(en″dō-kar-dīt′s )

[ endocardium + -itis ]
Infection or inflammation of the heart valves or of the lining of the heart. In casual clinical usage, “endocarditis” is often used for “infective endocarditis.”
SEE: infective endocarditis

ABBR: ABE Infective endocarditis with a rapid onset, usually a few days to 2 weeks. The infection is typically caused by virulent organisms such as Staphylococcus aureus, which may rapidly invade and destroy heart valvular tissue and also metastasize to other organs or tissues.
SEE: ulcerative endocarditis

An infrequently used term for nonbacterial thrombotic endocarditis.

Infective endocarditis produced by organisms that do not quickly or readily grow in blood cultures, usually because their growth is masked by the previous use of antibiotics or because the causative organisms require special culture media or grow slowly in the laboratory. Mycoplasma, Ricksettsia, HACEK (an acronym for Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella) organisms, and some fungi produce culture-negative endocarditis.
SEE: infective endocarditis

ABBR: IE Endocarditis caused by any microorganism, esp. any species of streptococci or staphylococci, and less often by Haemophilus spp. or other HACEK bacteria (such as Actinobacillus actinomycetem comitans, Cardiobacterium hominis, Eikenella corrodens, or Kingella kingae), enteric bacteria, ricksettsiae, chlamydiae, or fungi. Traditionally, IE can be categorized as acute if the illness has a fulminant onset; catheter-related if the causative microorganism gains access to the heart from an indwelling line; culture-negative if echocardiograms reveal that vegetations and other criteria for the disease are present, but the causative microbes have not been isolated in the laboratory; left-sided if it develops on the mitral or aortic valves; nosocomial if it occurs after 48 hr of hospitalization or an invasive surgical procedure; pacemaker-related if the disease occurs on an implanted pacemaker or cardioverter-defibrillator; prosthetic if it occurs on a surgically implanted heart valve; right-sided if it develops on the tricuspid or pulmonary valves; and subacute if it develops after several weeks or months of anorexia, low-grade fevers, and malaise. Patients who are older or have a history of injection drug abuse, diabetes mellitus, immunosuppressing illnesses, aortic stenosis, mitral valve prolapse, or rheumatic heart disease are more likely than others to become infected.

INCIDENCE
The incidence in the U.S. is about 3 to 9 cases per 100,000. Men have IE about twice as often as women.

PREDISPOSING CONDITIONS
IE is more likely to occur in previously infected patients than to arise de novo. It also occurs in: (1) patients with underlying structural abnormalities of the heart (congenital heart malformations, prosthetic heart valves or implanted devices, or rheumatic heart disease); (2) patients who inject drugs; (3) hospitalized patients; or (4) in people with chronic medical illnesses such as diabetes mellitus, kidney disease, and HIV/AIDS.

SYMPTOMS AND SIGNS
Patients with subacute IE may have vague symptoms, including low-grade fevers, loss of appetite, malaise, and muscle aches. Acutely infected patients often present with high fevers, prostration, chills and sweats, stiff joints or back pain, symptoms of heart failure (esp. if the infection has completely disrupted a heart valve or its tethers), heart block (if the infection erodes into the conducting system of the heart), symptoms caused by the spreading of the infection to lungs or meninges (such as cough, headache, stiff neck, or confusion), stroke symptoms, symptoms of renal failure, rashes (including petechiae), or other findings. Signs of the illness typically include documented fevers, cardiac murmurs, or (more rarely) nodular eruptions on the hands and feet (Osler nodes or Janeway lesions). Cottonwool spots may be seen on the retinas of some affected persons.

OSLER NODES AS SEEN IN INFECTIVE ENDOCARDITIS

DIAGNOSIS
Blood cultures, esp. if persistently positive, form the basis for the diagnosis of endocarditis. Contemporary criteria for diagnosis also include visual confirmation of endocardial infection (vegetations) by echocardiography, the presence of several other suggestive anomalies (such as persistent fevers in a patient who is known to inject drugs or a patient with an artificial heart valve), infective emboli in the lungs or other organs; and characteristic skin findings. Transthoracic echocardiography (TTE) is usually performed first because it is noninvasive. TTE may be used when needed for greater diagnostic sensitivity. In patients with visible valvular vegetations but negative blood cultures, serological tests for bacterial infections that are difficult to identify with cultures, such as bartonellosis, brucellosis or Q fever, may identify the pathogenic organism. Occasionally, a patient who dies of a febrile illness may be found to have infective vegetations on the heart valves at autopsy.

PREVENTION
The American Heart Association recommends that patients at high risk for endocarditis should receive prophylactic antibiotics before many procedures, including dental and periodontal cleanings and extractions, intraligamentary local anesthetic injections, tonsillectomy, adenoidectomy, bronchoscopy with a rigid instrument, and sclerotherapy for esophageal varices, esophageal stricture dilation, biliary tract procedures, barium enema or colonoscopy, surgery involving the respiratory or intestinal mucosa, prostate surgery, cystoscopy, and urethral dilation.

TREATMENT
Many patients recover after treatment with prolonged courses of parenteral antibiotics. Some (such as those with heart failure, systemic emboli, or infection that is not responding to medical therapy) may require surgery to replace damaged valves or débridement of abscesses within the myocardium.

IMPACT ON HEALTH
Endocarditis is deadly in about 10% to 25% of patients. Death is most likely to occur in patients who suffer strokes resulting from infected fragments embolizing to the brain, in patients with prosthetic valve endocarditis, and in patients who suffer congestive heart failure. Patients with right-sided endocarditis have a better prognosis than patients with other forms of the disease.

PATIENT CARE
During the acute phase of treatment, patients are monitored for signs and symptoms of heart failure (such as dyspnea, orthopnea, crackles, dependent edema, changes in the heart murmur, and a postsystolic gallop); cerebral emboli (such as paralysis, aphasias, changes in mental status), and embolization to the kidney (such as decreased urine output, hematuria); lung involvement (such as dyspnea, cough, egophony, hemoptysis, pleuritic pain, or friction rub), spleen involvement (such as left upper quadrant abdominal pain radiating to the left shoulder, abdominal rigidity); and peripheral vascular occlusion (such as numbness or tingling, changes in pulses, pallor, and coolness in an extremity). Blood cultures may be taken periodically to monitor the effectiveness of antibiotic therapy. Before the administration of antibiotics, a history of allergies is obtained. Treatment peak and trough drug levels are checked, e.g., when an aminoglycoside or vancomycin is given, to maintain therapeutic levels and prevent toxicity. Supportive treatment includes bed rest, sufficient fluid intake to preserve hydration, and aspirin or acetaminophen for fever and aches.

Passive and active limb exercises are used to maintain muscle tone and quiet, diversional activities to prevent excessive physical exertion until a slow, progressive activity program that limits cardiac workload can be established.

SEE: Libman-Sacks endocarditis

SEE: Löffler endocarditis

1. An obsolete term for endocarditis that is rapidly fatal.
2. Valvular vegetations composed of tumor cells.

Endocarditis of the lining of the heart but not the heart valves.

Infective endocarditis occurring on a patient's own heart valve(s), rather than on a prosthetic (surgically implanted) valve(s).

ABBR: NBTE The presence on the heart valves of vegetations that are produced not by bacteria but by sterile collections of platelets in fibrin. NBTE is characteristically found in severe cases of systemic lupus erythematosus, tuberculosis, or malignancy. The vegetations of NBTE readily embolize, causing infarctions in other organs.
SYN: SEE: verrucous endocarditis

Bacterial infection of a surgically implanted artificial heart valve.

Valvular inflammation and dysfunction (esp. mitral insufficiency) occurring during acute rheumatic fever.

Endocarditis affecting the tricuspid or pulmonary valve. It is usually the result of a percutaneous infection and is most often seen in injection drug users.

ABBR: SBE A heart valve infection that becomes clinically evident after weeks or months. It usually results from infection with streptococcal species that have relatively low virulence (such as viridans group streptococci). The infection often develops on a previously abnormal heart valve.
SYN: SEE: endocarditis viridans

Endocarditis caused by the extension of syphilis from the aorta to the aortic valves.

Endocarditis caused by Mycobacterium tuberculosis.

A rapidly destructive form of acute bacterial endocarditis characterized by necrosis or ulceration of the valves.

Endocarditis affecting the heart valves and not the inner lining of the heart.

Endocarditis associated with fibrinous clots on ulcerated valvular surfaces.

SEE: Nonbacterial thrombotic endocarditis.

SEE: Subacute bacterial endocarditis.