Introduction

Infective endocarditis (IE) may give rise to numerous extracardiac, cardiac, and valvular findings, including infected thrombi (vegetations), sequelae of local tissue destruction, and systemic manifestations including vasculitis, emboli, and ischemic events. This is an appropriate term as the causal organisms may be bacterial, fungal, rickettsial, or even viral or mycoplasmal. Traditionally a distinction between acute and subacute IE was made depending upon the severity and rate of disease progression. This reflected an organism's virulence and the presence of underlying cardiac disease. With antimicrobial treatment these clinical divisions have little pathologic significance, and it is preferable to think in terms of active, healing, and healed IE [1,2]. The disease is now probably best described by its anatomical location and the organism involved.

Infective endocarditis may arise in normal hearts with normal valves, or more commonly in patients with abnormal cardiac anatomy [2,3]. The most common preexisting cardiac valvular lesions are left-sided ones, including aortic stenosis (especially the congenitally bicuspid aortic valve), aortic insufficiency, and mitral insufficiency [4-6]. Valves damaged by rheumatic fever continue to be the most common type of predisposing cardiac valvular abnormality in developing countries. However, in developed countries degenerative or age-related diseases, including mitral valve prolapse, degenerative aortic stenosis, and mitral annular calcification are becoming a more predominant background for IE [2,5].

Other important predisposing conditions are congenital heart diseases, including ventricular septal defect, patent ductus arteriosus, coarctation, transposition of the great arteries, tricus-pid and pulmonary atresia or stenosis, and tetralogy of Fallot [7]. Hypertrophic cardiomyopathy and prosthetic grafts or valves may also predispose to IE [8].

For IE to occur there are usually three features—valvular thrombus, circulating bacteria, and bacterial growth on the valve [9,10]. Hearts may develop valvular thrombus due to abnormal flow and anatomy. Thrombus may develop due to regurgitant jet lesions, on contact surfaces, or other areas of mechanical trauma. It should be realized that many phenomena of modern medicine, including prolonged intubation, immuno-suppression, chemotherapy, complex surgical procedures, and increased use of antimicrobial agents might contribute to increased susceptibility to develop IE. Other predisposing conditions include immunodeficiency, alcoholism, malnutrition, and diabetes. Intravenous drug use (IVDU) may give rise to a repetitive bacteremia and is an important risk factor for IE.

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