Download Risk Factors for Mortality in Patients With Cardiac Device

Risk Factors for Mortality in Patients With Cardiac
Device-Related Infection
Timir S. Baman, MD; Sanjaya K. Gupta, MD; Javier A. Valle, MD; Elina Yamada, MD, FACC, FASE
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Background—Because of the increased use of pacemakers and implantable cardioverter defibrillators, infection has
become a complication with significant morbidity and mortality. Data on risk factors for mortality in patients with
cardiac-device related infection are limited. We evaluated the prognostic significance of key clinical and echocardiographic variables in a large retrospective population of patients with cardiac-device related infection.
Methods and Results—Two hundred ten patients with cardiac-device related infection were identified at the University of
Michigan between 1995 and 2006. Data were abstracted on key clinical and echocardiographic variables, treatment
strategy, and 6-month outcomes. We used multivariable Cox proportional hazards models to examine clinical and
echocardiographic variables that were associated with 6-month mortality. Mean age for our study population was 63⫾17
years, and 72 (44%) were women. All-cause 6-month mortality was 18% (n⫽37). Independent variables associated with
death were systemic embolization (hazard ratio 7.11; 95% CI 2.74 to 18.48), moderate or severe tricuspid regurgitation
(hazard ratio 4.24; 95% CI 1.84 to 9.75), abnormal right ventricular function (hazard ratio 3.59; 95% CI 1.57 to 8.24),
and abnormal renal function (hazard ratio 2.98; 95% CI 1.17 to 7.59). Size and mobility of cardiac device vegetations
were not independently associated with mortality.
Conclusions—We identified several clinical and echocardiographic variables that identify patients with cardiac-device
related infection who are at high-risk for mortality and may benefit from more aggressive evaluation. (Circ Arrhythmia
Electrophysiol. 2009;2:129-134.)
Key Words: infection 䡲 risk factors 䡲 mortality 䡲 outcome assessment
I
mplantation of electrophysiological cardiac devices such as
pacemakers and implantable cardioverter defibrillators
(ICDs) has become a widely available and routine procedure
in cardiovascular medicine. Numerous trials have shown that
pacemakers,1 biventricular pacemakers,2–3 and ICDs4 –7 decrease mortality and improve quality of life. A growing list of
indications, in conjunction with an aging population, projects
that even a greater number of patients will acquire such
devices in the future.
Methods
A retrospective chart review was conducted after identifying all
hospitalized patients with a discharge diagnosis of pacemaker or ICD
infection (International Classification of Diseases-9th RevisionClinical Modification [ICD-9-CM] code 996.61) at the University of
Michigan between 1995 and 2006. To ensure our search for these
patients was as exhaustive as possible, we also screened the medical
records of any patients with device explantation (ICD-9-CM codes
37.77, 37.79, 37.89, or 37.99) and a discharge diagnosis of sepsis
(ICD-9-CM code 038 or 785.59), bacteremia (ICD-9-CM code 790.7),
endocarditis (ICD-9-CM codes 421.0, 421.9, or 424.90), cellulitis
(ICD-9-CM code 682.9), or fever (ICD-9-CM code 780.6) to identify
additional cases. A total of 1163 patients were identified through this
database search with 210 noted as having CDI. The Institutional Review
Board of the University of Michigan approved this study.
Demographic, clinical, and echocardiographic data were collected
from the University of Michigan electronic medical record. The
demographic information consisted of age, gender, and length of
hospital stay. Clinical variables of interest included evidence of local
infection at the generator site, bacteremia, microbiological information, presence of diabetes, coronary artery disease, coronary artery
bypass surgery, hypertension, presence of HIV, steroid use, presence
of central line, renal dysfunction, pulmonary embolism, and systemic
embolization. Information on the type, age, and location of device
was also collected. Echocardiographic variables included presence
and description of vegetations, left and right ventricular (RV)
function, valvular endocarditis, valvular regurgitation, and estimation of pulmonary artery pressure via RV systolic pressure.
Clinical Perspective see p 134
One of the most feared complications of device placement
is infection, which can be associated with substantial morbidity and mortality. Infection rates for these devices reportedly vary from 0.7% to 7.0%8 –12 with a resultant 3.1-fold
increase in the number of associated hospitalizations in recent
years.13 Mortality rates attributable to infection have ranged
from 2.6% to 3.3%.14 –15 Although recent reports have identified several clinical characteristics associated with developing cardiac device-related infection (CDI), there are limited
data on outcomes after treatment. The purpose of the present
study was to determine risk factors associated with mortality
in a large study population of patients with CDI.
Received August 22, 2008; accepted January 7, 2009.
From the Department of Cardiology, University of Michigan, Ann Arbor.
Correspondence to Elina Yamada, MD, FACC, FASE, Department of Internal Medicine, Cardiovascular Center 2144, 1500 East Medical Center Dr.
SPC 5853, Ann Arbor, MI 48109-5853. E-mail [email protected]
© 2009 American Heart Association, Inc.
Circ Arrhythmia Electrophysiol is available at http://circep.ahajournals.org
129
DOI: 10.1161/CIRCEP.108.816868
130
Circ Arrhythmia Electrophysiol
Table 1.
April 2009
Unadjusted Hazard Ratios for 6-Month Mortality Associated With Age, Sex, and Treatment Group
Total (n⫽210)
Survived (n⫽173)
Died (n⫽37)
HR
95% CI
P Value
Age, y
63⫾17
61⫾17
71⫾11
1.04
1.01–1.06
ⱕ0.01
Male gender
138 (66)
112 (65)
26 (70)
1.56
2.91–3.45
0.28
Treatment option
Medical management
Percutaneous device removal
Cardiac surgical removal
23 (11)
15 (9)
8 (22)
1.00
...
170 (81)
142 (82)
28 (76)
0.44
0.20–0.96
(reference)
0.04
17 (8)
16 (9)
1 (3)
0.15
0.02–1.19
0.07
Values are n (%) or mean⫾SD.
Definitions
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CDI has been previously defined by other groups.12,16 The Duke
criteria17 for the diagnosis of endocarditis were applied to systemic
infections related to cardiac devices. Clinical evidence of pacemaker/
ICD infection included local signs of inflammation at the generator
site such as erythema, warmth, fluctuance, wound dehiscence, erosion,
tenderness, or purulent drainage. Device related endocarditis was
clinically confirmed if valvular or lead vegetations were detected by
echocardiography or if the Duke criteria for infective endocarditis were
met.18 The diagnosis of systemic embolization including cerebral, renal,
or spinal embolic infarction was based on high clinical suspicion as well
as data derived from diagnostic procedures.
Echocardiography
An experienced echocardiographer independently reviewed all the
transthoracic and transesophageal echocardiography studies without
knowledge of the patient’s clinical history or subsequent clinical
course. Vegetation was defined as a fixed or oscillating echodensity
adherent to a lead, valve leaflet, or other cardiac structure with
independent motion. The lesion had to be visible in multiple views.
The measurement of the vegetation was obtained in different planes
and the maximal length was used. In the presence of multiple
vegetations, the largest diameter was included in the analysis. The
mobility of the vegetation was evaluated using a 4-point scale
adopted from valvular endocarditis analysis: absent⫽fixed vegetation with no detectable independent motion; low⫽vegetation with a
fixed base but with a mobile free edge; moderate⫽pedunculated
vegetation that remains within the same chamber throughout the
cardiac cycle; severe⫽prolapsing vegetation that crosses the coaptation plane of the leaflets during the cardiac cycle.19 Severity of
valvular regurgitation was assessed using the standard guideline recommendations from the American Society of Echocardiography.20
End Points
The primary end point was death from all causes at 6 months. Death
status was ascertained in all patients by querying medical records and
the Social Security Death Index. Cause of mortality was determined
by review of medical record or through the National Death Index.21,22 For each patient submitted to the National Death Index a
social security number, date of birth, first and last names, and sex
were given to generate a true match.
A secondary end point of pulmonary embolism confirmed by
diagnostic imaging during hospitalization was also used.
Statistical Analysis
Continuous variables were expressed as mean⫾SD, and categorical
variables were expressed as frequencies. Six-month survival was
estimated by Kaplan–Meier method using size of lead vegetations as
a potential predictor of death. Clinical and echocardiographic variables were tested as independent predictors of 6-month all-cause
mortality using Cox proportional hazards analysis after controlling
for age, sex, and treatment method (surgical removal versus percutaneous removal versus medical management). Variables significantly associated with 6-month mortality were included as candidate
predictors in a multivariable analysis using Cox proportional hazards
model with stepwise forward regression (entry criterion Pⱕ0.10).
Age, sex, and treatment method were adjusted for in all statistical
analyses.
For the secondary end point of pulmonary embolism during
hospitalization, logistic regression analysis was performed using the
echocardiographic predictors of vegetation size and mobility as
previously defined. Variables were considered statistically significant at P⬍0.05. All analyses were performed using SPSS for
Windows (SPSS Inc, release 16.0). The authors had full access to the
data and take responsibility for its integrity. All authors have read
and agree to the manuscript as written.
Results
During the study period, 210 patients met criteria for CDI.
One hundred fifty-four patients underwent device implantation at an institution other than the University of Michigan
and were referred for further evaluation. Most patients had an
infected pacemaker (60%) followed by ICD (33%) and biventricular pacemaker (7%). Evidence of a generator pocket
infection was seen in 65%, whereas 34% displayed only
evidence of systemic infection. Pocket infection with concurrent systemic infection was noted in 20% of patients. The
mean length of hospital stay was 15 days, in-hospital mortality was 8%, and 6-month mortality was 18%.
Mean⫾SD age was 63⫾17 years (range, 20 to 93 years)
with 44% women in the study cohort. One hundred seventy
patients (81%) had percutaneous removal as opposed to 17
patients (8%) undergoing cardiac surgery. Twenty-three patients (11%) underwent medical management with retention
of infected hardware. One hundred eight patients (51%) had
evidence of positive blood cultures during admission,
whereas Staphylococcus aureus (S. aureus) was the leading
cause of systemic device infection (n⫽62). Of those in the S.
aureus group, 55% of cultures were found to be resistant to
methicillin. Twenty patients (10%) had blood cultures positive for coagulase-negative staphylococci.
Outcomes
Six-month all-cause mortality in our study was 18% (n⫽37).
Of this group, 17 patients had in-hospital mortality with
major causes of death including sepsis (76%) and cardiac
arrest (26%). With regards to all-cause 6-month mortality,
73% (n⫽27) were secondary to cardiovascular causes. Failure to thrive or hospice care accounted for 14% (n⫽5) of
deaths. Noncardiovascular causes of mortality accounted for
the remaining 14% (n⫽5).
Univariable Predictors of 6-Month Mortality
Table 1 shows unadjusted hazard ratios for 6-month mortality
using the clinical characteristics of age, sex, and treatment
Baman et al
Factors for Mortality in Device Infection
Table 2. Adjusted Hazard Ratios for 6-Month Mortality Associated With Patient Characteristics and Controlling for Age,
Sex, and Treatment Group
Total (n⫽210)
Survived (n⫽173)
Died (n⫽37)
HR
95% CI
P Value
Type of device
Pacemaker
126 (60)
103 (60)
23 (62)
1.00
ICD
69 (33)
59 (34)
10 (27)
0.93
0.47–2.41
(reference)
0.88
Biventricular PM/ICD
15 (7)
10 (6)
5 (14)
1.53
0.56–5.44
0.47
Previous device upgrade/replacement
38 (18)
34 (20)
4 (11)
1.37
0.48–3.94
0.56
57 (27)
45 (26)
12 (32)
1.59
0.78–3.22
0.20
110 (52)
83 (48)
27 (73)
2.12
1.10–5.00
0.07
Clinical variables
Diabetes
Coronary artery disease
CABG
Hypertension
Abnormal creatinine ⬎1.5 mg/dl
51 (24)
42 (24)
9 (24)
0.81
0.37–1.74
0.58
137 (65)
106 (61)
31 (84)
2.20
0.90–5.36
0.08
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99 (47)
70 (40)
29 (78)
3.99
1.71–9.30
ⱕ0.01
Positive blood culture
108 (51)
77 (45)
31 (84)
6.05
2.30–15.97
ⱕ0.01
Positive device culture
147 (70)
120 (69)
27 (73)
1.52
0.62–3.75
0.37
48 (23)
37 (21)
11 (30)
1.47
0.69–3.15
0.32
Echocardiographic variables
Lead vegetation visualized
Lead vegetation size
Absent/not obtained
168 (80)
139 (81)
29 (78)
1.00
...
1–10 mm
10 (5)
9 (5)
1 (3)
0.84
0.11–6.21
(reference)
0.86
11–20 mm
19 (9)
13 (8)
6 (16)
2.05
0.81–5.23
0.13
ⱖ21 mm
13 (6)
11 (6)
2 (5)
1.03
0.23–4.73
0.97
Lead vegetation mobility
Absent/not obtained
169 (80)
139 (80)
30 (81)
1.00
...
Low
16 (8)
12 (7)
4 (11)
1.65
0.56–4.83
(reference)
0.36
Moderate
13 (6)
12 (7)
1 (3)
0.37
0.05–2.74
0.33
Severe
12 (6)
9 (5)
3 (8)
2.04
0.54–7.67
0.29
Left ventricular dysfunction
Normal
93 (44)
79 (46)
14 (38)
1.00
...
Mild
14 (7)
13 (8)
1 (3)
0.43
0.06–3.33
(reference)
Moderate
22 (10)
17 (10)
5 (14)
1.33
0.47–3.77
0.59
Severe
42 (20)
30 (17)
12 (32)
1.68
0.75–3.74
0.21
Abnormal right ventricular function
35 (17)
22 (13)
13 (35)
4.22
1.91–9.29
ⱕ0.01
Moderate to severe tricuspid regurgitation
20 (10)
9 (5)
11 (30)
5.93
2.73–12.89
ⱕ0.01
RVSP not obtained
69 (33)
60 (35)
9 (24)
1.00
...
(reference)
10–39 mm Hg
52 (25)
46 (27)
6 (16)
0.74
0.26–2.09
0.57
40–59 mm Hg
35 (17)
23 (13)
12 (32)
2.19
0.88–5.44
0.09
ⱖ60 mm Hg
0.42
Right ventricular systolic pressure (RVSP)
15 (7)
9 (5)
6 (16)
4.40
1.48–13.02
0.01
Aortic stenosis
7 (3)
5 (3)
2 (5)
0.86
0.45–1.63
0.63
Aortic insufficiency
9 (4)
7 (4)
2 (5)
1.07
0.56–2.02
0.85
31 (15)
19 (11)
12 (32)
1.61
1.12–2.31
ⱕ0.01
Aortic
9 (4)
7 (4)
2 (5)
1.21
0.12–7.02
0.81
Mitral
6 (3)
5 (3)
1 (3)
1.08
0.09–13.36
0.94
Moderate to severe mitral regurgitation
Prosthetic valve
Clinical events
Pulmonary embolism
9 (4)
5 (3)
4 (11)
3.76
1.25–11.30
0.02
Systemic embolization
23 (11)
10 (6)
13 (35)
9.02
3.95–20.57
ⱕ0.01
PM indicates pacemaker; CABG, coronary artery bypass graft; RVSP, right ventricular systolic pressure.
Values are n (%) or mean⫾SD.
131
132
Circ Arrhythmia Electrophysiol
April 2009
Table 3. Independent Variables Associated With
6-Month Mortality*
HR
95% CI
P Value
Systemic embolization
7.11
2.74 –18.48
ⱕ0.01
Moderate or severe tricuspid regurgitation
4.24
1.84–9.75
ⱕ0.01
Abnormal right ventricular function
3.59
1.57–8.24
ⱕ0.01
Abnormal renal function (Cr ⬎1.5 mg/dl)
2.98
1.17–7.59
0.02
*All final models controlled for age, sex, and treatment group as well as
other variables listed in the table.
Figure. Kaplan–Meier plot of survival according to size of lead
vegetation in millimeters (mm) adjusting for age, sex, and treatment strategy.
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group, with age noted to be a significant predictor of
mortality (Pⱕ0.01). Among the treatment groups, percutaneous removal was found to be significantly associated with
better survival (hazard ratio 0.44; 95% CI 0.20 to 0.96;
P⫽0.04) as compared to medical management. Table 2
shows the univariate comparisons of patients with CDI who
survived longer than 6 months versus those who did not. A
device previously upgraded or replaced had no significant
effect on mortality (P⫽0.56). Patients with evidence of renal
impairment (creatinine ⬎1.5 mg/dL) had a significantly
worse 6-month survival rate compared to patients with
normal renal function (Pⱕ0.01). Another significant clinical
predictor of poor survival was the presence of positive blood
cultures (Pⱕ0.01). Adjusting for age, sex, and treatment
strategy, methicillin-resistant S. aureus (hazard ratio 8.75, CI
3.3 to 23.0; Pⱕ0.01), methicillin-resistant Staphylococcus
epidermidis (hazard ratio 8.73, CI 2.4 to 31.4; Pⱕ0.01), and
methicillin-sensitive S. aureus (hazard ratio 6.00, CI 1.9 to
19.1; Pⱕ0.01) bacteremia were associated with increased
mortality when compared to those with negative cultures.
Transthoracic echocardiography or transesophageal echocardiography was available for review in 171 patients. The
echocardiographic findings are shown in Table 2. Lead
vegetations were detected on echocardiography in 23% of
cases. Patients with moderate or severe tricuspid regurgitation
(Pⱕ0.01), abnormal right ventricular dysfunction (Pⱕ0.01),
an RV systolic pressure ⱖ60 mm Hg (P⫽0.01), or moderate
to severe mitral regurgitation (Pⱕ0.01) were found to have
significantly worse survival as compared to those who did
not. However, lead vegetation size was not significantly
associated with decreased 6-month survival (P⫽0.50; Figure). The clinical events related to cardiac device infection
are displayed at the end of Table 2. Patients with pulmonary
embolism (n⫽9; P⫽0.02) and systemic embolization (n⫽23;
Pⱕ0.01) had significantly higher 6-month mortality.
Multivariable Predictors of Six-Month Mortality
and Pulmonary Embolism
From univariate analysis, the factors associated with an
increased 6-month mortality include age (Pⱕ0.01), presence
of positive blood culture (Pⱕ0.01), abnormal renal function
(Pⱕ0.01), moderate or severe tricuspid regurgitation (Pⱕ0.01),
abnormal RV function (Pⱕ0.01), an RV systolic pressure
ⱖ60 mm Hg (P⫽0.01), moderate to severe mitral regurgitation (Pⱕ0.01), pulmonary embolism (P⫽0.02), and systemic
embolization (Pⱕ0.01; Table 2). Including these factors in a
multivariable analysis that also adjusted for age, gender, and
treatment group, we found systemic embolization (Pⱕ0.01),
moderate or severe tricuspid regurgitation (Pⱕ0.01), abnormal RV function (Pⱕ0.01), and abnormal renal function
(P⫽0.02) to remain independently associated with worse
6-month survival (Table 3). Tricuspid regurgitation remained
an independent predictor even when abnormal RV function
was included in the model (Pⱕ0.01). The proportionality
assumption was verified for all variables in the multivariate
model by testing for interaction with time.
In our cohort of 210 patients, 9 (4%) had documentation of
pulmonary embolism. Neither lead vegetation size (P⫽0.89)
nor mobility (P⫽0.31) was found to correlate with an
increased risk for pulmonary embolism (Table 4).
Discussion
With expanding indications for cardiac device implantation,
many physicians are witnessing a rapid increase in the
incidence of infection rates. In agreement with the study
recently published by Sohail et al,16 the majority of patients
with CDI in our cohort presented with evidence of infection
limited only to the generator site. It must be reemphasized
that such a benign clinical presentation can lead to an
outcome of substantial morbidity and mortality.
Table 4. Predictors of Pulmonary Embolism (Logistic
Regression Analysis)*
Pulmonary No Pulmonary
Embolism
Embolism
(n⫽9)
(n⫽201)
OR
95% CI
P Value
1.00
...
(reference)
Lead vegetation
size
0 –10 mm
6 (67)
172 (86)
⬎10 mm
3 (33)
29 (14)
Absent to low
6 (67)
179 (89)
Moderate to
severe
3 (33)
22 (11)
0.88 0.14–5.42
0.89
Lead vegetation
mobility
1.00
...
2.38 0.45–12.48
(reference)
0.31
*All final models controlled for age, sex, and treatment group as well as
other variables listed in the table.
Baman et al
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The findings of this retrospective analysis, which spans an
11-year period, highlight the mortality accompanying CDI
(18% at 6 months) and potential risk factors associated with
increased mortality in patients with infected cardiac devices.
Importantly, readily available clinical and echocardiographic
predictors do exist and allow clinicians to stratify patients
who are at highest risk for death and may play a role in
determining treatment strategies.
Several clinical characteristics have previously been identified as predictors for initially developing CDI. The most
comprehensive study was recently published by Klug et al.12
This study identified febrile illness before implantation, use
of temporary pacing before implantation, and early reintervention as factors associated with a higher probability of
infection. Other studies have shown that long-term corticosteroid
use and the presence of more than 2 pacing leads were predictors
of a higher risk of infectivity.23 Finally Bloom et al24 established
that diabetes mellitus, renal disease, and congestive heart
failure were also associated with the occurrence of device
infection. None of these studies examined the correlation of
clinical risk factors and outcome after treatment for CDI.
Accordingly, to the best of our knowledge, this study is the
first to evaluate the association of clinical and echocardiographic risk factors with subsequent mortality after treatment.
We have shown that independent predictors of mortality in
patients with infected cardiac devices include systemic embolization, moderate to severe tricuspid regurgitation, right
ventricle dysfunction, and abnormal creatinine. Abnormal
renal function appears to be a risk factor for initial device
infection24 as well as a predictor for mortality.
Echocardiographic findings of right ventricular dysfunction, moderate to severe tricuspid regurgitation, and increased
RV systolic pressure can be associated with elevated pulmonary artery pressures and right-sided failure secondary to
pulmonary embolism.25,26 In our cohort of patients, only a
small number had clinically significant pulmonary embolism
when confirmed by appropriate testing (4%). However, a
study performed by Klug and others27 showed that the
majority of patients with pacemaker infection and concurrent
pulmonary embolism displayed no clinical symptoms. The
results of our study also raise the concern whether a larger
number of patients may have had underlying silent pulmonary embolism leading to RV dysfunction and significant
tricuspid regurgitation, which were independent factors associated with increased 6-month mortality. Consequently, one
may question whether we should be more aggressively
pursuing this diagnosis in the CDI population.
Moreover, our results show that evidence of right-sided
failure and pulmonary embolism correlate with poor survival.
When reviewing the literature regarding right-sided endocarditis and subsequent risk for mortality, Hecht et al28 as well as
other studies29 have shown that size of valvular vegetations is
associated with significant 1-year mortality. In contrast, size
and mobility of lead vegetations in our CDI population are
not independent predictors of 6-month survival (Figure) or
pulmonary embolism (Table 4). Previous data on pacemaker
infections confirm that there is no statistical difference in lead
vegetation size between patients with and without pulmonary
embolism.27 One hypothesis may be that mortality and morbid-
Factors for Mortality in Device Infection
133
ity attributable to increased embolic risk is associated with
factors such as antiphospholipid antibodies, coagulation parameters, and endothelial cell activation,30 rather than the echocardiographic characteristics of the lead vegetations themselves.
Finally, because of small sample size in the surgical and
medical management groups, we were unable to confirm
whether a particular method of treatment has an effect on
mortality. In addition, examining this impact can be challenging given the high level of selection basis in determining
treatment options.
This study has the following limitations. First, it is an
observational and retrospective analysis. Our ability to adjust for
all the critical variables associated with mortality is limited by
the documentation available in the medical records that were
abstracted. Second, our study was limited to a single large
tertiary-care center with an extensive referral base for electrophysiological services. Similar to other studies,16 our CDI
population was predominately composed of pacemakers instead
of ICDs and cardiac resynchronization devices which currently
account for the majority of device implantations. Our findings
therefore may not be generalizable to other settings or institutions. Finally, data from transesophageal echocardiographys
were available in only 63% of patients where the study was
determined to be clinically indicated. Although this may have
underestimated the true frequency of some echocardiographic
findings (such as vegetations), we had surface echocardiograms
available in the great majority of patients.
In summary, we found 4 parameters that were independent
predictors of mortality in patients with CDI: systemic embolization, moderate to severe tricuspid regurgitation, abnormal
right ventricular function, and abnormal renal function. These
findings will require confirmation in additional future studies,
but suggest that patients with CDI who are at high-risk for
death after treatment may be identified and managed with
more aggressive evaluation.
Acknowledgments
We acknowledge Brahmajee Nallamothu, MD, MPH, Myra Kim,
PhD, and Ken Guire, PhD for their review of the statistical analyses
in this study.
Disclosures
None.
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CLINICAL PERSPECTIVE
Because of the increased use of pacemakers and implantable cardioverter defibrillators in medical practice, cardiac device
infection (CDI) has become a complication with significant mortality. Although recent studies have identified clinical
characteristics for developing CDI, risk factors for mortality have yet to be determined. The purpose of the present study
was to establish risk factors associated with mortality in a large study population of 210 patients with CDI. In our cohort,
6-month all-cause mortality was 18% with major causes of death including sepsis and cardiac arrest. After adjusting for
age, sex, and treatment strategy, independent variables associated with death were systemic embolization, moderate or
severe tricuspid regurgitation, abnormal right ventricular function, and abnormal renal function. Interestingly, size and
mobility of device vegetations were not clinical predictors of increased mortality. The presence of these clinical risk factors
target patients with CDI who are at high-risk for mortality and may benefit from more aggressive evaluation.
Risk Factors for Mortality in Patients With Cardiac Device-Related Infection
Timir S. Baman, Sanjaya K. Gupta, Javier A. Valle and Elina Yamada
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Circ Arrhythm Electrophysiol. 2009;2:129-134; originally published online February 13, 2009;
doi: 10.1161/CIRCEP.108.816868
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