Patients chiefly at risk are severe hypertensives and those who have angina or have had a myocardial infarct due to ischaemic heart disease. Anxiety or pain can cause outpouring of epinephrine which can both greatly increase the load on the heart and also precipitate dangerous dysrhythmias.

To die of fright is not a figure of speech but it can sometimes result from severe dysrhythmia. The first essential for these patients is therefore to ensure painless dentistry and to alleviate anxiety.

Patients should be asked whether routine dental treatment under local anaesthesia is acceptable and in any session of treatment as little or as much may be done as they feel able to tolerate.

Oral temazepam may be helpful (5 mg on the preceding night and again half an hour before treatment, and the patient accompanied by a responsible adult). If sedation is required, inhalational sedation is safer because nitrous oxide has no cardiorespiratory depressant effects and is more controllable, but it should be administered by an expert and not given within three months of a heart attack or recent angina.

Patients with severe or longstanding hypertension are at risk from ischaemic heart disease. Medical advice should be sought before treating those with blood pressures of 160–179/95–109. If considered at low risk from dental treatment, the same precautions should be taken for those with ischaemic heart disease.

Patients at risk are mainly those with congenital anomalies, such as valve or septal defects, or who have prosthetic heart valve replacements (Appendix 27.1). The majority of these patients have no symptoms and some valve defects, such as a bicuspid aortic valve, do not limit athletic activities.

Normally, bacteria entering the bloodstream are rapidly cleared by circulating leucocytes but, if there is a cardiac defect which can be colonised, infective endocarditis can develop.

There are many sources of bacteraemias, such as cardiac surgery, intravenous catheterisation and intravenous drug addiction. Bacteraemias can also be detected in over 80% of persons after extractions and even after toothbrushing, but the numbers of bacteria released are often very small. Even in a patient with a heart lesion, infective endocarditis does not necessarily follow.

Relatively few bacteria inhabit the oral mucosa and most are being constantly washed away by the saliva. By contrast, vast numbers of bacteria inhabit the gingival margins when oral hygiene is poor and even greater numbers occupy periodontal pockets. These bacteria are in close contact with dilated, thin-walled blood vessels (Fig. 27.2). Movement of teeth in their sockets repeatedly compresses and stretches or ruptures these vessels, so that bacteria can be pumped into the bloodstream.

Fewer than 15% of cases of infective endocarditis can be related to (but not necessarily caused by) dental operations but, in these cases, extractions have been preceded by the infection in over 95%. Viridans streptococci, such as those which colonise the teeth, are of low virulence, but may be able to colonise heart valves because of attachment mechanisms (Ch. 3) which also enable them to cause dental disease.

Factors determining susceptibility to infective endocarditis are unclear. For example, children with Down’s syndrome – who are prone to severe periodontal disease, have multiple immune defects and, frequently, congenital cardiac defects – are not particularly susceptible to infective endocarditis.

Currently, advanced age, especially if there is periodontal sepsis, is the main risk factor (Fig. 27.3). Infective endocarditis is rare in children and the peak incidence and mortality is after the age of 60 years. For cardiac transplantation, patients are deeply immunosuppressed and might be considered to be at high risk of infective endocarditis after dental operations. However, data are limited and there is no agreed protocol for such patients.

Once infective endocarditis develops, vegetations of bacteria and fibrin form on the valves, which are progressively destroyed (Fig. 27.4). Cardiac failure is the main cause of death, but emboli and bacteria released into the bloodstream can also cause renal or cerebral damage.

Prevention is all important. Patients in high-risk categories should receive preventive advice and, if treatment becomes necessary, antibiotic prophylaxis (see below and Appendix 27.1) before treatment that disturbs the gingival margin. This is likely to release significant numbers of bacteria from the gingivae or, particularly, periodontal pockets. Other dental procedures, such as fitting metal bands which extend deep to the gingival margins, though they may cause bacteraemias, have rarely been followed by infective endocarditis and antibiotic cover has not been officially recommended in the past. However, if the clinician considers the patient to fall into a high-risk group, then it may be prudent to give cover. Otherwise, orthodontic procedures in general are not recommended for antibiotic cover, particularly because most of these patients are children in whom infective endocarditis is rare. Endodontic treatment rarely, if ever, leads to infective endocarditis and the risks of antibiotic prophylaxis exceed any benefits.

Infective endocarditis does not appear to be a risk after myocardial infarction or coronary artery bypasses, or for wearers of cardiac pacemakers, and antibiotic cover is not recommended for them.