Infections that occur on the endocardial surface of the heart are known as infective endocarditis. One or more heart valves may be involved, and the condition is always fatal unless treated appropriately with antibiotics. The incidence of infective endocarditis in Australia is approximately five cases per 100,000 person–years and the in-hospital mortality is 15% to 20%. The condition affects males three times more frequently than females; Indigenous Australians are at a much greater risk than other Australians.

Acute endocarditis is a rapidly progressing form of endocarditis that usually involves Staphylococcus aureus or various streptococci species. This is a serious medical emergency and treatment should begin as soon as possible to prevent complications, including irreversible damage to the heart valves. Subacute endocarditis normally involves underlying structural valvular disease and may develop over the course of a few months to a year. Although treatment is crucial to decrease mortality and morbidity, subacute endocarditis is not the medical emergency of acute endocarditis and treatment may be delayed while blood cultures are performed. Subacute endocarditis normally involves alpha-haemolytic streptococci or enterococci.

Infective endocarditis can be further classified into the following four categories:

  1. Native valve endocarditis
  2. Prosthetic valve endocarditis
  3. Intravenous drug use endocarditis
  4. Health care associated endocarditis

Native valve infective endocarditis generally only occurs in patients with an underlying valvular disease. The most common underlying diseases are rheumatic valvular disease, congenital heart disease, mitral valve prolapse and degenerative heart disease.

Prosthetic valve endocarditis (PVE) can be classified as either early or late PVE. Early PVE is an infection occurring within 60 days of valve replacement; infection occurring after 60 days of valve replacement is classified as late PVE. Early PVE is shown to have a much higher mortality rate compared to late PVE. S. aureus is the main pathogen involved in both early and late PVE.

Infection may also occur in patients with permanent pacemaker devices or implanted cardioverter defibrillators. Modern surgical practices and appropriate antibiotic prophylaxis at the time of insertion may reduce the incidence and improve patient outcomes for this serious condition. In addition to antibiotic therapy, complete removal of the device is required.

Right sided infective endocarditis is predominantly due to intravenous drug use. S. aureus is the most common pathogen, however Pseudomonas aeruginosa, fungal infections and even rarer microbiological pathogens should not be ruled out in this group.

Health care associated infective endocarditis (HCIE) arises as a result of a stay in a hospital or other health care facility. S. aureus is the primary causative pathogen and is strongly associated with infection of intravascular lines. Procedures that increase the risk of bacteraemia may also be associated with endocarditis.

Studies showing the benefit of prophylactic antibiotics for the prevention of endocarditis following high-risk procedures are lacking. The United Kingdom’s National Institute for Health and Care Excellence (NICE) now recommend that prophylactic antibiotics should not be routinely given. Until further data is available, the Australian Therapeutic Guidelines continue to recommend prophylactic antibiotics in high-risk patients prior to certain high-risk procedures. High-risk patients include those with a prosthetic cardiac valve, previous history of infective endocarditis, and certain patients with congenital heart disease or rheumatic heart disease. High-risk procedures are those that carry a significant risk of bacteraemia with pathogens capable of causing endocarditis.The major goals of endocarditis treatment are to eradicate the underlying infection as well as treat any complications that may arise. Potential complications include, but are not limited to, congestive heart failure, systemic embolisation and end organ damage. Empirical antibiotic regimens can be found in the Therapeutic Guidelines; treatment should be directed as soon as sensitivity results are available. Blood cultures are an important part of endocarditis diagnosis. However, it is important to keep in mind that 5% of all cases will return negative blood cultures. This is normally due to previous treatment with antibiotics, but may also be due to the presence of fastidious bacteria or fungal pathogens. Fungal pathogens are more likely to be the causative agent in intravenous drug users and immuno-compromised patients.

Treatment of infective endocarditis includes aggressive intravenous antibiotic therapy for up to six weeks or longer. Hospital in the home services may be considered in medically stable patients after two weeks to reduce the costs and potential complications associated with a prolonged hospital stay. Surgery is often also required, particularly in cases of especially virulent or resistant pathogens or to repair or replace damaged cardiac valves. Currently, surgical intervention is indicated in 25% to 30% of patients during acute infection and 20% to 40% during convalescence. Evidence supporting early surgical intervention is increasing and contemporary practice appears to be shifting in this direction. International guidelines recommend surgical intervention in patients who develop congestive heart failure, uncontrolled infection and systemic embolism. Other rarer complications may also call for early surgical intervention.

Infective endocarditis is a serious condition that, if left untreated, will be fatal. The mortality rate during current therapies may still be as high as 30% one-year post-infection, depending upon the causative organism and other patient risk factors. Prolonged therapy is generally required, therefore health care professionals play a vital role in treating the infection as well as any complications of the condition or the therapy itself.

References:

  1. Antibiotic Expert Group. Therapeutic Guidelines: Antibiotic, Version 15. Melbourne: Therapeutic Guidelines Limited; 2014.
  2. Brusch J, Bronze M. Infective endocarditis. Medscape Drugs and Diseases; 2015.
  3. Le K, Sohail M, Friedman P, Uslan D, Cha S, Hayes D, et al. Clinical Predictors of cardiovascular implantable electronic-device related infective endocarditis. Pacing Clin Electrophysiol. 2011; 34(4): 450-9.
  4. Luk A, Kim M, Ross H, Rao V, David T, Butany J. Native and prosthetic valve infective endocarditis: clinicopathologic correlation and review of the literature. Malaysian J Pathol. 2014; 36(2): 71-81.
  5. Malhotra A, Rayner J, Williams T, Prendergast B. Infective endocarditis: therapeutic options and indications for surgery. Curr Cardiol Rep. 2014; 16(4): 464: p1-6.
  6. Nonaka M, Kusuhara T, An K, Nakatsuka D, Sekine Y, Iwakura A, et al. Comparison between early and late prosthetic valve endocarditis: clinical characteristics and outcomes. J Heart Valve Dis. 2013; 22(4): 567-74.
  7. Tattevin P, Revest M, Lefort A, Michelet C, Lortholary O. Fungal endocarditis: current challenges. Int J Antimicrob Ag. 2014; 44 (4): 290-4.
  8. Wang A, Athan E, Pappas PA, Fowler VG Jnr, Olaisan L, Pare C, et al. Contemporary Clinical Profile and Outcome of Prosthetic Valve Endocarditis. JAMA. 2007; 297(12): 1354-61.

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