What is endocarditis?

Causes and Symptoms

The lesions of endocarditis may be noninfective, as in some autoimmune conditions, or infective. The latter are characterized by direct invasion of the endocardium by microorganisms, most often bacteria.
Bacterial endocarditis may occur on normal or previously damaged heart
valves and also on artificial (prosthetic) heart valves. Rarely, endocarditis may occur on the wall (mural surface) of the heart or at the site of an abnormal hole between the pumping chambers of the heart, called a ventricular septal defect.

In areas of turbulent blood flow, platelet-fibrin deposition can occur, providing a nidus for subsequent bacterial colonization. Transient bacteremia may accompany infection elsewhere in the body or some medical and dental procedures, and these circulating bacteria can adhere to the endocardium, especially at platelet-fibrin deposition sites, and produce endocarditis. Intravenous drug abusers using unsterile equipment and drugs often inject bacteria along with the drugs, which can result in endocarditis. The lesions produced by these depositions plus bacteria are called vegetations. Clinical symptoms and signs usually begin about two weeks later.

Bacterial endocarditis usually involves either the mitral or the aortic heart valve. In intravenous drug abusers, the tricuspid heart valve is more commonly affected because it is the first valve to be reached by the endocardium-damaging drugs and contaminating bacteria. The pulmonic valve is only rarely the site of endocarditis. Occasionally, more than one heart valve is infected; this occurs most often in intravenous drug abusers or patients with multiple prosthetic heart valves.

Gram-positive cocci are the most common cause of bacterial endocarditis. Different species predominate in various conditions or situations: Streptococcus viridans in native valves, Staphylococcus aureus in the valves of intravenous drug abusers, and Staphylococcus epidermidis in prosthetic heart valves. Gram-negative bacilli are found in association with prosthetic heart valves or intravenous drug addiction.

The clinical manifestations of endocarditis are varied and often nonspecific. Early symptoms are similar to those encountered in most infections: fever, malaise, and fatigue. As the disease progresses, more cardiovascular and renal-related symptoms may appear: dyspnea, chest pain, and stroke. Fever and heart murmurs are found in most patients. Enlargement of the spleen, skin lesions, and evidence of emboli are commonly present.

The key to the diagnosis of bacterial endocarditis is to suspect the presence of the illness and obtain blood cultures. Febrile patients who have a heart murmur, cardiac failure, a prosthetic heart valve, history of intravenous drug abuse, preexisting valvular disease, stroke (especially in young adults), multiple pulmonary emboli, sudden arterial occlusion, unexplained prolonged fever, or multiple positive blood cultures are likely to have endocarditis. The hallmark of bacterial endocarditis is continuous bacteremia; thus, nearly all blood cultures will be positive. Other nonspecific blood tests, such as an erythrocyte
sedimentation rate, or specific blood tests, such as tests for teichoic acid antibodies, may be helpful in establishing a diagnosis.

Treatment and Therapy

Endocarditis may be prevented by administering prophylactic antibiotics to patients with preexisting heart abnormalities that predispose them to endocarditis when they are likely to have transient bacteremia. An example would be a patient with an artificial heart valve scheduled to have a dental cleaning.

Endocarditis is one of the few infections that is nearly always fatal if mistreated. Antibacterial therapy with agents capable of killing the offending bacteria, along with supportive medical care and cardiac surgery when indicated, cures most patients.

Perspective and Prospects

The first demonstration of bacteria in vegetations associated with endocarditis was by Emmanuel Winge of Oslo, Norway, in 1869. Fifty years later, a fresh section was cut from the preserved heart valve described by Winge, and staining by modern methods revealed a chain of streptococci verifying his discovery. It was not until 1943, when Leo Loewe successfully treated seven cases of bacterial endocarditis with penicillin, that the era of modern therapy of this serious illness began.

While the incidence of endocarditis remained fairly constant between the 1960s and the early 1990s, the patient profile changed: heroin addicts, the elderly, and those with prosthetic heart valves. Since the late 1990s there has been a steady increase in the number of heart valve infections. Recent studies have found that 40 percent of those who end up with endocarditis acquire their infections in health care facilities. Most of these patients are elderly, are suffering from other illnesses, and have received cardiac implants such as prosthetic heart valves, pacemakers, and defibrillators.

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