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Clinical Investigations: CARDIOLOGY |

The Impact of Hospital-Acquired Infections on the Microbial Etiology and Prognosis of Late-Onset Prosthetic Valve Endocarditis*

Pablo Rivas, MD; Julio Alonso, MD; Javier Moya, MD; Miguel de Górgolas, MD; Jorge Martinell, MD; Manuel L. Fernández Guerrero, MD
Author and Funding Information

*From the Division of Infectious Diseases (Drs. Rivas, Alonso, de Górgolas, and Fernández Guerrero), Department of Medicine, and the Service of Cardiac Surgery (Drs. Moya and Martinell), Fundación Jiménez Díaz., Universidad Autónoma de Madrid, Madrid, Spain.

Correspondence to: Pablo Rivas, MD, Fundación Jiménez Díaz., Avda. Reyes Católicos, 2., 28040, Madrid, Spain; e-mail: pablorivasg@hotmail.com



Chest. 2005;128(2):764-771. doi:10.1378/chest.128.2.764
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Study objectives: To study the changing etiology of prosthetic valve endocarditis (PVE) and the impact of nosocomial acquisition of the infection on prognosis in a single hospital.

Methods: Retrospective review of 121 cases of PVE during a period of 34 years. Two different periods (the period from 1970 to 1986 [P1], and the period from 1987 to 2003 [P2]) were analyzed.

Results: During P1, 58 patients with PVE were treated (30 early PVE and 28 late PVE); during P2, 63 patients with PVE were treated (13 early PVE and 50 late PVE). The frequency of early-onset PVE decreased from 0.94% in P1 to 0.34% in P2 (p < 0.001), but the incidence rate of late-onset PVE did not change (0.33% and 0.42% per year, respectively). The microbiology of early PVE changed over the years: Gram-negative bacilli decreased from 40% during P1 to 7.7% in P2 (p = 0.033). Staphylococci remained the main causes of early PVE in both periods. The microbial etiology of late PVE also changed over the years with enterococci and Staphylococcus aureus as the leading causes during P2. Streptococcus viridans decreased from a leading position to a fourth position. Methicillin-resistant S aureus endocarditis appeared first in 1992. Eleven cases of late-onset PVE in P2 were hospital acquired (22%). In comparison, only two cases (7.1%) of hospital-acquired, late-onset PVE were seen in P1 (p = 0.11). Mortality of early-onset PVE decreased from 80% in P1 to 46% in P2 (p = 0.026). The overall mortality of late-onset PVE did not change between periods: 39% vs 34%. Mortality associated with nosocomial PVE in P2 was 63.6% (7 of 11 patients). In comparison, the mortality of community-acquired cases was 25.6% (10 of 39 patients; p = 0.03). In the multivariate analysis, the presence of comorbidities and hospital acquisition were associated with an excess of mortality (odds ratio [OR], 13.9; 95% confidence interval [CI], 1.23 to 158 [p = 0.033]; and OR, 10.8; 95% CI, 2.16 to 54.7 [p = 0.0037], respectively).

Conclusion: Although the mortality associated with early-onset PVE has significantly decreased, in this series the mortality of patients with late-onset PVE remained high due mainly to an increasing number of patients with comorbidities who acquired the infection during admission for other diseases.


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