At one time, rheumatic heart disease was the leading risk factor for endocarditis. Nowadays, however, most cases of endocarditis occur in I.V. drug abusers, patients with prosthetic heart valves, and those with mitral valve prolapse (especially men with systolic murmurs). Other predisposing conditions include coarctation of the aorta, tetralogy of Fallot, subaortic and valvular aortic stenosis, ventricular septal defects, pulmonary stenosis, Marfan syndrome, degenerative heart disease (especially calcific aortic stenosis) and, rarely, a syphilitic aortic valve. Some patients with endocarditis have no underlying heart disease.

Infecting organisms differ among these groups. In patients with native valve endocarditis who aren’t I.V. drug abusers, causative organisms usually include—in order of frequency —streptococci (especially Streptococcus viridans), staphylococci, and enterococci. Although many other bacteria may cause the disorder, fungal causes are rare in this group. The mitral valve is usually involved, followed by the aortic valve.

In patients who are I.V. drug abusers, Staphylococcus aureus is the most common infecting organism. Less commonly, streptococci, enterococci, gram-negative bacilli, or fungi cause the disorder. The tricuspid valve is involved most often, followed by the aortic and then the mitral valve.

In patients with prosthetic valve endocarditis, early cases (those that develop within 60 days of valve insertion) are usually from staphylococcal infection. However, gram-negative aerobic organisms, fungi, streptococci, enterococci, or diphtheroids also may cause the disorder. The course is usually fulminant and fatal. Late cases (occurring after 60 days) are similar to native valve endocarditis.

Regardless of the cause, bacteremia—even transient bacteremia after dental or urogenital procedures—introduces the pathogen into the bloodstream. Fibrin and
platelets aggregate on valve tissue and engulf circulating bacteria or fungi, producing vegetative growths on the heart valves, endocardial lining of a heart chamber, or endothelium of a blood vessel.

(See Degenerative changes in endocarditis.)

Such vegetations may cover the valve surfaces, causing ulceration and necrosis. They also may extend to the chordae tendineae, leading to their rupture and subsequent valvular insufficiency. Ultimately, they may embolize to the spleen, kidneys, central nervous system (CNS), and lungs.

In the United States, endocarditis affects 2 to 4 people out of every 100,000 each year. Men are twice as likely as women to acquire this infection, and the mean age of onset is 50. Mortality rates vary with the infecting organism; death is more likely with increased age, infection of the aortic valve, heart failure and underlying heart disease, and CNS complications.

Early clinical features of endocarditis are usually nonspecific and include malaise, weakness, fatigue, weight loss, anorexia, arthralgia, night sweats, chills, valvular insufficiency and, in 90% of patients, an intermittent fever that may recur for weeks. Organisms of high pathogenicity, such as S. aureus, may cause a more acute onset. Endocarditis commonly causes a loud, regurgitant murmur typical of the underlying heart lesion. A suddenly changing murmur or the discovery of a new murmur with fever is a classic physical sign of endocarditis.