Non-bacterial thrombotic endocarditis pathophysiology: Difference between revisions
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==Overview== | ==Overview== | ||
Although the exact [[pathogenesis]] of [[non-bacterial thrombotic endocarditis]] is not completely understood, [[Endothelial dysfunction|endothelial injury]] correlated with a [[hypercoagulable state]] has been implicated. Pathogenesis can be sub-sectioned into four factors thought to be involved in instigating NBTE. These include; [[Immune complexes]][[Hypoxia|, Hypoxia]] , [[Hypercoagulability]], and[[Carcinomatosis]]. Conditions associated with nonbacterial thrombotic endocarditis include; [[Malignancies]], [[Systemic autoimmune diseases]] ([[Systemic lupus erythematosus|SLE]] is the most common,[[Hypercoagulable states]], Chronic inflammatory states, [[Heart failure]] with [[Valve dysfunction|valvulopathy]], e.t.c. | |||
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==Pathophysiology== | ==Pathophysiology== | ||
Revision as of 18:23, 6 August 2020
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aisha Adigun, B.Sc., M.D.[2]
Overview
Although the exact pathogenesis of non-bacterial thrombotic endocarditis is not completely understood, endothelial injury correlated with a hypercoagulable state has been implicated. Pathogenesis can be sub-sectioned into four factors thought to be involved in instigating NBTE. These include; Immune complexes, Hypoxia , Hypercoagulability, andCarcinomatosis. Conditions associated with nonbacterial thrombotic endocarditis include; Malignancies, Systemic autoimmune diseases (SLE is the most common,Hypercoagulable states, Chronic inflammatory states, Heart failure with valvulopathy, e.t.c.
Pathophysiology
Pathogenesis
- Although the exact pathogenesis of non-bacterial thrombotic endocarditis is not completely understood[1], endothelial injury correlated with a hypercoagulable state has been implicated.
- The main culprit that has been identified is damage to the endothelium and consequent exposure of subendothelial connective tissue to circulating platelets, platelet deposition and the formation of initial thrombi by the migration of inflammatory mononuclear cells[2].
- Pathogenesis can be sub-sectioned into four factors thought to be involved in instigating NBTE. These include[3];
Immune Complexes
- Circulating immune complexes were first identified in the formation of NBTE by Williams in 1980[9].
- Since that time, immunohistochemical techniques have been used to identify immunoglobulin and complement deposits within vessel walls in the zone of neovascularization of verrucose valvular lesions.[10]
- These findings are especially found in patients with systemic lupus erythematosus (SLE)[11].
Hypoxia
- Several studies have associated hypoxia with NBTE[12][13][14].
- These studies were conducted in both human[13][12] and animal[14] models and they found that, increased or persistent exposure to hypoxic insult can lead to an increase in circulating tissue factor.
- Tissue factor has been found to lead to a hypercoagulable state, which may have predisposed the studied patient populations to NBTE[12].
Hypercoagulability
- The association between thrombosis and malignancy was first described by Trousseau in 1866[15].
- In 1956 Robbins and MacDonald[16] hypothesized that valvular degeneration and hypercoagulable state played significant roles in the origin/formation of NBTE.
Carcinomatosis
- The relationship between carcinomatosis and NBTE has been vastly studied and established[17].
- 50% of malignancies associated with NBTEs are adenocarcinomas of the lung and ovary[18][19].
- It has been established that malignancies place patients in a hypercoagulable state which can then predispose them to valvular damage, clot formation, and NBTE[20].
- The mitral valve is most commonly affected in NBTE, followed by the aortic valve and less frequently, the tricuspid valve[21].
- The vegetations in NTBE are formed from the strands consisting of fibrin, immune complexes, neutrophils, lymphocytes, and histiocytes[22].
- As there is some inflammatory reaction at the site of attachment of vegetation, they can easily dislodge, embolize and cause serious infarctions[23].
Associated Conditions
Conditions associated with nonbacterial thrombotic endocarditis include[1][24]:
- Malignancies
- Systemic autoimmune diseases (SLE is the most common)
- Hypercoagulable states
- Chronic inflammatory states
- Heart failure with valvulopathy
Gross Pathology
- On gross pathology, small (1-5mm) and sterile vegetations that occur on normal cardiac valves, and are composed of platelets and fibrin are characteristic findings in NBTE[25].
Microscopic Pathology
On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
References
- ↑ 1.0 1.1 "Non-bacterial Thrombotic Endocarditis | IntechOpen".
- ↑ Liu J, Frishman WH (2016). "Nonbacterial Thrombotic Endocarditis: Pathogenesis, Diagnosis, and Management". Cardiol Rev. 24 (5): 244–7. doi:10.1097/CRD.0000000000000106. PMID 27501336.
- ↑ Beck ML, Freihaut B, Henry R, Pierce S, Bayer WL, Hendrickson WA, Ward KB, Wolf P, Feller K, Femmer K, Mohn GR (January 1975). "A serum haemagglutinating property dependent upon polycarboxyl groups". Br. J. Haematol. 29 (1): 149–56. doi:10.1111/j.1365-2141.1975.tb01808.x. PMID 32.
- ↑ Williams R.C.Jr.. Immune complexes in clinical and experimental medicine, 19801st ed. p. 12
- ↑ Nakanishi K., Tajima F., Nakata Y., Osada H., Ogata K., Kawai T., Torikata C., Suga T., Takishima K., Aurues T., Ikeda T.. Tissue factor is associated with the nonbacterial thrombotic endocarditis induced by a hypobaric hypoxic environment in rats, Virchows Arch, 1998, vol. 433 (pg. 375-379)
- ↑ Dutta T., Karas M.G., Segal A.Z., Kizer J.R.. Yield of transesophageal echocardiography for nonbacterial thrombotic endocarditis and other cardiac sources of embolism in cancer patients with cerebral ischemia, Am J Cardiol, 2006, vol. 97 6(pg. 894-898)
- ↑ MacDonald R.A., Robbins S.L.. The significance of nonbacterial thrombotic endocarditis: an autopsy and clinical study of 78 cases, Am Intern Med, 1957, vol. 46 (pg. 255-273)
- ↑ "Nonbacterial thrombotic endocarditis in cancer patients: Comparison of characteristics of patients with and without concomitant disseminated intravascular coagulation - Bedikian - 1978 - Medical and Pediatric Oncology - Wiley Online Library".
- ↑ Williams R.C.Jr.. Immune complexes in clinical and experimental medicine, 19801st ed. p. 12
- ↑ Shapiro RF, Gamble CN, Wiesner KB, Castles JJ, Wolf AW, Hurley EJ, Salel AF (December 1977). "Immunopathogenesis of Libman-Sacks endocarditis. Assessment by light and immunofluorescent microscopy in two patients". Ann. Rheum. Dis. 36 (6): 508–16. doi:10.1136/ard.36.6.508. PMC 1000155. PMID 339850.
- ↑ Nydegger UE, Lambert PH, Gerber H, Miescher PA (August 1974). "Circulating immune complexes in the serum in systemic lupus erythematosus and in carriers of hepatitis B antigen. Quantitation by binding to radiolabeled C1q". J. Clin. Invest. 54 (2): 297–309. doi:10.1172/JCI107765. PMC 301557. PMID 4847246.
- ↑ 12.0 12.1 12.2 Dutta T, Karas MG, Segal AZ, Kizer JR (March 2006). "Yield of transesophageal echocardiography for nonbacterial thrombotic endocarditis and other cardiac sources of embolism in cancer patients with cerebral ischemia". Am. J. Cardiol. 97 (6): 894–8. doi:10.1016/j.amjcard.2005.09.140. PMID 16516597.
- ↑ 13.0 13.1 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.
- ↑ 14.0 14.1 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.
- ↑ Metharom P, Falasca M, Berndt MC (January 2019). "The History of Armand Trousseau and Cancer-Associated Thrombosis". Cancers (Basel). 11 (2). doi:10.3390/cancers11020158. PMC 6406548. PMID 30708967.
- ↑ "THE SIGNIFICANCE OF NONBACTERIAL THROMBOTIC ENDOCARDITIS: AN AUTOPSY AND CLINICAL STUDY OF 78 CASES | Annals of Internal Medicine".
- ↑ Sanjay Asopa, Anish Patel, Omar A. Khan, Rajan Sharma, Sunil K. Ohri, Non-bacterial thrombotic endocarditis, European Journal of Cardio-Thoracic Surgery, Volume 32, Issue 5, November 2007, Pages 696–701, https://doi.org/10.1016/j.ejcts.2007.07.029
- ↑ Borowski A, Ghodsizad A, Cohnen M, Gams E (June 2005). "Recurrent embolism in the course of marantic endocarditis". Ann. Thorac. Surg. 79 (6): 2145–7. doi:10.1016/j.athoracsur.2003.12.024. PMID 15919332.
- ↑ Suzuki S, Tanaka K, Nogawa S, Umezawa A, Hata J, Fukuuchi Y (2002). "Expression of interleukin-6 in cerebral neurons and ovarian cancer tissue in Trousseau syndrome". Clin. Neuropathol. 21 (5): 232–5. PMID 12365726.
- ↑ "www.cancertherapyadvisor.com".
- ↑ Zakka K, Zakka P, Davarpanah A, Koshkelashvili N, Bilen MA, Owonikoko T, El-Rayes B, Akce M (2020). "Nonbacterial Thrombotic Endocarditis and Widespread Skin Necrosis in Newly Diagnosed Lung Adenocarcinoma". Case Rep Oncol. 13 (1): 239–244. doi:10.1159/000506453. PMC 7154248 Check
|pmc=value (help). PMID 32308583 Check|pmid=value (help). - ↑ Eiken PW, Edwards WD, Tazelaar HD, McBane RD, Zehr KJ (December 2001). "Surgical pathology of nonbacterial thrombotic endocarditis in 30 patients, 1985-2000". Mayo Clin. Proc. 76 (12): 1204–12. doi:10.4065/76.12.1204. PMID 11761501.
- ↑ Roldan CA, Sibbitt WL, Qualls CR, Jung RE, Greene ER, Gasparovic CM, Hayek RA, Charlton GA, Crookston K (September 2013). "Libman-Sacks endocarditis and embolic cerebrovascular disease". JACC Cardiovasc Imaging. 6 (9): 973–83. doi:10.1016/j.jcmg.2013.04.012. PMC 3941465. PMID 24029368.
- ↑ "Nonbacterial Thrombotic Endocarditis: Clinicopathologic Study of a Necropsy Series | Revista Española de Cardiología (English Edition)".
- ↑ "Cvs ie-csbrp".