Skip Navigation

Nonvalvular Cardiovascular Device—Related Infections

  1. Larry M. Baddour1,
  2. Michael A. Bettmann3,
  3. Ann F. Bolger4,
  4. Andrew E. Epstein6,
  5. Patricia Ferrieri2,
  6. Michael A. Gerber7,
  7. Michael H. Gewitz8,
  8. Alice K. Jacobs9,
  9. Matthew E. Levison11,
  10. Jane W. Newburger10,
  11. Thomas J. Pallasch5,
  12. Walter R. Wilson1,
  13. Robert S. Baltimore12,
  14. Donald A. Falace13,
  15. Stanford T. Shulman14,
  16. Lloyd Y. Tani15, and
  17. Kathryn A. Taubert16
  1. 1Department of Medicine, Mayo Clinic College of Medicine, Rochester
  2. 2Department of Pediatrics, University of Minnesota, Minneapolis, Minnesota
  3. 3Department of Radiology, Dartmouth-Hitchcock Medical Center, Lebanon, New Hampshire
  4. 4Department of Medicine, University of California, San Francisco
  5. 5Department of Dentistry, University of Southern California, Los Angeles
  6. 6Department of Medicine, University of Alabama, Birmingham
  7. 7Department of Pediatrics, Cincinnati Children's Hospital and Medical Center, Ohio
  8. 8Department of Pediatrics, New York Medical Center, New York
  9. 9Department of Medicine, Boston Medical Center, Boston, Massachusetts
  10. 10Department of Pediatrics, Harvard Medical School, Boston, Massachusetts
  11. 11Department of Medicine, Drexel University, Philadelphia, Pennsylvania
  12. 12Department of Pediatrics, Yale University School of Medicine, New Haven, Connecticut
  13. 13College of Dentistry, University of Kentucky, Lexington
  14. 14Department of Pediatrics, Northwestern University, Evanston, Illinois
  15. 15Department of Pediatrics, Primary Children's Medical Center, Salt Lake City, Utah
  16. 16American Heart Association, Dallas, Texas
  1. Reprints or correspondence: Dr. Larry M. Baddour, Mayo Clinic-Rochester, 200 First St. SW, Rochester, MN 55905 (baddour.larry{at}mayo.edu).

The American Heart Association's Committee on Rheumatic Fever, Endocarditis, and Kawasaki Disease recently published a scientific statement [1] that addresses nonvalvular cardiovascular device-related infections. This is the first time that the committee has reviewed this topic, and it did so to emphasize to clinicians the importance and variety of these infections.

For discussion purposes, the document classifies each device into 1 of 3 categories: intracardiac, intra-arterial, and intravenous (table 1). Because the diagnosis, management, and prevention of intravascular catheter-related infections has received considerable attention in other publications, these device-related infections were not included in the statement. For similar reasons, infections of prosthetic cardiac valves were also not reviewed.

Table 1

Incidence of infection associated with use of a nonvalvular cardiovascular device (NVD).

Table 2

Antibiotic prophylaxis recommendations for use with placement of nonvalvular cardiovascular devices.

The incidence of nonvalvular cardiovascular device-related infections varies widely according to the device. For example, infectious complications associated with ventricular assist devices are frequently seen. In contrast, infections involving coronary artery stents or vena caval filters are extremely rare. Because of the large and increasing number of these devices that are being placed in patients globally, it is critical that a discussion of infectious complications be available to clinicians, even for devices that are rarely associated with infection.

Staphylococcus aureus and coagulase-negative staphylococci account for the majority of nonvalvular cardiovascular device-related infections. Because many of these infections are nosocomially acquired, multidrug resistance, including resistance to oxacillin, is characteristic of many of the isolates involved in such infections. For S. aureus, several adhesins—known as microbial surface components recognizing adhesive matrix molecules, or MSCRAMM—function as extracellular matrix-binding proteins that coat the surface of medical devices and allow for bacterial attachment to the device to initiate infection [2, 3]. For both coagulase-negative staphylococci and S. aureus, biofilm production on the surface of the nonvalvular cardiovascular device may be pivotal in the pathogenesis of these infections [4, 5]. In addition, other factors, including host response to the devices and the physical and chemical characteristics of the devices, are operative in infection pathogenesis.

The clinical presentation of nonvalvular cardiovascular device-related infection can be systemic, local, or both. Local manifestations include signs and symptoms of inflammation at the device placement site. Fever may or may not be present. Systemic findings of infection are seen when endarteritis, endocarditis, or septic phlebitis are present as a complication of intravascular or intracardiac device infection. Results of blood cultures are usually positive in cases of systemic infection and, when positive, often lead to the correct diagnosis. Imaging studies, such as ultrasonography and CT scanning, are often used to support a diagnosis of nonvalvular cardiovascular device-related infection.

Treatment is based on the principle that removal of the entire device system is usually required to eradicate infection. This is tempered by the reality that many of these devices are life sustaining, and, because of underlying medical or surgical conditions, selected patients may not be candidates for device removal. For members of this group of patients who are otherwise stable from a cardiovascular standpoint and who have clinically and microbiologically responded to induction therapy, long-term antimicrobial suppressive therapy may be a treatment option. Because many of these patients are device-dependent, and because newer oral antimicrobials that have excellent bioavailability are available, long-term (and even lifelong) suppressive therapy is used. Overall, drug tolerability has been good. Nevertheless, patients should be monitored for and educated about drug-related adverse events and possible drug-drug interactions.

Prevention of infection is the ultimate goal, and for some devices, primary prophylaxis that is modeled after the prophylaxis used to prevent surgical site infections is appropriate (table 2). In contrast, secondary (episodic) prophylaxis, modeled on that used to prevent infective endocarditis [6] in patients with prosthetic cardiac valves, is not recommended in the statement. Unlike the pathogens involved in prosthetic valve endocarditis, viridans group streptococci and enterococci rarely cause nonvalvular device-related infections, and dental, respiratory, gastrointestinal, and genitourinary procedures have not been implicated as causes of subsequent nonvalvular cardiovascular device-related infection.

As technical advances continue, future versions of the scientific statement will include a review of newer types and generations of devices. For example, we anticipate learning more about whether infection will complicate the use of the artificial heart. Newer devices, such as annular valve rings and occluders of left atrial appendages and atrial septal defects and/or patent foramen ovalae, will need to be addressed as clinical experience accumulates. In addition, it is hoped that novel antimicrobial agents will some day be capable of curing infection, thereby obviating the need for device removal. Active and passive immunization with antistaphylococcal vaccines prior to device placement to prevent infection will also be an important topic for future review.

  • Received December 1, 2003.
  • Accepted December 2, 2003.

References

| Table of Contents

Navigate This Article