79] Pansini S, di Summa M, Patane F, Forsennati PG, Serra M, Del Ponte S. Risk of recurrence after reoperation for prosthetic valve endocarditis. J Heart Valve Dis 1997;6:
847.
[80] Davenport J, Hart RG. Prosthetic valve endocarditis 19761987: antibiotics, anticoagulation, and stroke. Stroke 1990;21:9939.
504
[81] Delahaye JP, Poncet PH, Malquarti V, Beaune J, Gare JP, Mann JM. Cerebrovascular
accidents in infective endocarditis: role of anticoagulation. Eur Heart J 1990;11:10748.
[82] Horskotte D, Piper C, Niehues R, Wiemer M, Schultheiss HP. Late prosthetic valve endocarditis. Eur Heart J 1995;16(Suppl B):3947.
[83] Leport C, Vilde JL, Bricaire F, et al. Fifty cases of late prosthetic valve endocarditis:
improvement in prognosis over a 15 year period. Br Heart J 1987;58:6671.
[84] Wilson WR, Geraci JE, Danielson GK, et al. Anticoagulant therapy and central nervous
system complications in patients with prosthetic valve endocarditis. Circulation 1978;57:
10047.
[85] Chua JD, Wilko BL, Lee I, Juratli N, Longworth DL, Gordon SM. Diagnosis and
management of infections involving implantable electrophysiologic cardiac devices. Ann
Int Med 2000;133:6048.
[86] Frame R, Brodman RF, Furman S, Andrews CA, Gross JN. Surgical removal of infected
transvenous pacemaker leads. Pacing Clin Electrophysiol 1993;16:23438.
[87] Kearney RA, Eisen HJ, Wolf JE. Nonvalvular infections of the cardiovascular system.
Ann Int Med 1994;121:21930.
[88] Lai KK, Fontecchio SA. Infections associated with implantable cardioverter-debrillators
placed transvenously and via thoracotomies: epidemiology, infection control, and
management. Clin Infect Dis 1998;27:2659.
[89] Smith PN, Vidaillet HJ, Hayes JJ. Infections with non-thoracotomy implantable
cardioverter-debrillators: can these be prevented? Pacing Clin Electrophysiol 1998;21:
4255.
[90] Bryan CS, Sutton JP, Saunders DE Jr., Longaker DW, Smith CW. Endocarditis related to
transvenous pacemakers. Syndromes and surgical implications. J Thorac Cardiovasc Surg
1978;75:75862.
[91] Trappe HJ, Ptzner P, Klein H. Infections after cardioverter-debrillator implantation:
observations in 335 patients over 10 years. Br Heart J 1995;73:204.
[92] Bluhm G. Pacemaker infections: a clinical study with special reference to prophylactic use
of some isoxaazoyl penicillins. Acta Med Scand 1985;699:162.
[93] Camus C, Leport C, Ra F, Michelet C, Cartier F, Vilde JL. Sustained bacteremia in 26
patients with a permanent endocardial pacemaker: assessment of wire removal. Clin Infect
Dis 1993;17:4655.
[94] Chamis AL, Peterson GE, Cabell CH, et al. Staphylococcus aureus bacteremia in patients
with permanent pacemakers or implantable cardioverter-debrillators. Circulation 2001;104:
102933.
[95] Beeler BA. Infections of permanent transvenous epicardial pacemakers in adults. Heart
Lung 1982;11:1526.
[96] Lewis AB, Hayes DL, Holmes DR Jr, Vliestra RE, Pluth JR, Osborn MJ. Update on
infections involving permanent pacemakers: characterization and management. J Thorac
Cardiovasc Surg 1985;89:75863.
[97] Borbola J, Denes P, Ezri MD, Hauser RD, Serry C, Goldin MD. The automatic
implantable cardioverter-debrillator. Clinical experience, complications, and follow-up
in 25 patients. Arch Intern Med 1988;148:706.
[98] Spratt KA, Blumberg EA, Wood CA, Kutalek SP, Reboli AC. Infections of implantable
cardioverter debrillators: approach to management. Clin Infect Dis 1993;17:67985.
[99] Arber N, Pras E, Copperman Y, et al. Pacemaker endocarditis: report of 44 cases and
review of the literature. Medicine (Baltimore) 1994;73:299305.
[100] Cacoub P, Leprince P, Nataf P, et al. Pacemaker infective endocarditis. Am J Cardiol
1998;82:4804.
[101] Klug D, Lacroix D, Savoye C, et al. Systemic infection related to endocarditis on
pacemaker leads: clinical presentation and management. Circulation 1997;95:2098107.
[102] Molina JE. Undertreatment and overtreatment of patients with infected antiarrhythmic
implantable devices. Ann Thorac Surg 1997;63:5049.
505
[103] ONunain S, Perez I, Roelke M, et al. The treatment of patients with infected implantable
cardioverter-debrillator systems. J Thorac Cardiovasc Surg 1997;113:1219.
[104] Samuels LE, Samuels FL, Kaufman MS, Morris RJ, Brockman SK. Management of
infected implantable cardiac debrillators. Ann Thorac Surg 1997;64:17026.
[105] Victor F, DePlace C, Camus C, et al. Pacemaker lead infection: echocardiographic
features, management and outcome. Heart 1999;81:827.
[106] Amin M, Gross J, Andrews C, Furman S. Pacemaker infection with Mycobacterium avium
complex. Pacing Clin Electrophysiol 1991;14:1524.
[107] Cohen T, Pons V, Schwartz J, Grin J. Candida albicans pacemaker site infections.
Pacing Clin Electrophysiol 1991;14:1468.
[108] Kramer L, Rojas-Corona RR, She D, Eisenberg ES. Disseminated aspergillosis and
pacemaker endocarditis. Pacing Clin Electrophysiol 1985;8:2259.
[109] Turkisher V, Priel I, Dan M. Successful management of an infected implantable cardioverter debrillator with oral antibiotics and without removal of the device. Pacing Clin
Electrophysiol 1997;20:226870.
[110] Lee JH, Geha AS, Rattehalli NM, et al. Salvage of infected ICDs: management without
removal. Pacing Clin Electrophysiol 1996;19:43742.
[111] Wilko BL, Byrd CL, Love CJ, et al. Pacemaker lead extraction with the laser sheath:
results of the pacing lead extraction with the excimer sheath (PLEXES) trial. J Am Coll
Cardiol 1999;33:16716.
[112] Byrd C. Management of implant complications. In: Ellenbogen K, Kay G, Wilko BL,
editors. Clinical cardiac pacing. Philadelphia (PA): W.B. Saunders; 2000. p. 66994.
[113] Rose EA, Geligns AC, Moskowitz AJ, et al. Long-term use of a left-ventricular assist
device for end-stage heart failure. New Engl J Med 2001;345:143543.
[114] De Jonge KC, Laube HR, Dohmen PM, et al. Diagnosis and management of left
ventricular assist device valve-endocarditis: LVAD valve replacement. Ann Thorac Surg
2000;70:14045.

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Infect Dis Clin N Am 16 (2002) 477505

Infections of intracardiac devices

Division of Infectious Diseases, Beth Israel Deaconess Medical Center,

Prosthetic cardiac valves, pacemakers, and implanted debrillators are

Prosthetic valve endocarditis

A.W. Karchmer, D.L. Longworth / Infect Dis Clin N Am 16 (2002) 477505

Study (years valves

Initial number valve

Rutledge et al. (195681) [6]

Aortic position only.

A.W. Karchmer, D.L. Longworth / Infect Dis Clin N Am 16 (2002) 477505

A.W. Karchmer, D.L. Longworth / Infect Dis Clin N Am 16 (2002) 477505

A.W. Karchmer, D.L. Longworth / Infect Dis Clin N Am 16 (2002) 477505

A.W. Karchmer, D.L. Longworth / Infect Dis Clin N Am 16 (2002) 477505

positive in patients with PVE caused by Candida spp or C. neoformans,

A.W. Karchmer, D.L. Longworth / Infect Dis Clin N Am 16 (2002) 477505

congestive heart failure, persistent fever in spite of optimal antimicrobial

A.W. Karchmer, D.L. Longworth / Infect Dis Clin N Am 16 (2002) 477505

Prosthesis type and position

Aortic position (34)

Patients had pathoanatomic or clinically conrmed (Von Reyn criteria) PVE.

administration of antibiotics, and full echocardiographic assessment. The

A.W. Karchmer, D.L. Longworth / Infect Dis Clin N Am 16 (2002) 477505

infected prosthetic valve should be treated empirically immediately after

3. Enterococci (in vitro

1824 million units IV

2430 million units IV

2430 million units IV

Dose and routea

Streptomycin can be used instead

Preferred for nutritionally variant

Can be used in patients

May omit aminoglycoside

(continued on next page)

Cefotaxime or other third generation

Use gentamicin during the initial two

Penicillin 1824 million units daily in divided

Use for patients with penicillin allergy.

A.W. Karchmer, D.L. Longworth / Infect Dis Clin N Am 16 (2002) 477505

1824 million units IV

Dose and Routea

Use if organism resistant

Bactericidal synergy results if isolate

A.W. Karchmer, D.L. Longworth / Infect Dis Clin N Am 16 (2002) 477505

For fungal PVE, amphotericin B (0.7 to 1.0 mg/kg/d) is recommended;

A.W. Karchmer, D.L. Longworth / Infect Dis Clin N Am 16 (2002) 477505

Indications for cardiac surgery in patients with PVEa

postoperative mortality is proportional to the severity of hemodynamic

A.W. Karchmer, D.L. Longworth / Infect Dis Clin N Am 16 (2002) 477505

A.W. Karchmer, D.L. Longworth / Infect Dis Clin N Am 16 (2002) 477505

rifampin accelerates the hepatic clearance of warfarin, patients being treated

Infections involving implantable electrophysiologic cardiac devices

A.W. Karchmer, D.L. Longworth / Infect Dis Clin N Am 16 (2002) 477505

electrodes in the venous system or right atrium (Fig. 2) [90]. Myocardial

A.W. Karchmer, D.L. Longworth / Infect Dis Clin N Am 16 (2002) 477505

Fig. 2. Implantable cardioverterdebrillator lead with a large, attached, infected vegetation.

Epidemiology and risk factors

A.W. Karchmer, D.L. Longworth / Infect Dis Clin N Am 16 (2002) 477505

surgeons [88]. In recent years, electrophysiologic studies have been followed

A.W. Karchmer, D.L. Longworth / Infect Dis Clin N Am 16 (2002) 477505

Includes pacemakers (87) and cardioverter debrillators (36).

A.W. Karchmer, D.L. Longworth / Infect Dis Clin N Am 16 (2002) 477505