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Antimicrobial prophylaxis for endocarditis: Letter to the Editor (1)
  1. John A C Chalmers,
  2. D M Pullan
  1. The Cardiothoracic Centre, Liverpool, UK
  1. Correspondence to:
    Mr J A C Chalmers
    The Cardiothoracic Centre, Thomas Drive, Liverpool L14 3PE, UK; john.chalmers{at}ctc.nhs.uk

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To the Editor: The title of the editorial by Ashrafian and Bogle1 was clear enough, but the editorial was not.

The representative cardiological bodies in UK, USA and Europe have all published guidelines on the prevention of infective endocarditis (IE). Their guidance is clear. The guidance from the British Society for Antimicrobial Chemotherapy2 on the other hand carries with it a feeling of self-righteousness, but its position is not rational.

The science of endocarditis is clear enough—valves become infected secondary to bacteraemia. The argument that rabbit models do not replicate strictly the pathogenesis of endocarditis in humans2 and that as such the evidence is questionable confines much of the progress made in the 20th century to the intellectual dustbin. The incidence of endocarditis will depend on the organism type, the immune status of the patient and the bacteriological load. The risk of antibiotic-related death from penicillin anaphylaxis (quoted in the editorial), given as five times higher than the risk of IE, is unreferenced (and in our experience unbelievable) and gives no indication of the risk of IE without antibiotics. Patients undergoing dental procedures develop bacteraemias with a higher bacteriological load than the background risk from chewing or brushing. Doctors and dentists cannot cover patient risk at all times. However, they have a duty to reasonably cover risks that are recognisable and potentially treatable. No treatment is 100% effective: antibiotic prophylaxis should not be expected to be so. Failure to stop all events does not indicate ineffectiveness in the majority. Endocarditis as a whole carries a mortality of at least 20%, despite best available management. If the background risk is so small, why should a patient who has had endocarditis represent a risk of infection higher than one, with equivalent pathology, who has not had endocarditis? This does not seem to be a rational stance2 (from a group who require hard evidence).

Recommendations of this nature adopted unilaterally against the best advice of representative cardiological bodies put dentists in an invidious position. They will be liable for omissions in cover and are unlikely to be supported if the treatment given runs contrary to the recommendations of the patient’s cardiologist.

Patients deserve clear and consistent advice from their clinicians. Unfortunately, the advice inherent in the guidelines and your editorial would not have helped to foster either.

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