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Regional drug slang for five US dollars’ worth of drugs—named after Abraham Lincoln, who appears on $5-dollar bills.
Segen's Medical Dictionary. © 2012 Farlex, Inc. All rights reserved.


(en?do-kar-di'tis) [? + ? + itis, inflammation]
Infection or inflammation of the heart valves or of the lining of the heart. In day-to-day clinical speech, this word is often used to mean “infective endocarditis.” See: infective endocarditis

acute bacterial endocarditis

Abbreviation: 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

atypical verrucous endocarditis

An infrequently used term for nonbacterial thrombotic endocarditis.

culture-negative 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
Enlarge picture

infective endocarditis

Abbreviation: IE
Endocarditis caused by any microorganism, esp. any species of streptococci or staphylococci, and less often by Haemophilus spp. or other HACEK bacteria (e.g., 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 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. The incidence in the U.S. is about 2 to 4 cases per 100,000. Patients who are elderly 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.


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 (e.g., 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's nodes or Janeway lesions). Cottonwool spots may be seen on the retinas of some affected persons. See: illustration


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 (e.g., 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. Occasionally, a patient who dies of a febrile illness may be found to have infective vegetations on the heart valves at autopsy.


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 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.


Many patients recover after treatment with prolonged courses of parenteral antibiotics. Some (e.g., those with heart failure or severely injured hearts) may not respond without surgery to replace damaged valves or débride abscesses within the myocardium.

Patient care

During the acute phase of treatment, patients are monitored for signs and symptoms of heart failure (e.g., dyspnea, orthopnea, crackles, dependent edema, changes in the heart murmur, and a postsystolic gallop), cerebral emboli (e.g., paralysis, aphasias, changes in mental status), and embolization to the kidney (e.g., decreased urine output, hematuria); lung involvement (e.g., dyspnea, cough, egophony, hemoptysis, pleuritic pain, or friction rub) or spleen involvement (e.g., left upper quadrant abdominal pain radiating to the left shoulder, abdominal rigidity); and peripheral vascular occlusion (e.g., 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 aminoglycoside or vancomycin is given) to maintain therapeutic levels and prevent toxicity. Supportive treatment includes bedrest, 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.


The American Heart Association recommends that patients at high risk for endocarditis should receive prophylactic antibiotics prior to many procedures, including dental and periodontal cleanings and extractions, intraligamentary local anesthetic injections, tonsillectomy, adenoidectomy, bronchoscopy with rigid instrument, 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.

Libman-Sacks endocarditis

See: Libman-Sacks endocarditis

Löffler's endocarditis

See: Löffler's endocarditis

malignant endocarditis

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

mural endocarditis

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

native valve endocarditis

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

nonbacterial thrombotic endocarditis

Abbreviation: 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. Synonym: verrucous endocarditis

prosthetic valve endocarditis

Bacterial infection of a surgically implanted artificial heart valve.

rheumatic endocarditis

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

right-sided endocarditis

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.

subacute bacterial endocarditis

Abbreviation: 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 (e.g., viridans group streptococci). The infection often develops on a previously abnormal heart valve. Synonym: endocarditis viridans

syphilitic endocarditis

Endocarditis due to syphilis having extended from the aorta to the aortic valves.

tuberculous endocarditis

Endocarditis caused by Mycobacterium tuberculosis.

ulcerative endocarditis

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

valvular endocarditis

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

vegetative endocarditis

Endocarditis associated with fibrinous clots on ulcerated valvular surfaces.

verrucous endocarditis

Nonbacterial thrombotic endocarditis.

endocarditis viridans

Subacute bacterial endocarditis.

acute bacterial endocarditis

Abbreviation: 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
See also: endocarditis
Medical Dictionary, © 2009 Farlex and Partners