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* The exact pathogenesis of nonbacterial thrombotic endocarditis is not completely understood.
* The exact pathogenesis of nonbacterial thrombotic endocarditis is not completely understood.
*[[Nonbacterial thrombotic endocarditis]] (NBTE), also called '''marantic endocarditis''' is most commonly found on previously undamaged valves.
*The vegetations in nonbacterial thrombotic endocarditis are sterile and small.
*The vegetations mostly aggregate at the edges of the valve or the cusps.
* We can divide the pathogenesis pathway of nonbacterial endocarditis into to phase:
* We can divide the pathogenesis pathway of nonbacterial endocarditis into to phase:
** Initiating phase
** Initiating phase
Line 58: Line 61:
****Some studies demonstrated that hypoxia may lead to tissue factor activation.
****Some studies demonstrated that hypoxia may lead to tissue factor activation.
****Higher tissue factor level has an association with higher rate of endocarditis.
****Higher tissue factor level has an association with higher rate of endocarditis.
****Other studies implies that the rate of endocarditis is higher in smokers and patients with chronic lung disease and possibly hypoxia.  
****Other studies implies that the rate of endocarditis is higher in smokers and patients with chronic lung disease and possibly hypoxia.
*** Hypercoagulability<ref name="pmid13403513">{{cite journal |vauthors=MACDONALD RA, ROBBINS SL |title=The significance of nonbacterial thrombotic endocarditis:  an autopsy and clinical study of 78 cases |journal=Ann. Intern. Med. |volume=46 |issue=2 |pages=255–73 |date=February 1957 |pmid=13403513 |doi=10.7326/0003-4819-46-2-255 |url=}}</ref><ref name="pmid834136">{{cite journal |vauthors=Sack GH, Levin J, Bell WR |title=Trousseau's syndrome and other manifestations of chronic disseminated coagulopathy in patients with neoplasms: clinical, pathophysiologic, and therapeutic features |journal=Medicine (Baltimore) |volume=56 |issue=1 |pages=1–37 |date=January 1977 |pmid=834136 |doi= |url=}}</ref>
*** Hypercoagulability<ref name="pmid13403513">{{cite journal |vauthors=MACDONALD RA, ROBBINS SL |title=The significance of nonbacterial thrombotic endocarditis:  an autopsy and clinical study of 78 cases |journal=Ann. Intern. Med. |volume=46 |issue=2 |pages=255–73 |date=February 1957 |pmid=13403513 |doi=10.7326/0003-4819-46-2-255 |url=}}</ref><ref name="pmid834136">{{cite journal |vauthors=Sack GH, Levin J, Bell WR |title=Trousseau's syndrome and other manifestations of chronic disseminated coagulopathy in patients with neoplasms: clinical, pathophysiologic, and therapeutic features |journal=Medicine (Baltimore) |volume=56 |issue=1 |pages=1–37 |date=January 1977 |pmid=834136 |doi= |url=}}</ref>
****There is an association between hypercoagulable state and clotting factor abnormalities with initiation of nonbacterial thrombotic endocarditis.
****There is an association between hypercoagulable state and clotting factor abnormalities with initiation of nonbacterial thrombotic endocarditis.
Line 69: Line 72:
*****
*****
** Verrucae formation
** Verrucae formation
*[[Nonbacterial thrombotic endocarditis]] (NBTE), also called '''marantic endocarditis''' is most commonly found on previously undamaged valves.
*The vegetations in NBTE are small, sterile, and tend to aggregate along the edges of the valve or the cusps.
*Unlike infective endocarditis, NBTE does not cause an inflammation response from the body.
*NBTE usually occurs due to hypercoaguable states such as systemic bacterial infection or pregnancy.
*NBTE may also occur in patients with [[cancer]], particularly mucinous [[adenocarcinoma]].
*[[Libman-Sacks endocarditis]] is another form of sterile endocarditis; this form occurs more often in patients with [[lupus erythematosus]] and is thought to be due to the deposition of immune complexes.
*[[Libman-Sacks endocarditis]] involves small vegetations, while infective endocarditis is composed of large vegetations.
*These immune complexes precipitate an inflammatory reaction, which helps to differentiate it from NBTE.
*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.<ref name="endo"> Endocarditis. Wikipedia (2015). https://en.wikipedia.org/wiki/Endocarditis Accessed on September 21, 2015</ref>


== Genetics ==
== Genetics ==

Revision as of 16:35, 2 January 2020

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Maliha Shakil, M.D. [2]

Overview

The pathogenesis of infective endocarditis includes valvular damage, altered and turbulent flow, bacteremia, and lack of blood supply to the valves. Damaged endothelium becomes a site for attachment of infectious agents in infectious endocarditis. Nonbacterial thrombotic endocarditis is related to hypercoaguable states such as pregnancy or systemic bacterial infection. The characteristic lesion of endocarditis is a vegetation. Vegetations are composed of fibrin, inflammatory cells, platelets, and microorganisms.

Pathophysiology

Pathogenesis

Infective Endocarditis

  • The pathogenesis of infective endocarditis includes:[1][2]
Pathogenic Factors Mechanism
Valvular Damage
  • Altered and turbulent flow
  • Catheters, electrodes, and other intracardiac devices
  • Solid particles from repeated intravenous injections
  • Chronic inflammation
Bacteremia
Lack of blood supply to valves
  • Blunted immune response
  • Therapeutic drugs have difficulty reaching infected valves

Nonbacterial Thrombotic Endocarditis

  • The exact pathogenesis of nonbacterial thrombotic endocarditis is not completely understood.
  • Nonbacterial thrombotic endocarditis (NBTE), also called marantic endocarditis is most commonly found on previously undamaged valves.
  • The vegetations in nonbacterial thrombotic endocarditis are sterile and small.
  • The vegetations mostly aggregate at the edges of the valve or the cusps.
  • We can divide the pathogenesis pathway of nonbacterial endocarditis into to phase:
    • Initiating phase
      • Immune complexes[3][4]
        • circulating immune complexes and complement deposition can initiate the process.
        • The example for this initiating factor in libman sacks endocarditis in lupus patients.
      • Hypoxia[5][6]
        • Some studies demonstrated that hypoxia may lead to tissue factor activation.
        • Higher tissue factor level has an association with higher rate of endocarditis.
        • Other studies implies that the rate of endocarditis is higher in smokers and patients with chronic lung disease and possibly hypoxia.
      • Hypercoagulability[7][8]
        • There is an association between hypercoagulable state and clotting factor abnormalities with initiation of nonbacterial thrombotic endocarditis.
      • Carcinomatosis[9]
        • The association between cancer and nonbacterial thrombotic endocarditis is well established.
        • In most of the cases of cancer related endocarditis we have abnormal activity of tissue factor.
        • Tissue factor may be secreted from promyelocytic leukaemia cells.
        • Tissue factor may be expressed on the surface of adenocarcinoma cells which leads to increased expression of tissue factor by endothelial cells.
    • Verrucae formation

Genetics

Associated Conditions

Gross Pathology

Microscopic Pathology

Gross and Microscopic Pathology

The characteristic lesion of endocarditis is a vegetation. Vegetations are composed of fibrin, inflammatory cells, platelets, and microorganisms.[10] Characteristic features of endocarditis on gross pathology and histopathological analysis include:[11]

Endocarditis Subtype Features on Gross Pathology Features on Histopathological Microscopic Analysis
Infective Endocarditis
  • Left-sided valve involvement (mitral, aortic) more common generally
  • Right-sided valve involvement (pulmonic, tricuspid valve) more common in intravenous drug abusers
  • Valvular vegetations
  • Valvular destruction
  • Inflammatory infiltrate
  • Abundant neutrophils
  • Plasma cells may be present in subacute endocarditis
  • Microorganisms present
Nonbacterial Thrombotic Endocarditis
  • Round non-destructive vegetations, usually at the line of closure
  • Vegetations without inflammation and microorganisms

Image courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology

  • Heart; Breast intraductal papilloma metastasis. Thrombotic Nonbacterial Endocarditis (Infected): Gross mitral valve natural color vegetations well illustrated these were secondarily infected with staphylococcus case of 8 year survival breast intraductal papillary adenocarcinoma with extensive metastases. Aortic valve also involved.

    Heart; Breast intraductal papilloma metastasis. Thrombotic Nonbacterial Endocarditis (Infected): Gross mitral valve natural color vegetations well illustrated these were secondarily infected with staphylococcus case of 8 year survival breast intraductal papillary adenocarcinoma with extensive metastases. Aortic valve also involved.

  • Nonbacterial Thrombotic Endocarditis Infected: Micro low mag H&E fibrin vegetation with masses of staphylococci and inflammatory cells in valve secondarily infected case 8 year survival breast papillary intraductal adenocarcinoma with extensive metastases gross is aortic valve lesions.

    Nonbacterial Thrombotic Endocarditis Infected: Micro low mag H&E fibrin vegetation with masses of staphylococci and inflammatory cells in valve secondarily infected case 8 year survival breast papillary intraductal adenocarcinoma with extensive metastases gross is aortic valve lesions.

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References

  1. ↑ Infective endocarditis. Wikipedia (2015). https://en.wikipedia.org/wiki/Infective_endocarditis#Pathogenesis Accessed on September 21, 2015
  2. ↑ Endocarditis. Wikipedia (2015). https://en.wikipedia.org/wiki/Endocarditis Accessed on September 21, 2015
  3. ↑ Ford PM, Ford SE, Lillicrap DP (April 1988). "Association of lupus anticoagulant with severe valvular heart disease in systemic lupus erythematosus". J. Rheumatol. 15 (4): 597–600. PMID 3135393.
  4. ↑ Williams, Ralph (1980). Immune complexes in clinical and experimental medicine. Cambridge, Mass: Harvard University Press. ISBN 978-0674444386.
  5. ↑ Nakanishi K, Tajima F, Nakata Y, Osada H, Ogata K, Kawai T, Torikata C, Suga T, Takishima K, Aurues T, Ikeda T (October 1998). "Tissue factor is associated with the nonbacterial thrombotic endocarditis induced by a hypobaric hypoxic environment in rats". Virchows Arch. 433 (4): 375–9. doi:10.1007/s004280050262. PMID 9808440.
  6. ↑ Truskinovsky AM, Hutchins GM (April 2001). "Association between nonbacterial thrombotic endocarditis and hypoxigenic pulmonary diseases". Virchows Arch. 438 (4): 357–61. doi:10.1007/s004280000372. PMID 11355169.
  7. ↑ MACDONALD RA, ROBBINS SL (February 1957). "The significance of nonbacterial thrombotic endocarditis: an autopsy and clinical study of 78 cases". Ann. Intern. Med. 46 (2): 255–73. doi:10.7326/0003-4819-46-2-255. PMID 13403513.
  8. ↑ Sack GH, Levin J, Bell WR (January 1977). "Trousseau's syndrome and other manifestations of chronic disseminated coagulopathy in patients with neoplasms: clinical, pathophysiologic, and therapeutic features". Medicine (Baltimore). 56 (1): 1–37. PMID 834136.
  9. ↑ Gralnick HR, Abrell E (January 1973). "Studies of the procoagulant and fibrinolytic activity of promyelocytes in acute promyelocytic leukaemia". Br. J. Haematol. 24 (1): 89–99. doi:10.1111/j.1365-2141.1973.tb05730.x. PMID 4577065.
  10. ↑ Mylonakis E, Calderwood SB (2001). "Infective endocarditis in adults". N Engl J Med. 345 (18): 1318–30. doi:10.1056/NEJMra010082. PMID 11794152.
  11. ↑ Infective Endocarditis. Libre Pathology (2015). URL=http://librepathology.org/wiki/index.php/Infective_endocarditis Accessed on September 21, 2015

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