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The average age of patients with endocarditis is 58 years and men outnumber women. A falling incidence of rheumatic heart disease, the aging population, recognition of diseases such as mitral valve prolapse, surgical correction of congenital heart disease, and placement of prosthetic heart valves have changed the population at risk. Between 1938 and 1967, rheumatic heart disease was implicated in 38 per cent of cases compared with 6 per cent between 1980 and 1984

(McKinsey,. etal 1987). The proportion of endocarditis associated with the aortic and mitral valves is now similar, whereas mitral valve disease used to be twice as common.

Underlying cardiac lesions were present in 73 per cent (46 out of 63) of patients in one series, with mitral valve prolapse being the most usual, followed by degenerative disease of aortic or mitral valves, congenital heart disease, and rheumatic heart disease ( McKinseyefa/ 1987). Aortic regurgitation precedes endocarditis in a third of patients compared with a sixth of patients for aortic stenosis. Mitral regurgitation precedes another 21 to 33 per cent of cases ( MlcheLand. Acar.1995). Mitral valve prolapse is present in 5 per cent of the population, and the risk of endocarditis is increased in those with valvular thickening (> 5 mm), occurring in up to 6 per cent of such patients. Tricuspid valve disease is rare.

Congenital heart disease is present in 10 to 20 per cent of patients with infective endocarditis ( McKinsey,eta[ 1987). Patent ductus arteriosus, ventricular septal defect, tetralogy of Fallot, and a bicuspid aortic valve are the most common. Of 1347 patients with ventricular septal defect followed for 16 years, 32 developed endocarditis (Mj.chel and Acar.1995). Ventricular septal defect is most likely to predispose to endocarditis if uncorrected and associated with aortic regurgitation. Partial correction of congenital heart disease is associated with a greater risk of endocarditis than if correction is complete. A patch or residual ventricular septal defect is the usual site of infection in tetralogy of Fallot. The risk of endocarditis in congenital aortic stenosis depends on the severity of the lesion. A bicuspid aortic valve is present in 1 to 2 per cent of the population and accounts for 20 per cent of cases of endocarditis. Patent ductus arteriosus and coarctation of the aorta are rarely associated with endocarditis because these malformations are now usually corrected in infancy.

Hypertrophic obstructive cardiomyopathy predisposes to endocarditis, particularly on the aortic or mitral valves or the subaortic endocardium. Vegetations of the aortic and pulmonary valves occur on the ventricular surface of the valve, and those of the mitral and tricuspid valves occur on the atrial surface. Approximately 5 per cent of patients may develop endocarditis, depending on the severity of obstruction.

Previous infective endocarditis is a frequent risk factor, particularly in patients with cardiac disease, continued drug abuse, or dental decay. Intravenous drug abuse is commonly associated with the development of endocarditis in the younger patient. Central venous and pulmonary artery catheters, feeding lines, and intracardiac pacemakers present other risk factors, usually for right-sided endocarditis, if not quickly removed following infection ( Fig 3 and Fig 4).

Fig. 3 A massive vegetation caused by a coagulase-negative staphylococcus originally seeded from an infected Hickman catheter in a leukemic patient. The patient had been treated with large doses of teicoplanin for 3 months, but the vegetation continued to enlarge. The patient died during removal of the valve.

Up to a third of cases of infective endocarditis are due to infection of a prosthetic valve. In a review of 21 series, prosthetic valve endocarditis was found to occur in

0.3 to 1 patient per 100 patient-years (de^Gevigney eta[ 1995). Infection of the aortic valve may be more common than that of the mitral valve and is more likely when more than one prosthetic valve is present. Opinion is divided as to the relative risk of infection of bioprosthetic and mechanical valves, but age and length of cardiopulmonary bypass are important (Fig 5). The risk of endocarditis rises from 3 per cent at 1 year to 5 per cent at 10 years after insertion. Endocarditis occurs in

0.1 to 7 per cent of patients with permanent pacemakers (d.e.G.e.vi.g.D.e,y., §L§L 1995).

Fig. 5 A Starr-Edwards valve showing a large vegetation.

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