Myxoma pathophysiology: Difference between revisions
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==Overview== | ==Overview== | ||
Cardiac myxoma is a benign intracavitary endocardial mass that represents the most common primary tumor of the heart.<ref name="pmid10903697">{{cite journal |vauthors=Grebenc ML, Rosado de Christenson ML, Burke AP, Green CE, Galvin JR |title=Primary cardiac and pericardial neoplasms: radiologic-pathologic correlation |journal=Radiographics |volume=20 |issue=4 |pages=1073–103; quiz 1110–1, 1112 |year=2000 |pmid=10903697 |doi=10.1148/radiographics.20.4.g00jl081073 |url=}}</ref> | Cardiac myxoma is a benign intracavitary endocardial mass that represents the most common primary tumor of the heart.<ref name="pmid10903697">{{cite journal |vauthors=Grebenc ML, Rosado de Christenson ML, Burke AP, Green CE, Galvin JR |title=Primary cardiac and pericardial neoplasms: radiologic-pathologic correlation |journal=Radiographics |volume=20 |issue=4 |pages=1073–103; quiz 1110–1, 1112 |year=2000 |pmid=10903697 |doi=10.1148/radiographics.20.4.g00jl081073 |url=}}</ref> Myxoma cells are characterized by undifferentiated mesenchymal cells, which potentially differentiate into many [[tissues]] such as [[blood vessels]], [[glandular]] structures, [[bones]], and source of extramedullary [[hematopoiesis]].<ref name="pmid433739">{{cite journal |vauthors=Bulkley BH, Hutchins GM |title=Atrial myxomas: a fifty year review |journal=Am. Heart J. |volume=97 |issue=5 |pages=639–43 |year=1979 |pmid=433739 |doi= |url=}}</ref> The primary distribution of cardiac myxoma is the [[left atrium]] (75%) of the heart, regularly they tend to be located in the [[fossa ovalis]] and endocardium of the [[atrial septum]]. | ||
==Pathogenesis== | ==Pathogenesis== | ||
Cardiac myxoma arises from remnants of subendocardial vasoformative reserve cells, which are primitive [[mesenchymal]] cells that are normally involved in the supportive structure of the [[endocardium]]. <ref name="pmid10064365">{{cite journal |vauthors=Roscher AA, Kato NS, Quan H, Padmanabhan M |title=Intra-atrial myxomas, clinical-pathologic correlation based on two case studies including historical review |journal=J Cardiovasc Surg (Torino) |volume=37 |issue=6 Suppl 1 |pages=131–7 |year=1996 |pmid=10064365 |doi= |url=}}</ref> <ref name="pmid11737312">{{cite journal |vauthors=Acebo E, Val-Bernal JF, Gómez-Román JJ |title=Prichard's structures of the fossa ovalis are not histogenetically related to cardiac myxoma |journal=Histopathology |volume=39 |issue=5 |pages=529–35 |year=2001 |pmid=11737312 |doi= |url=}}</ref>The true origin of cardiac myxomas still remains unclear. Recent studies<ref name="pmid16508920">{{cite journal |vauthors=Orlandi A, Ciucci A, Ferlosio A, Genta R, Spagnoli LG, Gabbiani G |title=Cardiac myxoma cells exhibit embryonic endocardial stem cell features |journal=J. Pathol. |volume=209 |issue=2 |pages=231–9 |year=2006 |pmid=16508920 |doi=10.1002/path.1959 |url=}}</ref><ref name="pmid13129418">{{cite journal |vauthors=Amano J, Kono T, Wada Y, Zhang T, Koide N, Fujimori M, Ito K |title=Cardiac myxoma: its origin and tumor characteristics |journal=Ann Thorac Cardiovasc Surg |volume=9 |issue=4 |pages=215–21 |year=2003 |pmid=13129418 |doi= |url=}}</ref> | Cardiac myxoma arises from remnants of subendocardial vasoformative reserve cells, which are primitive [[mesenchymal]] cells that are normally involved in the supportive structure of the [[endocardium]].<ref name="pmid10064365">{{cite journal |vauthors=Roscher AA, Kato NS, Quan H, Padmanabhan M |title=Intra-atrial myxomas, clinical-pathologic correlation based on two case studies including historical review |journal=J Cardiovasc Surg (Torino) |volume=37 |issue=6 Suppl 1 |pages=131–7 |year=1996 |pmid=10064365 |doi= |url=}}</ref><ref name="pmid11737312">{{cite journal |vauthors=Acebo E, Val-Bernal JF, Gómez-Román JJ |title=Prichard's structures of the fossa ovalis are not histogenetically related to cardiac myxoma |journal=Histopathology |volume=39 |issue=5 |pages=529–35 |year=2001 |pmid=11737312 |doi= |url=}}</ref> The true origin of cardiac myxomas still remains unclear. Recent studies suggest several theories to support the histopathogensis of this type of myxoid tumor; such as, the neoplastic theory, dysembryoplastic theory, histopathogenesis of glandular cells in myxoma and the thrombotic theory.<ref name="pmid16508920">{{cite journal |vauthors=Orlandi A, Ciucci A, Ferlosio A, Genta R, Spagnoli LG, Gabbiani G |title=Cardiac myxoma cells exhibit embryonic endocardial stem cell features |journal=J. Pathol. |volume=209 |issue=2 |pages=231–9 |year=2006 |pmid=16508920 |doi=10.1002/path.1959 |url=}}</ref><ref name="pmid13129418">{{cite journal |vauthors=Amano J, Kono T, Wada Y, Zhang T, Koide N, Fujimori M, Ito K |title=Cardiac myxoma: its origin and tumor characteristics |journal=Ann Thorac Cardiovasc Surg |volume=9 |issue=4 |pages=215–21 |year=2003 |pmid=13129418 |doi= |url=}}</ref> | ||
==Genetics== | ==Genetics== | ||
Single cardiac myxomas and familial forms are related with several chromosome and gene alterations which involve cardiac development. | Single cardiac myxomas and familial forms are related with several chromosome and gene alterations which involve cardiac development. | ||
Inherited myxomas are usually presented in the [[Carney complex]]. The development of this syndrome is a result of [[PRKAR1A]] gene inactivation mutation that is associated with [[chromosome]] 17q24.2-q24.3. This gene plays an important role in cardiac development and myxomagenesis. The expression of PRKAR1A causes myxomatous changes in the endocardium.<ref name="pmid26416542">{{cite journal |vauthors=Sun Y, Chen X, Sun J, Wen X, Liu X, Zhang Y, Hoffman AR, Hu JF, Gao Y |title=A Novel Inherited Mutation in PRKAR1A Abrogates PreRNA Splicing in a Carney Complex Family |journal=Can J Cardiol |volume=31 |issue=11 |pages=1393–401 |year=2015 |pmid=26416542 |doi=10.1016/j.cjca.2015.05.018 |url=}}</ref> | Inherited myxomas are usually presented in the [[Carney complex]]. The development of this syndrome is a result of [[PRKAR1A]] gene inactivation mutation that is associated with [[chromosome]] 17q24.2-q24.3. This gene plays an important role in cardiac development and myxomagenesis. The expression of PRKAR1A causes myxomatous changes in the endocardium.<ref name="pmid26416542">{{cite journal |vauthors=Sun Y, Chen X, Sun J, Wen X, Liu X, Zhang Y, Hoffman AR, Hu JF, Gao Y |title=A Novel Inherited Mutation in PRKAR1A Abrogates PreRNA Splicing in a Carney Complex Family |journal=Can J Cardiol |volume=31 |issue=11 |pages=1393–401 |year=2015 |pmid=26416542 |doi=10.1016/j.cjca.2015.05.018 |url=}}</ref> | ||
The encoded protein of [[PRKAR1A]] is a type 1A regulatory subunit of protein kinase A. Inactivating germline mutations of this gene are found in 70% of people with Carney complex. Less commonly, the molecular pathogenesis of Carney complex is a variety of genetic changes at chromosome 2p16.Both types of Carney complex are [[autosomal dominant]]. Despite dissimilar genetics, there appears to be no [[phenotype|phenotypic]] difference between PRKAR1A and chromosome 2p16 mutations.<ref> Carney Complex.Wikipedia. https://en.wikipedia.org/wiki/Carney_complex Accessed on November 24, 2015</ref> | |||
==Associated Conditions== | ==Associated Conditions== | ||
Carney complex is | The [[Carney complex]] is characterized by myxomatous neoplasms (cardiac, endocrine, cutaneous and neural), and a host of pigmented lesions of the skin and mucosae, including the rarely occurring epitheloid blue [[nevus]].<ref>Carney JA, Gordon H, Carpenter PC, Shenoy BV, Go VL. The complex of myxomas, spotty pigmentation, and endocrine overactivity. ''Medicine'' (Baltimore). 1985;64(4):270-83.</ref><ref>Iglesias C, Torrelo A, Colmenero I, Mediero IG, Zambrano A, Requenca L. Isolated multiple congential epithelioid blue naevus. ''British Journal of Dermatology'' 2005;152:391-393.</ref><ref>Gaissmaier et al. (letter and response) Carney Complex. ''Circulation'' 1999;100 (25); e150 http://circ.ahajournals.org/cgi/reprint/100/25/e150</ref> Approximately 7% of all cardiac myxomas are associated with Carney complex.<ref name="Reynen1995">{{Cite journal | last1 = Reynen | first1 = K. | title = Cardiac Myxomas | journal = New England Journal of Medicine | volume = 333 | issue = 24 | pages = 1610–1617 | year = 1995 | pmid = 7477198 | doi = 10.1056/NEJM199512143332407}}</ref> | ||
==Gross Pathology== | ==Gross Pathology== | ||
On gross pathology, external appearance, consistency size and weight are extremely variable findings of cardiac myxoma. Tumor consistency depends on the quantity and distribution of fibrous tissue and calcification (It can be smooth, lobulated, friable or gelatinous). <ref name="pmid25297937">{{cite journal |vauthors=Di Vito A, Mignogna C, Donato G |title=The mysterious pathways of cardiac myxomas: a review of histogenesis, pathogenesis and pathology |journal=Histopathology |volume=66 |issue=3 |pages=321–32 |year=2015 |pmid=25297937 |doi=10.1111/his.12531 |url=}}</ref> Usually a macroscopic gelatinous, irregular surface that fills the [[left atrium]] is a characteristic finding of myxoma. Myxomas that have irregular consistency are more likely to form surface thrombi and embolize. | On gross pathology, external appearance, consistency size and weight are extremely variable findings of cardiac myxoma. Tumor consistency depends on the quantity and distribution of fibrous tissue and calcification (It can be smooth, lobulated, friable or gelatinous). <ref name="pmid25297937">{{cite journal |vauthors=Di Vito A, Mignogna C, Donato G |title=The mysterious pathways of cardiac myxomas: a review of histogenesis, pathogenesis and pathology |journal=Histopathology |volume=66 |issue=3 |pages=321–32 |year=2015 |pmid=25297937 |doi=10.1111/his.12531 |url=}}</ref> Usually a macroscopic gelatinous, irregular surface that fills the [[left atrium]] is a characteristic finding of myxoma. Myxomas that have irregular consistency are more likely to form surface thrombi and embolize. | ||
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==Immunohistochemistry== | ==Immunohistochemistry== | ||
Cardiac myxoma cells exhibit immuno-reactivity mainly for calretinin (75–100%) followed by vimentin (>50%), Notch-1, alpha-1 antichymotrypsin and plakophilin- 2.<ref name="pmid11642722">{{cite journal |vauthors=Acebo E, Val-Bernal JF, Gómez-Roman JJ |title=Thrombomodulin, calretinin and c-kit (CD117) expression in cardiac myxoma |journal=Histol. Histopathol. |volume=16 |issue=4 |pages=1031–6 |year=2001 |pmid=11642722 |doi= |url=}}</ref>Calretinin plays an important role in the discrimination of mural thrombi and papillary fibroelastoma.<ref name="pmid11642722">{{cite journal |vauthors=Acebo E, Val-Bernal JF, Gómez-Roman JJ |title=Thrombomodulin, calretinin and c-kit (CD117) expression in cardiac myxoma |journal=Histol. Histopathol. |volume=16 |issue=4 |pages=1031–6 |year=2001 |pmid=11642722 |doi= |url=}}</ref>. Another immunohistochemical marker, survivin (an apoptosis inhibitor) has been detected to play an important role in the development and growth of cardiac myxomas.<ref name="pmid21880190">{{cite journal |vauthors=Lin YS, Jung SM, Wu HH, Shiu TF, Tzai FC, Chu JJ, Lin PJ, Chu PH |title=Survivin expression in cardiac myxoma |journal=Chang Gung Med J |volume=34 |issue=4 |pages=360–6 |year=2011 |pmid=21880190 |doi= |url=}}</ref> | Cardiac myxoma cells exhibit immuno-reactivity mainly for calretinin (75–100%) followed by vimentin (>50%), Notch-1, alpha-1 antichymotrypsin and plakophilin- 2.<ref name="pmid11642722">{{cite journal |vauthors=Acebo E, Val-Bernal JF, Gómez-Roman JJ |title=Thrombomodulin, calretinin and c-kit (CD117) expression in cardiac myxoma |journal=Histol. Histopathol. |volume=16 |issue=4 |pages=1031–6 |year=2001 |pmid=11642722 |doi= |url=}}</ref>Calretinin plays an important role in the discrimination of mural thrombi and papillary fibroelastoma.<ref name="pmid11642722">{{cite journal |vauthors=Acebo E, Val-Bernal JF, Gómez-Roman JJ |title=Thrombomodulin, calretinin and c-kit (CD117) expression in cardiac myxoma |journal=Histol. Histopathol. |volume=16 |issue=4 |pages=1031–6 |year=2001 |pmid=11642722 |doi= |url=}}</ref>. Another immunohistochemical marker, survivin (an apoptosis inhibitor) has been detected to play an important role in the development and growth of cardiac myxomas.<ref name="pmid21880190">{{cite journal |vauthors=Lin YS, Jung SM, Wu HH, Shiu TF, Tzai FC, Chu JJ, Lin PJ, Chu PH |title=Survivin expression in cardiac myxoma |journal=Chang Gung Med J |volume=34 |issue=4 |pages=360–6 |year=2011 |pmid=21880190 |doi= |url=}}</ref> | ||
{| style="border: 0px; font-size: 90%; margin: 3px; width: 500px" | |||
|valign=center| | |||
|+ '''Cardiac Myxoma''' | |||
! style="background: #4479BA; width: 200px; color: #FFFFFF;"|'''Features''' | |||
! style="background: #4479BA; width: 600px; color: #FFFFFF;"|'''Description''' | |||
|- | |||
| style="padding: 5px 5px; background: #DCDCDC; font-weight: bold" align=center | '''General aspects'''|| style="padding: 5px 5px; background: #F5F5F5;" | | |||
:*Isolated cells with irregular cellular borders, mild or no atypia, no mitosis | |||
|- | |||
| style="padding: 5px 5px; background: #DCDCDC; font-weight: bold" align=center | '''Genetics'''|| style="padding: 5px 5px; background: #F5F5F5;"| | |||
:*[[PRKAR1A]] gene plays an important role in cardiac development and myxomagenesis | |||
|- | |||
| style="padding: 5px 5px; background: #DCDCDC; font-weight: bold" align=center | '''Gross Pathology'''|| style="padding: 5px 5px; background: #F5F5F5;"| | |||
:*Smooth, lobulated mass can be friable or gelatinous | |||
|- | |||
| style="padding: 5px 5px; background: #DCDCDC; font-weight: bold" align=center | '''Micropathology'''|| style="padding: 5px 5px; background: #F5F5F5;" | | |||
:*Inflammatory infiltrate with hemosiderin, calcifications and extramedullary hemopoyesis | |||
|- | |||
| style="padding: 5px 5px; background: #DCDCDC; font-weight: bold" align=center | '''Inmunohistochemistry'''|| style="padding: 5px 5px; background: #F5F5F5;" | | |||
:*Vimentin, endothelial and neural markers | |||
|} | |||
==References== | ==References== | ||
Revision as of 14:55, 24 November 2015
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Myxoma pathophysiology On the Web |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Cafer Zorkun, M.D., Ph.D. [2]Ahmad Al Maradni, M.D. [3]Maria Fernanda Villarreal, M.D. [4]
Overview
Cardiac myxoma is a benign intracavitary endocardial mass that represents the most common primary tumor of the heart.[1] Myxoma cells are characterized by undifferentiated mesenchymal cells, which potentially differentiate into many tissues such as blood vessels, glandular structures, bones, and source of extramedullary hematopoiesis.[2] The primary distribution of cardiac myxoma is the left atrium (75%) of the heart, regularly they tend to be located in the fossa ovalis and endocardium of the atrial septum.
Pathogenesis
Cardiac myxoma arises from remnants of subendocardial vasoformative reserve cells, which are primitive mesenchymal cells that are normally involved in the supportive structure of the endocardium.[3][4] The true origin of cardiac myxomas still remains unclear. Recent studies suggest several theories to support the histopathogensis of this type of myxoid tumor; such as, the neoplastic theory, dysembryoplastic theory, histopathogenesis of glandular cells in myxoma and the thrombotic theory.[5][6]
Genetics
Single cardiac myxomas and familial forms are related with several chromosome and gene alterations which involve cardiac development. Inherited myxomas are usually presented in the Carney complex. The development of this syndrome is a result of PRKAR1A gene inactivation mutation that is associated with chromosome 17q24.2-q24.3. This gene plays an important role in cardiac development and myxomagenesis. The expression of PRKAR1A causes myxomatous changes in the endocardium.[7]
The encoded protein of PRKAR1A is a type 1A regulatory subunit of protein kinase A. Inactivating germline mutations of this gene are found in 70% of people with Carney complex. Less commonly, the molecular pathogenesis of Carney complex is a variety of genetic changes at chromosome 2p16.Both types of Carney complex are autosomal dominant. Despite dissimilar genetics, there appears to be no phenotypic difference between PRKAR1A and chromosome 2p16 mutations.[8]
Associated Conditions
The Carney complex is characterized by myxomatous neoplasms (cardiac, endocrine, cutaneous and neural), and a host of pigmented lesions of the skin and mucosae, including the rarely occurring epitheloid blue nevus.[9][10][11] Approximately 7% of all cardiac myxomas are associated with Carney complex.[12]
Gross Pathology
On gross pathology, external appearance, consistency size and weight are extremely variable findings of cardiac myxoma. Tumor consistency depends on the quantity and distribution of fibrous tissue and calcification (It can be smooth, lobulated, friable or gelatinous). [13] Usually a macroscopic gelatinous, irregular surface that fills the left atrium is a characteristic finding of myxoma. Myxomas that have irregular consistency are more likely to form surface thrombi and embolize.
Morphologically, these lesions tend to be attached to the endocardium by a broad-based pedunculated stalk. In some cases, the attachment to the endocardium can also be without a clear stalk, or sessile. Cardiac myxomas are non-invasive tumors, thus there is no infiltration to underlying tissues.
Cardiac myxomas are intracavitary tumors. The distribution is normally within the interatrial septum or adjacent to foramen ovale (75%). However, they can also be found in other cardiac chambers, such as right atrium (15%), ventricles(˜2%) or cardiac valves (rare).[14] Large cardiac myxomas are usually located in fossa ovalis. The average tumor size is from 0.6 to 12 cm, with a mean weight of 40 g.[1]
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A gelatinous tumor is attached by a narrow pedicle to the atrial septum. The myxoma has an irregular surface and nearly fills the left atrium.
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Left Atrial Myxoma
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Gross pathology Atrial Myxoma: Myxomas are brownish or white and are frequently covered with thrombus
Microscopic Pathology
On microscopic histopathological analysis, myxoma cells have an ovoid nucleus with large nucleoli, abundant eosinophilic cytoplasm, and indistinct cell borders.[15] They are usually arranged in perivascular ring structures (typically, infiltrated by lymphocytes and macrophages). The Gamna-Bodies consist of fibrosis and deposition of iron pigments are a characteristic finding of myxoma tumors.
The extracellular matrix forms an Alcian blue-positive myxoid stroma, composed of variable amounts of proteoglycans, elastin and collagen. There is a diffuse reticulated stroma with fine collagen fibrils on which iron encrustation often occurs. [13]
It is also common to find hemosiderin within the histiocytes. Thrombosis, fibrosis and calcification are a frequent histological finding. In some cases, extramedular hematopoises is present and mucin-producing glands can be also seen in the base of the tumor.
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![1) Black arrow(top):Endothelium 2) Black arrow(bottom): Hemosiderin macrophage. [16]](/images/3/3e/800px-Atrial_myxoma_edge_high_mag.jpg)
1) Black arrow(top):Endothelium 2) Black arrow(bottom): Hemosiderin macrophage. [16]
![1) Black arrow(top):Endothelium 2) Black arrow(bottom): Hemosiderin macrophage. [16]](/index.php/File:800px-Atrial_myxoma_edge_high_mag.jpg)
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Cardiac Myxoma: Gamna Bodies: A peculiar form of fibrosis with deposition of iron pigment, identical to that seen in the spleens of patients with sickle cell anemia, is not uncommon in myxoma.
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Cardiac Myxoma Common features at the interface with the atrial septum include lymphoid aggregates, smooth muscle bundles, and thick walled vessels which angiographically may look like neovascularization.
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Cardiac Myxoma The extramedullary hematopoiesis seen here is present in about 7 percent of cardiac myxomas.
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Cardiac Myxoma Glandular structures are seen in less than 5 percent of cases. In this example, they were limited to the base of the myxoma
Immunohistochemistry
Cardiac myxoma cells exhibit immuno-reactivity mainly for calretinin (75–100%) followed by vimentin (>50%), Notch-1, alpha-1 antichymotrypsin and plakophilin- 2.[17]Calretinin plays an important role in the discrimination of mural thrombi and papillary fibroelastoma.[17]. Another immunohistochemical marker, survivin (an apoptosis inhibitor) has been detected to play an important role in the development and growth of cardiac myxomas.[18]
| Features | Description |
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| General aspects |
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| Genetics |
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| Gross Pathology |
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| Micropathology |
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| Inmunohistochemistry |
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References
- ↑ 1.0 1.1 Grebenc ML, Rosado de Christenson ML, Burke AP, Green CE, Galvin JR (2000). "Primary cardiac and pericardial neoplasms: radiologic-pathologic correlation". Radiographics. 20 (4): 1073–103, quiz 1110–1, 1112. doi:10.1148/radiographics.20.4.g00jl081073. PMID 10903697.
- ↑ Bulkley BH, Hutchins GM (1979). "Atrial myxomas: a fifty year review". Am. Heart J. 97 (5): 639–43. PMID 433739.
- ↑ Roscher AA, Kato NS, Quan H, Padmanabhan M (1996). "Intra-atrial myxomas, clinical-pathologic correlation based on two case studies including historical review". J Cardiovasc Surg (Torino). 37 (6 Suppl 1): 131–7. PMID 10064365.
- ↑ Acebo E, Val-Bernal JF, Gómez-Román JJ (2001). "Prichard's structures of the fossa ovalis are not histogenetically related to cardiac myxoma". Histopathology. 39 (5): 529–35. PMID 11737312.
- ↑ Orlandi A, Ciucci A, Ferlosio A, Genta R, Spagnoli LG, Gabbiani G (2006). "Cardiac myxoma cells exhibit embryonic endocardial stem cell features". J. Pathol. 209 (2): 231–9. doi:10.1002/path.1959. PMID 16508920.
- ↑ Amano J, Kono T, Wada Y, Zhang T, Koide N, Fujimori M, Ito K (2003). "Cardiac myxoma: its origin and tumor characteristics". Ann Thorac Cardiovasc Surg. 9 (4): 215–21. PMID 13129418.
- ↑ Sun Y, Chen X, Sun J, Wen X, Liu X, Zhang Y, Hoffman AR, Hu JF, Gao Y (2015). "A Novel Inherited Mutation in PRKAR1A Abrogates PreRNA Splicing in a Carney Complex Family". Can J Cardiol. 31 (11): 1393–401. doi:10.1016/j.cjca.2015.05.018. PMID 26416542.
- ↑ Carney Complex.Wikipedia. https://en.wikipedia.org/wiki/Carney_complex Accessed on November 24, 2015
- ↑ Carney JA, Gordon H, Carpenter PC, Shenoy BV, Go VL. The complex of myxomas, spotty pigmentation, and endocrine overactivity. Medicine (Baltimore). 1985;64(4):270-83.
- ↑ Iglesias C, Torrelo A, Colmenero I, Mediero IG, Zambrano A, Requenca L. Isolated multiple congential epithelioid blue naevus. British Journal of Dermatology 2005;152:391-393.
- ↑ Gaissmaier et al. (letter and response) Carney Complex. Circulation 1999;100 (25); e150 http://circ.ahajournals.org/cgi/reprint/100/25/e150
- ↑ Reynen, K. (1995). "Cardiac Myxomas". New England Journal of Medicine. 333 (24): 1610–1617. doi:10.1056/NEJM199512143332407. PMID 7477198.
- ↑ 13.0 13.1 Di Vito A, Mignogna C, Donato G (2015). "The mysterious pathways of cardiac myxomas: a review of histogenesis, pathogenesis and pathology". Histopathology. 66 (3): 321–32. doi:10.1111/his.12531. PMID 25297937.
- ↑ Yoon DH, Roberts W (2002). "Sex distribution in cardiac myxomas". Am. J. Cardiol. 90 (5): 563–5. PMID 12208428.
- ↑ Vaideeswar P, Butany JW (2008). "Benign cardiac tumors of the pluripotent mesenchyme". Semin Diagn Pathol. 25 (1): 20–8. PMID 18350919.
- ↑ Cardiac Myxoma. Libre Pathology URL http://librepathology.org/wiki/index.php/Cardiac_myxoma Accessed on November 19,2015
- ↑ 17.0 17.1 Acebo E, Val-Bernal JF, Gómez-Roman JJ (2001). "Thrombomodulin, calretinin and c-kit (CD117) expression in cardiac myxoma". Histol. Histopathol. 16 (4): 1031–6. PMID 11642722.
- ↑ Lin YS, Jung SM, Wu HH, Shiu TF, Tzai FC, Chu JJ, Lin PJ, Chu PH (2011). "Survivin expression in cardiac myxoma". Chang Gung Med J. 34 (4): 360–6. PMID 21880190.