ABSTRACT
Although almost any structural heart disease can predispose to the development of endocarditis, certain cardiac conditions are associated with IE more frequently than others. Acquired valvular dysfunction due to rheumatic heart disease (RHD) was a common predisposing condition in the past, involving the mitral valve in 85% of cases, either alone or in combination, and the aortic valve in about half of cases. However, rheumatic valvular disease is now much less common in Western countries, found in fewer than 15% of patients in many recent series. In developing nations, RHD remains a common disorder
and a frequent predisposing factor in the development of IE. Congenital cardiac conditions including patent ductus arteriosus, ventricular septal defect, primum atrial septal defect, bicuspid aortic valve, coarctation of the aorta, tetralogy of Fallot, and pulmonic stenosis together account for approximately 6%–24% of cases. The congenitally bicuspid aortic valve is a common condition, found in 1%–2% of the general population, and is becoming an increasingly important predisposing factor for native valve endocarditis. IE involving bicuspid aortic valves tends to be severe, requiring surgery in 80%–90% of cases, and carries a significant mortality rate even with prompt surgical intervention. The mitral valve prolapse (MVP) syndrome is also associated with endocarditis. This relatively common condition is found in 0.5%–20% of otherwise healthy individuals, particularly young women. The risk of IE appears to be increased in the group of patients who manifest the holosystolic murmur, rather than those with the isolated midsystolic click, presumably because it is the regurgitant flow and not the valve prolapse itself that creates the turbulence that predisposes to IE. Patients exhibiting myxomatous degeneration of the mitral valve, with mitral valve leaflet thickening and redundancy on echocardiogram, are also at increased risk for IE. Idiopathic hypertrophic subaortic stenosis (IHSS) is another cardiac condition that can lead to IE, which occurs in 5% of patients with IHSS. This has been attributed to turbulent flow at the aortic valve, which is distal to the hypertrophied portion of the interventricular septum, as well as to coexisting mitral regurgitation due to displacement of the anterior leaflet by the abnormally shaped ventricle. The role of ‘‘degenerative’’ cardiac conditions such as calcified lesions due to arteriosclerotic cardiovascular disease or a calcified mitral annulus in predisposition to IE remains unclear. In a number of series, the majority of patients with acute IE had no known underlying cardiac disease. As these degenerative conditions are common in the elderly population, it is possible though unproved that they play a role in the development of IE.
