Published online before print February 13, 2009, doi: 10.1161/CIRCEP.108.816868
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Original Articles |
Risk Factors for Mortality in Patients With Cardiac Device-Related Infection
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 elinay{at}umich.edu
Received August 22, 2008; accepted January 7, 2009.
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Abstract |
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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.
Key Words: infection • risk factors • mortality • outcome assessment
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Introduction |
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Implantation 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.
Clinical Perspective see p 129
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.
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Methods |
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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 Revision-Clinical 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.
Definitions
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 P
0.10). 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.
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Results |
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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 group, with age noted to be a significant predictor of mortality (P0.01). 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 (P0.01). Another significant clinical predictor of poor survival was the presence of positive blood cultures (P0.01). Adjusting for age, sex, and treatment strategy, methicillin-resistant S. aureus (hazard ratio 8.75, CI 3.3 to 23.0; P0.01), methicillin-resistant Staphylococcus epidermidis (hazard ratio 8.73, CI 2.4 to 31.4; P0.01), and methicillin-sensitive S. aureus (hazard ratio 6.00, CI 1.9 to 19.1; P0.01) bacteremia were associated with increased mortality when compared to those with negative cultures.
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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 (P
0.01), abnormal right ventricular dysfunction (P0.01), an RV systolic pressure 
60 mm Hg (P=0.01), or moderate to severe mitral regurgitation (P0.01) 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; P0.01) had significantly higher 6-month mortality.
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Multivariable Predictors of Six-Month Mortality and Pulmonary Embolism
From univariate analysis, the factors associated with an increased 6-month mortality include age (P
0.01), presence of positive blood culture (P0.01), abnormal renal function (P0.01), moderate or severe tricuspid regurgitation (P0.01), abnormal RV function (P0.01), an RV systolic pressure 60 mm Hg (P=0.01), moderate to severe mitral regurgitation (P0.01), pulmonary embolism (P=0.02), and systemic embolization (P0.01; Table 2). Including these factors in a multivariable analysis that also adjusted for age, gender, and treatment group, we found systemic embolization (P0.01), moderate or severe tricuspid regurgitation (P0.01), abnormal RV function (P0.01), 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 (P0.01). The proportionality assumption was verified for all variables in the multivariate model by testing for interaction with time.
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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).
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Discussion |
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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.
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 morbidity 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.
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Acknowledgments |
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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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References |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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1. Parsonnet V, Zucker R, Gilbert L, Myers GH. Clinical use of an implantable standby pacemaker. JAMA. 1966; 196: 784–786.
2. Cleland JG, Daubert JC, Erdmann E, Freemantle N, Gras D, Kappenberger L, Tavazzi L. The effect of cardiac resynchronization on morbidity and mortality in heart failure. N Engl J Med. 2005; 352: 1539–1549.
3. Bristow MR, Saxon LA, Boehmer J, Krueger S, Kass DA, De Marco T, Carson P, DiCarlo L, DeMets D, White BG, DeVries DW, Feldman AM. Cardiac-resynchronization therapy with or without an implantable defibrillator in advanced chronic heart failure. N Engl J Med. 2004; 350: 2140–2150.
4. Moss AJ, Fadl Y, Zareba W, Cannom DS, Hall WJ. Survival benefit with an implanted defibrillator in relation to mortality risk in chronic coronary heart disease. Am J Cardiol. 2001; 88: 516–520.[CrossRef][Medline]
5. Moss AJ, Zareba W, Hall WJ, Klein H, Wilber DJ, Cannom DS, Daubert JP, Higgins SL, Brown MW, Andrews ML. Prophylactic implantation of a defibrillator in patients with myocardial infarction and reduced ejection fraction. N Engl J Med. 2002; 346: 877–883.
6. Buxton AE, Lee KL, Fisher JD, Josephson ME, Prystowsky EN, Hafley G. A randomized study of the prevention of sudden death in patients with coronary artery disease. N Engl J Med. 1999; 341: 1882–1890.
7. Bardy GH, Lee KL, Mark DB, Poole JE, Packer DL, Boineau R, Domanski M, Troutman C, Anderson J, Johnson G, McNulty SE, Clapp-Channing N, Davidson-Ray LD, Fraulo ES, Fishbein DP, Luceri RM, Ip JH. Amiodarone or an implantable cardioverter-defibrillator for congestive heart failure. N Engl J Med. 2005; 352: 225–237.
8. Frame R, Brodman RF, Furman S, Andrews CA, Gross JN. Surgical removal of infected transvenous pacemaker leads. Pacing Clin Electrophysiol. 1993; 16: 2343–2348.[CrossRef][Medline]
9. Kearney RA, Eisen HJ, Wolf JE. Nonvalvular infections of the cardiovascular system. Ann Intern Med. 1994; 121: 219–230.
10. Lai KK, Fontecchio SA. Infections associated with implantable cardioverter defibrillators placed transvenously and via thoracotomies: epidemiology, infection control, and management. Clin Infect Dis. 1998; 27: 265–269.[Medline]
11. Trappe HJ, Pfitzner P, Klein H, Wenzlaff P. Infections after cardioverter-defibrillator implantation: observations in 335 patients over 10 years. Br Heart J. 1995; 73: 20–34.
12. Klug D, Balde M, Pavin D, Hidden-Lucet F, Clementy J, Sadoul N, Rey JL, Lande G, Lazarus A, Victor J, Barnay C, Grandbastien B, Kacet S. Risk factors related to infections of implanted pacemakers and cardioverter-defibrillators: results of a large prospective study. Circulation. 2007; 116: 1349–1355.
13. Voigt A, Shalaby A, Saba S. Rising rates of cardiac rhythm management device infections in the United States: 1996 through 2003. J Am Coll Cardiol. 2006; 48: 590–591.
14. Catanchin A, Murdock CJ, Athan E. Pacemaker infections: a 10-year experience. Heart Lung Circ. 2007; 16: 434–439.[CrossRef][Medline]
15. Villamil Cajoto I, Rodríguez Framil M, Van den Eynde Collado A, José Villacián Vicedo M, Canedo Romero C. Permanent transvenous pacemaker infections: an analysis of 59 cases. Eur J Intern Med. 2007; 18: 484–488.[CrossRef][Medline]
16. Sohail MR, Uslan DZ, Khan AH, Friedman PA, Hayes DL, Wilson WR, Steckelberg JM, Stoner S, Baddour LM. Management and outcome of permanent pacemaker and implantable cardioverter-defibrillator infections. J Am Coll Cardiol. 2007; 49: 1851–1859.
17. Durack DT, Lukes AS, Bright DK. New criteria for diagnosis of infective endocarditis: utilization of specific echocardiographic findings. Am J Med. 1994; 96: 200–219.[CrossRef][Medline]
18. Uslan DZ, Sohail MR, Friedman PA, Hayes DL, Wilson WR, Steckelberg JM, Baddour LM. Frequency of permanent pacemaker or implantable cardioverter-defibrillator infection in patients with gram-negative bacteremia. Clin Infect Dis. 2006; 43: 731–736.[CrossRef][Medline]
19. Vilacosta I, Graupner C, San Román JA, Sarriá C, Ronderos R, Fernández C, Mancini L, Sanz O, Sanmartín JV, Stoermann W. Risk of embolization after institution of antibiotic therapy for infective endocarditis. J Am Coll Cardiol. 2002; 39: 1489–1495.
20. Zoghbi WA, Enriquez-Sarano M, Foster E, Grayburn PA, Kraft CD, Levine RA, Nihoyannopoulos P, Otto CM, Quinones MA, Rakowski H, Stewart WJ, Waggoner A, Weissman NJ; American Society of Echocardiography. Recommendations for evaluation of the severity of native valvular regurgitation with two-dimensional and Doppler echocardiography. J Am Soc Echocardiogr. 2003; 16: 777–802.[CrossRef][Medline]
21. National Death Index User’s Manual. Hyattsville, MD: Department of Vital Statistics, Centers for Disease Control; 2003.
22. Calle EE, Terrell DD. Utility of the National Death Index for ascertainment of mortality among cancer prevention study II participants. Am J Epidemiol. 1993; 137: 235–241.
23. Sohail MR, Uslan DZ, Khan AH, Friedman PA, Hayes DL, Wilson WR, Steckelberg JM, Stoner SM, Baddour LM. Risk factor analysis of permanent pacemaker infection. Clin Infect Dis. 2007; 45: 166–173.[CrossRef][Medline]
24. Bloom H, Heeke B, Leon A, Mera F, Delurgio D, Beshai J, Langberg J. Renal insufficiency and the risk of infection from pacemaker or defibrillator surgery. Pacing Clin Electrophysiol. 2006; 29: 142–155.[CrossRef][Medline]
25. Gibson NS, Sohne M, Buller HR. Prognostic value of echocardiography and spiral computed tomography in patients with pulmonary embolism. Curr Opin Pulm Med. 2005; 11: 380–394.[CrossRef][Medline]
26. Come PC. Echocardiographic evaluation of pulmonary embolism and its response to therapeutic interventions. Chest. 1992; 101: 151S–162S.[Medline]
27. Klug D, Lacroix D, Savoye C, Goullard L, Grandmougin D, Hennequin JL, Kacet S, Lekieffre J. Systemic infection related to endocarditis on pacemaker leads. Circulation. 1997; 95: 2098–2107.
28. Hecht SR, Berger M. Right-sided endocarditis in intravenous drug users. Prognostic features in 102 episodes. Ann Intern Med. 1992; 117: 560–566.
29. Martín-Dávila P, Navas E, Fortún J, Moya JL, Cobo J, Pintado V, Quereda C, Jiménez-Mena M, Moreno S. Analysis of mortality and risk factors associated with native valve endocarditis in drug users: the importance of vegetation size. Am Heart J. 2005; 150: 1099–1106.[CrossRef][Medline]
30. Kupferwasser LI, Hafner G, Mohr-Kahaly S, Erbel R, Meyer J, Darius H. The presence of infection-related antiphospholipid antibodies in infective endocarditis determines a major risk factor for embolic events. J Am Coll Cardiol. 1999; 33: 1365–1371.
Related Article
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.
Circ Arrhythm Electrophysiol 2009 2: 129-134.
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