Epidemiology

Endocarditis usually occurrs more frequently in men, gender derived ratios range from 1.6 to 2.5.The age specific incidence of endocarditis increased progressively after 30 years of age and exceed 15 to 30 cases per 100,000 person-years in the sixth through eighth decades of life. From 55 to 75 per cent of patients with native valve endocarditis (NVE) have predisposing conditions like rheumatic heart disease, congenital heart disease, mitral valve prolapse, degenerative heart disease, asymmetrical septal hypertrophy, or intravenous drug abuse. From 7 to 25 per cent of cases involve prosthetic valves. Predisposing conditions cannot be identified in 25 to 45 per cent of patients. The nature of predisposing conditions and in part the microbiology of IE correlate with the age of patients.

Rheumatic fever with subsequent rheumatic heart disease in children and young adults is still the most common predisposing cause for IE in developing countries. In recent decades, only the increasing role of intravenous (IV) drug abuse as predisposition for IE and the high IE risk in children and young adults surviving after correction of complex congenital heart disease favour the occurrence of infection in younger patients and the incidence has increased in the elderly because of the increased longeivity and the associated prevalence of degenerative valvular heart disease.

Table : Predisposing Conditions and Microbiology of Native Valve Endocarditis

Children

Among neonates, IE typically involves the tricuspid valve of structurally normal hearts and is associated with very high mortality rates. It is likely that many of these episodes arise as a consequence of infected intra venous and right heart catheters as well as cardiac surgery.The vast majority of children with IE occurring after the neonatal period have identifiable structural cardiac abnormalities. Rheumatic heart disease is the major predisposition for IE in developing countries. Congenital heart abnormalities, particularly those involving the aortic valve; ventricular septal defects; tetralogy of Fallot; and other complex structural anomalies associated with cyanosis (TGA, single ventricle) are found in remaining cases. Of children with IE on congenital defects, 50 per cent develop infection after cardiac surgery; in these children,infection frequently involves prosthetic valves, valved conduits, or synthetic patches. Mitral valve prolapse generally in association with a regurgitant murmur has been recognized to predispose to IE in children.

Endocarditis among neonates is caused primarily by S.aureus, coagulase-negative staphylococci, and group B streptococci. Occasionally infection is caused by gram- negative bacilli and candida species. Among older children, streptococci, the predominant cause account for at least 40 per cent of cases, and S. aureus occurring as a nosocomial or community acquired acute infection is the second most common cause of IE.The clinical features and echocardiographic findings of IE in children are similar to those noted among adults with NVE or PVE, respectively. In contrast, IE among neonates is more cryptic; the clinical picture is dominated by bacteremia, and classical signs of IE are rare.

Adults

Mitral valve prolapse (MVP) has emerged as a prominent, predisposing structural cardiac abnormality and in adults accounts for 7 to 30 per cent of NVE in cases not related to drug abuse or nosocomial infection. This increased risk of endocarditis is largely confined to patients with both prolapse and a mitral regurgitation murmur. Risk is also increased among men and patients older than 45 years. Valve redundancy and thickened leaflets (> 5mm) by echocardiography also identify a population at increased risk for IE.
 

Rheumatic heart disease was the predisposing cardiac lesion for IE in 20 to 25 per cent. In patients with rheumatic heart disease, endocarditis occurs most frequently on the mitral valve, a site at which women are more commonly infected. The aortic valve is the next most common site for IE; infection in this setting occurs more commonly in men.Congenital heart disease is the substrate for IE in 10 to 20 per cent of younger adults and 8 per cent of older adults. Among adults, the common predisposing lesions are patent ductus arteriosus,ventricular septal defect, and bicuspid aortic value, the latter particularly found among older men (> 60 years).
Intravenous Drug Abusers

The risk for IE among IV drug abusers, 2 to 5 per cent per patient- year, is estimated to be several fold greater than that of patients with rheumatic heart disease or prosthetic valves.Endocarditis occurring in IV drug abusers has a unique propensity to infect right heart valves. In clinical series, distribution of valve involvement is tricuspid in 46 to 78 per cent, mitral in 32 to
24 per cent, and aortic in 8 to 19 per cent, (as many as 16 per cent of patients have infection at multiple sites). In IV drug abusers, the valves were normal before infection in 75 to 93 per cent of patients. In contrast to NVE among adults in general, S aureus causes more than 50 per cent of these infections overall and 60 to 70 per cent of those involving the tricuspid valve.
Prosthetic Valve Endocarditis The risk of PVE is greatest during the initial 6 months after valve surgery (particularly during the
initial 5 to 6 weeks) and thereafter declines to a lower but persistent risk (0.2 to 0.35 per cent per year)

PVE has been called “early” when symptoms begin within 60 days of valve surgery and “late” with onset thereafter. These terms were established to distinguish early PVE that arose as a complication of valve surgery from late infection that was more likely community acquired. In fact, many cases with onset between 60 days and 1 year after surgery are likely to be nosocomial and, despite their delayed presentation, derive from events during the surgical admission. Data suggest that during the initial months after valve implantation, mechanical prostheses are at greater risk of infection than bioprosthetic valves but that after 12 months the risk of infection of bioprostheses exceeds that of mechanical valves.

The intracardiac pathology of PVE differs notably from the largely leaflet-confined pathology of NVE. Infection on mechanical prostheses commonly extends beyond the valve ring into the annulus and periannular tissue as well as the mitral-aortic intravalvular fibrosa, resulting in ring abscesses, septal abscesses, fistulous tracts, and dehiscence of the prosthesis with hemodynamically significant paravalvular regurgitation.

Table: Microbiology of Prosthetic Valve Endocarditis