Endocarditis overview
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Associate Editor-in-Chief: Cafer Zorkun, M.D., Ph.D. [2]
Please Join in Editing This Page and Apply to be an Editor-In-Chief for this topic: There can be one or more than one Editor-In-Chief. You may also apply to be an Associate Editor-In-Chief of one of the subtopics below. Please mail us [3] to indicate your interest in serving either as an Editor-In-Chief of the entire topic or as an Associate Editor-In-Chief for a subtopic. Please be sure to attach your CV and or biographical sketch.
Overview of Endocarditis
Endocarditis is an inflammation of the inner layer of the heart, the endocardium. The most common structures involved are the heart valves.
Endocarditis can be classified by etiology as either non-infective or infective, depending on whether a microorganism is the source of the problem.
Traditionally, infective endocarditis has been clinically divided into acute and subacute (because the patients tend to live longer in subacute as opposed to acute) endocarditis. This classifies both the rate of progression and severity of disease. Thus subacute bacterial endocarditis (SBE) is often due to streptococci of low virulence and mild to moderate illness which progresses slowly over weeks and months, while acute bacterial endocarditis (ABE) is a fulminant illness over days to weeks, and is more likely due to Staphylococcus aureus which has much greater virulence, or disease-producing capacity.
This terminology is now discouraged. The terms short incubation (meaning less than about six weeks), and long incubation (greater than about six weeks) are preferred.
Infective endocarditis may also be classified as culture-positive or culture-negative. Culture-negative endocarditis is due to micro-organisms that require a longer period of time to be identified in the laboratory. Such organisms are said to be 'fastidious' because they have demanding growth requirements. Some pathogens responsible for culture-negative endocarditis include Aspergillus species, Brucella species, Coxiella burnetii, Chlamydia species, and HACEK bacteria.
Finally, the distinction between native-valve endocarditis and prosthetic-valve endocarditis is clinically important. Prosthetic-valve endocarditis constitutes 10-20% of cases of endocarditis. The greatest risk is during the first 6 months after valve surgery. Staphylococcus epidermidis is the most common cause. The infection often extends into the anulus and cardiac tissues.
Patients who inject narcotics intravenously may introduce infection which will travel to the right side of the heart. In other patients without a history of intravenous exposure, endocarditis is more frequently left-sided.
Non-infective endocarditis
Non-infective or marantic endocarditis is rare. A form of sterile endocarditis is termed Libman-Sacks endocarditis; this form occurs more often in patients with lupus erythematosus and the antiphospholipid syndrome. Non-infective endocarditis may also occur in patients with cancer, particularly mucinous adenocarcinoma.
Infective endocarditis
Given the poor vascular supply of the heart valves, entrance of infection fighting components of the bloodstream (such as white blood cells) are reduced. So if an organism (such as bacteria) establishes a foothold in the valves, the bodies ability to fight the infection inside the valve structures is reduced.
Normally, blood flows smoothly through these valves. If they have been damaged (for instance in rheumatic fever) the trauma of non-laminar flow can increase the risk of infection.