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The most common heart valve affected by infective endocarditis (IE) is the aortic valve. Fortunately, significant progress has been made in our understanding and management of aortic valve IE. Clinical manifestations include fever, heart murmur, splenomegaly, embolic events, and bacteremia or fungemia. Early diagnosis is extremely important because progression invariably leads to devastating complications, including acute heart failure, cerebral embolism, and death, if the infection is not treated with antibiotics, surgery, or both. Increasingly, IE has become a “surgical disease,” particularly for aortic valve IE, and during the last decade, more than half of all patients have been operated on during the active phase of the disease (early surgery).1


Among patients with aortic valve IE, congenitally bicuspid aortic valve is the most common predisposing lesion.2 Other congenital abnormalities of the aortic valve predisposing to infection are degenerative calcific aortic stenosis, aortic regurgitation due to any cause, and rheumatic aortic valve disease. Occasionally, highly virulent microorganisms infect normal aortic valves. Patients with prosthetic heart valves run a constant higher risk of developing IE.

It is difficult to determine the incidence and prevalence of native aortic valve IE in the general population because the disease is continuously changing.3,4 The annual incidence is estimated to range from 1.7 to 7.0 episodes per 100,000 person-years in North America,5-7 and patients with prosthetic aortic valves are reported to have an incidence of 0.2 to 1.4 episodes per 100 patient-years.8-10 Approximately 1.4% of patients undergoing aortic valve replacement develop prosthetic valve IE during the first postoperative year.11

The incidence of nosocomial IE is increasing because more patients are undergoing invasive procedures. IE in hemodialysis patients is fortunately relatively infrequent, but when it happens, it is associated with high mortality.12 Dental procedures, extractions in particular, have been shown to produce bacteremia. However, daily dental flossing can also produce bacteremia in periodontally healthy individuals at a rate comparable with that caused by dental procedures for which antibiotic prophylaxis is usually given to patients with valve disease to prevent endocarditis, suggesting that prophylaxis may be futile.13 Endoscopic procedures may also produce bacteremia. Intravenous drug users using nonsterile syringes and needles most often infect their structurally normal tricuspid valves (see “Prophylaxis of Infective Endocarditis” later in this chapter).


The key to understanding IE is appreciating the pathology progression.6,14,15 Circulating organisms adhere and attach to areas with endocardial (valve) injury; such damaged areas often have deposition of platelets, fibrin, or clots, facilitating attachment and growth of the organisms. In 1928, Grant and colleagues16 theorized that platelet-fibrin thrombi on the heart valve serve as a nidus for bacteria to adhere, and in 1963, Angrist and Oka17 introduced the term nonbacterial thrombotic endocarditis to describe such sterile vegetations, providing experimental evidence ...

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