Endocarditis: Difference between revisions
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* [http://www.mitralvalverepair.org/content/view/163/Acute Endocarditis, Embolic Stroke] |
* [http://www.mitralvalverepair.org/content/view/163/Acute Endocarditis, Embolic Stroke] |
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*[http://www.biofilmcommunity.org/ Biofilm Research, News, Biofilm-specific Interviews] |
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Revision as of 16:36, 31 March 2012
| Endocarditis | |
|---|---|
| Specialty | Cardiology, infectious disease  |
Endocarditis is an inflammation of the inner layer of the heart, the endocardium. It usually involves the heart valves (native or prosthetic valves). Other structures that may be involved include the interventricular septum, the chordae tendineae, the mural endocardium, or even on intracardiac devices. Endocarditis is characterized by a prototypic lesion, the vegetation, which is a mass of platelets, fibrin, microcolonies of microorganisms, and scant inflammatory cells.[1] In the subacute form of infective endocarditis, the vegetation may also include a center of granulomatous tissue, which may fibrose or calcify.[2]
There are multiple ways to classify endocarditis. The simplest classification is based on etiology: either infective or non-infective, depending on whether a microorganism is the source of the inflammation or not. Regardless, diagnosis of endocarditis is based on the clinical features, investigations such as echocardiogram, as well as any blood cultures demonstrating the presence of endocarditis-causing microorganisms.
Infective endocarditis
Since the valves of the heart do not receive any dedicated blood supply, defensive immune mechanisms (such as white blood cells) cannot directly reach the valves via the bloodstream. If an organism (such as bacteria) attaches to a valve surface and forms a vegetation, the host immune response is blunted. The lack of blood supply to the valves also has implications on treatment, since drugs also have difficulty reaching the infected valve.
Normally, blood flows smoothly through these valves. If they have been damaged (from rheumatic fever, for example) the risk of bacteria attachment is increased.[2]
Non-infective endocarditis
Nonbacterial thrombic endocarditis (NBTE) or marantic endocarditis is most commonly found on previously undamaged valves.[2] As opposed to infective endocarditis, the vegetations in NBTE are small, sterile, and tend to aggregate along the edges of the valve or the cusps.[2] Also unlike infective endocarditis, NBTE does not cause an inflammation response from the body.[2] NBTE usually occurs during a hypercoagulable state such as system wide bacterial infection, or pregnancy, though it is also sometimes seen in patients with venous catheters.[2] NBTE may also occur in patients with cancers, particularly mucinous adenocarcinoma[2] where Trousseau syndrome can be encountered. Typically NBTE does not cause many problems on its own, but parts of the vegetations may break off and embolize to the heart or brain, or they may serve as a focus where bacteria can lodge, thus causing infective endocarditis.[2]
Another form of sterile endocarditis, is termed Libman-Sacks endocarditis; this form occurs more often in patients with lupus erythematosus and is thought to be due to the deposition of immune complexes.[2] Like NBTE, Libman-Sacks endocarditis involves small vegetations, while infective endocarditis is composed of large vegetations.[2] These immune complexes precipitate an inflammation reaction, which helps to differentiate it from NBTE. Also unlike NBTE, Libman-Sacks endocarditis does not seem to have a preferred location of deposition and may form on the undersurfaces of the valves or even on the endocardium.[2]
References
- ^ Kasper DL, Brunwald E, Fauci AS, Hauser S, Longo DL, Jameson JL (2005). Harrison's Principles of Internal Medicine. McGraw-Hill. pp. 731–40. ISBN 0-07-139140-1. OCLC 54501403 56437106 56801936 56967424.
{{cite book}}: Check|oclc=value (help); Unknown parameter|month=ignored (help)CS1 maint: multiple names: authors list (link) - ^ a b c d e f g h i j k Mitchell RS, Kumar V, Robbins SL, Abbas AK, Fausto N (2007). Robbins Basic Pathology (8th ed.). Saunders/Elsevier. pp. 406–8. ISBN 1-4160-2973-7.
{{cite book}}: CS1 maint: multiple names: authors list (link)
3. Filsoufi F, Carpentier A. www.themitralvalve.org