Difference between revisions of "Heart"

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===Coronary arteries===
===Coronary arteries===
*These are often done first, i.e. before the heart is opened.
*These are often done first, i.e. before the heart is opened.
*They should be sectioned at ~2 mm intervals.
*They should be sectioned (axially) at ~2 mm intervals.
**Longitudinally opening the coronaries does '''not''' allow accurate assessment of luminal stenosis.<ref>URL: [http://www.histopathology-india.net/CAEx.htm http://www.histopathology-india.net/CAEx.htm]. Accessed on: 7 July 2011.</ref>
*A significant stenosis (defined by ''diameter'' narrowing) is 70-75%.<ref name=Ref_HospAuto147>{{Ref HospAuto|147}}</ref>
*A significant stenosis (defined by ''diameter'' narrowing) is 70-75%.<ref name=Ref_HospAuto147>{{Ref HospAuto|147}}</ref>


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===Right ventricle===
===Right ventricle===
*Make cut throught the apex (transverse/biventicular section).
*Make cut through the apex (transverse/biventicular section).
*Open along lateral edge (from RA cut).
*Open along lateral edge (from RA cut).


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*After the heart is opened it should be sliced at 5-10 mm intervals to the semilunar valves.
*After the heart is opened it should be sliced at 5-10 mm intervals to the semilunar valves.


==Standard measures==
==Standard measures of the heart==
*Mass (weight).
*Mass (weight).
*Left ventricle (LV) - 2 cm below the MV.
*Left ventricle (LV) - 2 cm below the MV.
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*Pulmonic valve (PV) circumference.
*Pulmonic valve (PV) circumference.
*Tricuspid valve (TV) circumference.
*Tricuspid valve (TV) circumference.
===Normal measures===
====Younger adults (20-60 years)====
Based on ''Ludwig'':<ref name=Ref_Ludwig569>{{Ref Ludwig|569}}</ref>
{| class="wikitable sortable"
! Measure
! Men
! Women
|-
|Aortic valve
| 6.7 (6.0-7.4)
| 6.3 (5.7-6.9)
|-
|Pulmonary valve
| 6.6 (6.1-7.1)
| 6.2 (5.7-6.7)
|-
|Mitral valve
| 9.6 (9.4-9.9)
| 8.6 (8.2-9.1)
|-
|Tricuspid valve
| 11.4 (11.2-11.7)
| 10.6 (10.2-10.9)
|}
Based on ''Ludwig'':<ref name=Ref_Ludwig569>{{Ref Ludwig|569}}</ref>
{| class="wikitable sortable"
! Feature
! Measure
|-
|Left ventricle
| 1.25 (1.00-1.50)
|-
|Right ventricle
| 0.4 (0.25-0.50)
|-
|}
====Older adults (>60 years)====
Based on ''Ludwig'':<ref name=Ref_Ludwig569>{{Ref Ludwig|569}}</ref>
{| class="wikitable sortable"
! Measure
! Men
! Women
|-
|Aortic valve
| 8.3 (8.1-8.5)
| 7.6 (7.3-7.9)
|-
|Pulmonary valve
| 7.3 (7.2-7.5)
| 7.1 (6.8-7.4)
|-
|Mitral valve
| 9.5 (9.2-9.8)
| 8.6 (8.2-9.0)
|-
|Tricuspid valve
| 11.6 (11.4-11.8)
| 10.5 (10.0-11.1)
|}
Based on ''Ludwig'':<ref name=Ref_Ludwig569>{{Ref Ludwig|569}}</ref>
{| class="wikitable sortable"
! Feature
! Measure
|-
|Left ventricle
| 1.15 (1.05-1.25)
|-
|Right ventricle
| 0.38 (0.35-0.40)
|-
|}


==Standard sections==
==Standard sections==
Minimalist approach (Cybulsky):
Minimalist approach (Dr. C.):
#LV and PPM (left ventricle and posterior papillary muscle).
#LV and PPM (left ventricle and posterior papillary muscle).
#LV and APM (left ventricle and anterior papillary muscle).
#LV and APM (left ventricle and anterior papillary muscle).
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#RV.
#RV.


Make the lab work hard approach (Butany):
Make the lab work hard approach (Dr. B.):
#PRV (post. RV) with tricuspid valve.
#PRV (post. RV) with tricuspid valve.
#ARV (ant. RV) with pulm. valve.
#ARV (ant. RV) with pulm. valve.
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==Conducting system==
==Conducting system==
===Indications for examining the conducting system<ref>KC. 1 October 2010.</ref>===
===Indications for examining the conducting system<ref>KC. 1 October 2010.</ref>===
#History of asyncope.
#History of syncope.
#History of arrhythmia.
#History of [[cardiac arrhythmia|arrhythmia]].
#[[Autopsy#Negative autopsy|Negative autopsy]].
#[[Autopsy#Negative autopsy|Negative autopsy]].


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Histologic characteristics:
Histologic characteristics:
*Spindle cell morphology + wavy nucleus.
*Spindle cell morphology + wavy nucleus.
*Cytoplasms stains lighter with eosin than cardiac muscle.
*Cytoplasm stains lighter with eosin than cardiac muscle.
*+/-Vacuoles.
*+/-Vacuoles.


Images:
=====Images=====
*[http://commons.wikimedia.org/wiki/File:Sinoatrial_node_low_mag.jpg SA node - low mag. - vignetting (WC)].
<gallery>
*[http://commons.wikimedia.org/wiki/File:Sinoatrial_node_2_low_mag.jpg SA node - low mag. (WC)].
Image:Sinoatrial_node_low_mag.jpg | SA node - low mag. - vignetting (WC)
*[http://commons.wikimedia.org/wiki/File:Sinoatrial_node_high_mag.jpg SA node - high mag.(WC)].
Image:Sinoatrial_node_2_low_mag.jpg | SA node - low mag. (WC)
Image:Sinoatrial_node_high_mag.jpg | SA node - high mag.(WC)
</gallery>


===Atrioventricular node===
===Atrioventricular node===
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The pathologist (like radiologists) can say...
The pathologist (like radiologists) can say...
*Pericardial effusion.
*[[Pericardial]] [[effusion]].
**Hemopericardium.
**Hemopericardium.


Image: [http://en.wikipedia.org/wiki/File:CT_pericardial_effusion.jpg Pericardial effusion - CT scan (wikipedia.org)].
Image: [http://en.wikipedia.org/wiki/File:CT_pericardial_effusion.jpg Pericardial effusion - CT scan (wikipedia.org)].


==Myocardial infarction==
==Fibrinous pericarditis==
===Clinical===
*[[AKA]] ''bread and butter pericarditis''.
*Usually diagnosed clinically - with blood work (troponin, CK-MB) or EKG.
*Post-[[myocardial infarction]] this is known as ''Dressler's syndrome''.<ref name=Ref_PCPBoD8_293>{{Ref PCPBoD8|293}}</ref>
*MI may be precipitated by cocaine use... and further exacerbated by treatment with a beta-blocker.<ref name=pmid19127137>{{cite journal |author=Mohamad T, Kondur A, Vaitkevicius P, Bachour K, Thatai D, Afonso L |title=Cocaine-induced chest pain and beta-blockade: an inner city experience |journal=Am J Ther |volume=15 |issue=6 |pages=531-5 |year=2008 |pmid=19127137 |doi=10.1097/MJT.0b013e3181758cfc |url=}}</ref>
===General===
Etiology:
*Radiation.<ref name=pmid436483 >{{Cite journal  | last1 = Schneider | first1 = JS. | last2 = Edwards | first2 = JE. | title = Irradiation-induced pericarditis. | journal = Chest | volume = 75 | issue = 5 | pages = 560-4 | month = May | year = 1979 | doi = | PMID = 436483 }}</ref>
*Uremia.
*[[Myocardial infarction]] (MI).
**Classically occurs at 2-3 days following a MI.<ref name=Ref_PCPBoD8_293>{{Ref PCPBoD8|293}}</ref>
 
Note:
*Roberts suggests that ''pericardial heart disease'' may be a better term for this, as this isn't really an inflammatory process.<ref name=pmid16200146>{{Cite journal | last1 = Roberts | first1 = WC. | title = Pericardial heart disease: its morphologic features and its causes. | journal = Proc (Bayl Univ Med Cent) | volume = 18 | issue = 1 | pages = 38-55 | month = Jan | year = 2005 | doi = | PMID = 16200146 }}</ref>


Classic symptoms:
===Gross===
*Chest pain (with radiation down the arms).
*Pericardium with a shaggy rough appearance.  
*Nausea & vomiting.
**Described as "buttered bread dropped-on-the-floor look".<ref name=pmid14991530>{{Cite journal  | last1 = Cohen | first1 = MB. | last2 = Laennec | first2 = RT. | title = Cross your heart: Some historical comments about fibrinous pericarditis. | journal = Hum Pathol | volume = 35 | issue = 2 | pages = 147-9 | month = Feb | year = 2004 | doi =  | PMID = 14991530 }}</ref>
*Diaphoresis.


Post-MI:
Image:
*''Dressler's syndrome'' [[AKA]] ''postmyocardial infarction syndrome'';<ref name=pmid5039567>{{cite journal |author=Hutchcroft BJ |title=Dressler's syndrome |journal=Br Med J |volume=3 |issue=5817 |pages=49 |year=1972 |month=July |pmid=5039567 |pmc=1788531 |doi= |url=}}</ref> pericarditis post-myocardial infarction +/- pericardial effusion (clinically tamponade).
*[http://library.med.utah.edu/WebPath/CVHTML/CV047.html Bread and butter pericarditis (utah.edu)].
===Microscopic===
Features:
*Fibrin - pink amorphous material.


Enzymatic tests:<ref>[http://pro2services.com/Lectures/Fall/CardEnz/a6mienz.gif http://pro2services.com/Lectures/Fall/CardEnz/a6mienz.gif]</ref><ref>[http://www.hope-academic.org.uk/biochem/pbl/IMG00030.GIF http://www.hope-academic.org.uk/biochem/pbl/IMG00030.GIF]</ref>
Note:
*CK: peaks at day 1, resolves after 2-3 days.
*Inflammation is not a strict requirement for the diagnosis.<ref name=pmid16200146>{{Cite journal  | last1 = Roberts | first1 = WC. | title = Pericardial heart disease: its morphologic features and its causes. | journal = Proc (Bayl Univ Med Cent) | volume = 18 | issue = 1 | pages = 38-55 | month = Jan | year = 2005 | doi =  | PMID = 16200146 }}</ref>
*AST: peaks close to day 2, resolves after 4-5 days.
*LDH: peaks day 2, resolves after ~6 days.
Images:
*[http://autopsy.stanford.edu/images/FibrinousPericarditis.jpg Fibrinous pericarditis (stanford.edu)].<ref>URL: [http://autopsy.stanford.edu/fellowships.html http://autopsy.stanford.edu/fellowships.html]. Accessed on: 21 January 2012.</ref>
<gallery>
Image:Pericarditis_fibrinosa.jpg | Fibrinous pericarditis. (WC)
</gallery>


===Pathologic===
===Sign out===
====Microscopic====
<pre>
Sequence:<ref>[http://library.med.utah.edu/WebPath/TUTORIAL/MYOCARD/MYOCARD.html http://library.med.utah.edu/WebPath/TUTORIAL/MYOCARD/MYOCARD.html]</ref>
Pericardium, Excision:
*1-3 hours - Wavy (myocardial) fibers
- Fibrinous pericardial heart disease.
*4-12 hours - Coagulative necrosis & loss of cross striations, contraction bands, edema, hemorrhage, PMN infiltrate.
</pre>
*18-24 hours - Coagulative necrosis, pyknosis of nuclei, and marginal contraction bands.
*1-3 days - Loss of nuclei (karyolysis), loss of striations, abundant PMNs.
*3-7 days - Macrophage and mononuclear infiltration, fibrovascular response.
*10-21 days - Fibrovascular response, prominent granulation tissue.
*6 weeks - Fibrosis.


====Gross====
==Myocardial infarction==
Sequence:<ref>[http://library.med.utah.edu/WebPath/TUTORIAL/MYOCARD/MYOCARD.html http://library.med.utah.edu/WebPath/TUTORIAL/MYOCARD/MYOCARD.html]</ref>
*Abbreviated ''MI''.
*18-24 hours - myocardial pallor.
*[[AKA]] ''myocardial infarct''.
*1-3 days - pallor, moderate hyperemia (redness due to congestion with blood).
{{Main|Myocardial infarction}}
*3-7 days - yellow lesion with hyperemic border.
*10-21 days - maximally yellow.
*6 weeks - white (fibrosis).


==Coronary artery atherosclerosis==
==Coronary artery atherosclerosis==
*Greater than 75% (diameter) stenosis - considered significant.<ref>Chamberlain. March 7, 2008.</ref>
{{Main|Atherosclerosis}}
*[[AKA]] ''coronary artery disease'', abbreviated ''CAD''.
*[[AKA]] ''atherosclerotic heart disease'', abbreviated ''ASHD''.
*[[AKA]] ''atherosclerotic coronary artery disease''.


Stenosis definition (as per NASCET):<ref name="pmid9811916">{{cite journal |author=Barnett HJ, Taylor DW, Eliasziw M, ''et al.'' |title=Benefit of carotid endarterectomy in patients with symptomatic moderate or severe stenosis. North American Symptomatic Carotid Endarterectomy Trial Collaborators |journal=The New England Journal of Medicine |volume=339 |issue=20 |pages=1415–25 |year=1998 |month=November |pmid=9811916 |doi= |url=http://content.nejm.org/cgi/pmidlookup?view=short&pmid=9811916&promo=ONFLNS19}}</ref><br>
===General===
<math>percent stenosis = ( 1 - ( minimal\ diameter ) / ( poststenotic\ diameter ) ) x 100%.</math>
*Greater than 75% (diameter) stenosis - considered significant.<ref>Chamberlain, D. March 7, 2008.</ref>
*Leading cause of morbidity and mortality, esp. in the elderly.
*''Left main coronary artery (LMCA) disease'' is particularly fatal.<ref name=pmid10580359>{{Cite journal | last1 = Kanjwal | first1 = MY. | last2 = Carlson | first2 = DE. | last3 = Schwartz | first3 = JS. | title = Chronic/subacute total occlusion of the left main coronary artery--a case report and review of literature. | journal = Angiology | volume = 50 | issue = 11 | pages = 937-45 | month = Nov | year = 1999 | doi = | PMID = 10580359 }}</ref>


With a bit of allegbra one can show:<br>
Clinical presentations:
*Stable angina.
*Unstable angina.
*[[Myocardial infarction]].
*[[Sudden cardiac death]].
 
Note:
*''Coronary artery atherosclerosis'' is '''not''' the only type of ''coronary artery disease''... but it is by far the most common; thus, CAD is generally considered synonymous with ''coronary artery atherosclerosis''.
 
Treatment:
*Medical management (blood pressure control (antihypertensives), cholesterol control (e.g. statins, exercise), [[diabetes mellitus|diabetes]] control, smoking cessation).
*[[Coronary artery bypass surgery]] (CABG).
*Percutaneous coronary intervention (PCI).
 
====Stenosis definition====
Definition (as per NASCET):<ref name="pmid9811916">{{cite journal |author=Barnett HJ, Taylor DW, Eliasziw M, ''et al.'' |title=Benefit of carotid endarterectomy in patients with symptomatic moderate or severe stenosis. North American Symptomatic Carotid Endarterectomy Trial Collaborators |journal=The New England Journal of Medicine |volume=339 |issue=20 |pages=1415–25 |year=1998 |month=November |pmid=9811916 |doi= |url=http://content.nejm.org/cgi/pmidlookup?view=short&pmid=9811916&promo=ONFLNS19}}</ref><br>
<math>percent\ stenosis = ( 1 - ( minimal\ diameter ) / ( poststenotic\ diameter ) ) x 100%.</math>
 
With a bit of algebra one can show:<br>
<math>A_x=x^2 A_o</math><br>
<math>A_x=x^2 A_o</math><br>
Where:
Where:
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*A 75% diameter reduction results in a 93.75% area reduction.
*A 75% diameter reduction results in a 93.75% area reduction.
*A 90% diameter reduction results in a 99% area reduction.
*A 90% diameter reduction results in a 99% area reduction.
===Microscopic===
:See ''[[Atherosclerosis]]''.


==Abnormal hearts==
==Abnormal hearts==
===Cardiac hypertrophy===
Can be by:
*Mass criteria described in a couple of articles from the ''Mayo Clinic Proceedings''.<ref name=pmid3276973>{{cite journal |author=Scholz DG, Kitzman DW, Hagen PT, Ilstrup DM, Edwards WD |title=Age-related changes in normal human hearts during the first 10 decades of life. Part I (Growth): A quantitative anatomic study of 200 specimens from subjects from birth to 19 years old |journal=Mayo Clin. Proc. |volume=63 |issue=2 |pages=126–36 |year=1988 |month=February |pmid=3276973 |doi= |url=}}</ref><ref name=pmid3276974>{{cite journal |author=Kitzman DW, Scholz DG, Hagen PT, Ilstrup DM, Edwards WD |title=Age-related changes in normal human hearts during the first 10 decades of life. Part II (Maturity): A quantitative anatomic study of 765 specimens from subjects 20 to 99 years old |journal=Mayo Clin. Proc. |volume=63 |issue=2 |pages=137–46 |year=1988 |month=February |pmid=3276974 |doi= |url=}}</ref>
*Thickness criteria.
Rules of thumb:<ref>KC. 14 October 2010.</ref>
*>400 g is ''often'' abnormal.
*>500 g is abnormal.
*>1.5 cm left ventricle thickness.
*>0.5 cm right ventricle thickness.
===Common patterns===
====Dilated hearts====
Dilated pattern DDx:<ref name=Ref_PBoD602>{{Ref PBoD|602}}</ref>
Dilated pattern DDx:<ref name=Ref_PBoD602>{{Ref PBoD|602}}</ref>
*Hypertensive heart disease.  
*Hypertensive heart disease.  
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*[[Amyloidosis]].
*[[Amyloidosis]].


==Concentric LV hypertrophy==
====Concentric left ventricular hypertrophy====
Concentric left ventricular hypertrophy is a common gross pathologic finding.
Concentric left ventricular hypertrophy is a common gross pathologic finding.


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*[[Valvular heart disease|Aortic stenosis]].
*[[Valvular heart disease|Aortic stenosis]].


==Cardiomyopathy==
Other considerations:
*Hypertrophic [[cardiomyopathy]] (usually eccentric).
 
<gallery>
Image: Heart_left_ventricular_hypertrophy_sa.jpg | Concentric LVH. (WC)
</gallery>
====Eccentric left ventricular hypertrophy====
*[[Hypertrophic cardiomyopathy]], includes [[hypertrophic obstructive cardiomyopathy]] (HOCM).
 
==Detail articles==
===Cardiomyopathy===
{{main|Cardiomyopathy}}
{{main|Cardiomyopathy}}
In the land of cardiology... there is a thing called cardiomyopathy.
In the land of cardiology... there is a thing called cardiomyopathy.  This article deals with it. 
 
It includes discussion of ''dilated cardiomyopathy'', ''hypertrophic cardiomyopathy'' and ''arrhythmogenic right ventricular cardiomyopathy''.


==Congenital heart disease==
===Congenital heart disease===
{{main|Congenital heart disease}}
{{main|Congenital heart disease}}
Congential heart disease... a domain of paediatric cardiac surgery and occasionally adult cardiac surgery.
Congenital heart disease... a domain of pediatric cardiac surgery and occasionally adult cardiac surgery.


==Tumours==
The article covers shunts, both left-to-right and right-to-left.
 
===Tumours===
{{main|Tumours of the heart}}
{{main|Tumours of the heart}}
These are rare buggers.
These are rare buggers.


==Valvular disease==
===Valvular disease===
{{main|Valvular heart disease}}
{{main|Valvular heart disease}}
This is the domain of cardiac surgery... only seen in hospitals with cardiac surgery.
This is the domain of cardiac surgery... only seen in hospitals with cardiac surgery.


==Endocarditis==
===Endocarditis===
See [[Valvular heart disease]].
{{Main|Infective endocarditis}}
 
==Shunts==
Most shunts are a consequence of congenital heart disease, which is dealt with in the [[congenital heart disease]] article.  They are only listed here briefly and grouped into ''left-to-right'' and ''right-to-left''.
 
===Left-to-right===
Mnemonic ''the Ds'':<ref name=Ref_PBoD566>{{Ref PBoD|566}}</ref>
*ASD = atrial septal defect.
*VSD = ventricular septal defect.
*AVSD = atrioventricular defect.
*PDA = patent ductus arteriosus.
 
Note: The word ''Left'' has four letters and there are four L->R shunts.
===Right-to-left===
Mnemonic ''5 Ts'':<ref name=Ref_PBoD568>{{Ref PBoD|568}}</ref>
*Tetralogy of Fallot (TOF),
*Transposition of great arteries,
*Truncus arteriosus,
*Tricuspid valve atresia,
*Total anomalous pulmonary venous return.
 
Clinical: TOF is the classic cause of "blue babies".


==Cardiac sarcoidosis==
==Cardiac sarcoidosis==
{{main|Sarcoidosis}}
{{main|Sarcoidosis}}
===General===
===General===
*Can be in insolation or part of systemic sarcoidosis.<ref name=pmid9608713>{{cite journal |author=Veinot JP, Johnston B |title=Cardiac sarcoidosis--an occult cause of sudden death: a case report and literature review |journal=J. Forensic Sci. |volume=43 |issue=3 |pages=715–7 |year=1998 |month=May |pmid=9608713 |doi= |url=}}</ref>
*Can be in isolation or part of systemic sarcoidosis.<ref name=pmid9608713>{{cite journal |author=Veinot JP, Johnston B |title=Cardiac sarcoidosis--an occult cause of sudden death: a case report and literature review |journal=J. Forensic Sci. |volume=43 |issue=3 |pages=715–7 |year=1998 |month=May |pmid=9608713 |doi= |url=}}</ref>
*May mimic hypertrophic [[cardiomyopathy]] clinically.<ref name=pmid10981852>{{cite journal |author=Matsumori A, Hara M, Nagai S, ''et al.'' |title=Hypertrophic cardiomyopathy as a manifestation of cardiac sarcoidosis |journal=Jpn. Circ. J. |volume=64 |issue=9 |pages=679–83 |year=2000 |month=September |pmid=10981852 |doi= |url=}}</ref>
*May mimic hypertrophic [[cardiomyopathy]] clinically.<ref name=pmid10981852>{{cite journal |author=Matsumori A, Hara M, Nagai S, ''et al.'' |title=Hypertrophic cardiomyopathy as a manifestation of cardiac sarcoidosis |journal=Jpn. Circ. J. |volume=64 |issue=9 |pages=679–83 |year=2000 |month=September |pmid=10981852 |doi= |url=}}</ref>
*Clinical: associated with heart block.<ref name=pmid9608713/>
*Clinical: associated with heart block.<ref name=pmid9608713/>
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*Anterior LV - 18.0%.
*Anterior LV - 18.0%.
*RV - 17.9%.
*RV - 17.9%.
**RV involvement may lead to confusion with arrhythmogenic right ventricular cardiomyopathy (ARVC).
**RV involvement may lead to confusion with [[arrhythmogenic right ventricular cardiomyopathy]] (ARVC).
*Lateral LV - 14.1%.
*Lateral LV - 14.1%.


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*Advanced lesions are fibrotic and may mimic old infarcts (grossly) due to coronary artery atherosclerosis.
*Advanced lesions are fibrotic and may mimic old infarcts (grossly) due to coronary artery atherosclerosis.


===Histology===
===Microscopic===
Features:<ref name=pmid19660614/>
Features:<ref name=pmid19660614/>
*Non-caseating granulomas.  
*Non-caseating [[granulomas]].  
*Subepicardial predominance.
*Subepicardial predominance.
*+/-Fibrosis - old lesions are fibrotic.
*+/-Fibrosis - old lesions are fibrotic.
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Notes:
Notes:
*Myocyte necrosis and eosinophils are features of ''granulomatous myocarditis''.<ref name=pmid19660614/>
*Myocyte necrosis and [[eosinophil]]s are features of ''granulomatous myocarditis''.<ref name=pmid19660614/>


==Myocarditis==
==Myocarditis==
===Work-up===
{{Main|Myocarditis}}
*Requires 10 sections to exclude;<ref>KC. 1 October 2010.</ref> sections should include RV and LV.
**It is often missed with five.<ref>{{Cite journal  | last1 = Kubo | first1 = N. | last2 = Morimoto | first2 = S. | last3 = Hiramitsu | first3 = S. | last4 = Uemura | first4 = A. | last5 = Kimura | first5 = K. | last6 = Shimizu | first6 = K. | last7 = Hishida | first7 = H. | title = Feasibility of diagnosing chronic myocarditis by endomyocardial biopsy. | journal = Heart Vessels | volume = 12 | issue = 4 | pages = 167-70 | month =  | year = 1997 | doi =  | PMID = 9559966 }}</ref>


===Classification<ref name=emedicine1612533>[http://emedicine.medscape.com/article/1612533-overview http://emedicine.medscape.com/article/1612533-overview]</ref>===
==Idiopathic granulomatous myocarditis==
*Eosinophilic - ''hypersensitivity myocarditis'' - most common.
*[[AKA]] ''giant cell myocarditis''<ref name=emedicine1612533>[http://emedicine.medscape.com/article/1612533-overview http://emedicine.medscape.com/article/1612533-overview]</ref> and less ambiguously ''idiopathic giant cell myocarditis''.
*Lymphocytic - viral, autoimmune.
*Granulomatous.
*Neutrophilic.
*Reperfusion (associated with myocardial infarction).


==Granulomatous myocarditis==
===General===
===General===
*AKA ''giant cell myocarditis''.<ref name=emedicine1612533>[http://emedicine.medscape.com/article/1612533-overview http://emedicine.medscape.com/article/1612533-overview]</ref>
*Unknown etiology.<ref name=upmc175>URL: [http://path.upmc.edu/cases/case175/dx.html http://path.upmc.edu/cases/case175/dx.html]. Accessed on: 8 January 2012.</ref>


===Histology===
===Microscopic===
Features:<ref name=pmid19660614/>
Features:<ref name=pmid19660614/>
*Granulomas.  
*[[Granuloma]]s.  
*Myocyte necrosis.
*Myocyte [[necrosis]].
*Eosinophils.
*Eosinophils.


Note:
Note:
*Eosinophils and myocyte necrosis differentiate this entity from ''cardiac sarcoidosis''.
*Eosinophils and myocyte necrosis differentiate this entity from ''[[cardiac sarcoidosis]]''.
**Granulomas in sarcoidosis are well formed and also involve the fat.<ref name=upmc175>URL: [http://path.upmc.edu/cases/case175/dx.html http://path.upmc.edu/cases/case175/dx.html]. Accessed on: 8 January 2012.</ref>
 
DDx:
*Infectious granulomatous myocarditis, e.g. [[tuberculosis]].
*[[Rheumatic myocarditis]].
*Lymphocytic myocarditis.
 
Images:
*[http://path.upmc.edu/cases/case175.html Giant cell myocarditis (upmc.edu)].
 
===Stains===
*[[Ziehl-Neelsen stain]] -ve.
*[[GMS stain]] -ve.
 
==Chagas disease==
*[[AKA]] ''American trypanosomiasis''.
{{Main|Chagas disease}}


==Cardiac amyloidosis==
==Cardiac amyloidosis==
{{main|amyloidosis}}
{{main|Amyloidosis}}
===General===
===General===
*Amyloid in the heart.
*Amyloid in the heart.
*Rare.
*Common in the elderly - see ''[[senile systemic amyloidosis]]''.


===Histology===
===Microscopic===
Features (H&E stain):
Features ([[H&E stain]]):
*Acellular fluffy pink material.
*Acellular fluffy pink material.


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Notes:
Notes:
*ABCs of pink on H&E = '''a'''myloid, '''b'''lood (fibrin), '''c'''ollagen, '''s'''mooth muscle.
*ABCs of pink on H&E = '''a'''myloid, '''b'''lood (fibrin), '''c'''ollagen, '''s'''mooth muscle.
==Mesothelial/monocytic incidental cardiac excrescence==
*[[AKA]] ''Cardiac MICE''.
===General===
*Very rare.
*Benign.
*May be confused with a tumour.<ref name=pmid12879644>{{Cite journal  | last1 = de Gouveia | first1 = RH. | last2 = Ramos | first2 = S. | last3 = Ribeiro | first3 = MA. | last4 = Ferreira | first4 = M. | last5 = Martins | first5 = AP. | title = Cardiac MICE--tumor or thrombus? | journal = Rev Port Cardiol | volume = 22 | issue = 4 | pages = 523-9 | month = Apr | year = 2003 | doi =  | PMID = 12879644 }}</ref>
===Microscopic===
Features:<ref name=pmid12879644/>
*Mesothelial cells.


==Cocaine toxicity==
==Cocaine toxicity==
===General===
{{Main|Cocaine toxicity}}
*Anatomical pathology findings at autopsy are uncommon (most common situation) or non-specific (atherosclerosis +/- acute thrombosis).<ref name=pmid1749414>{{cite journal |author=Virmani R |title=Cocaine-associated cardiovascular disease: clinical and pathological aspects |journal=NIDA Res. Monogr. |volume=108 |issue= |pages=220–9 |year=1991 |pmid=1749414 |doi= |url=}}</ref>
 
*Toxicity mechanisms:
No distinctive pathologic findings. May appear older than one would expect, e.g. advanced [[atherosclerosis]] in a young man.
**Direct effects of norepinephrine on myocytes
**Vasospasm leading to myocardial ischemia.


===Gross===
==Heart transplant pathology==
Features:<ref name=pmid1346509>{{cite journal |author=Kloner RA, Hale S, Alker K, Rezkalla S |title=The effects of acute and chronic cocaine use on the heart |journal=Circulation |volume=85 |issue=2 |pages=407–19 |year=1992 |month=February |pmid=1346509 |doi= |url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=1346509}}</ref>
{{Main|Heart transplant pathology}}
*+/-Atherosclerosis out of keeping with age.
*+/-Large areas of confluent necrosis.
*+/-Fibrosis.


===Microscopic===
Comes in different flavours... cellular, acute vascular chronic.
Features:<ref name=pmid1346509/>
*+/-Large areas of confluent necrosis.
*+/-Contraction band necrosis.
*+/-Fibrosis.
*+/-Myocarditis (usu. eosinophilic).


==See also==
==See also==

Latest revision as of 05:33, 21 July 2016

The heart is an important organ. It moves the blood around. For orthopods, it gets the Ancef (cefazolin) to the bones. When it stops for an extended time... people end-up in the morgue or being seen by a pathologist for an autopsy.

An introduction to cardiovascular pathology is found in the cardiovascular pathology article.

Obscure anatomy

Main article: Heart anatomy

Heart dissection

Pericardium

If adhesions are present decide whether they are:

  1. Fibrinous (recent) or,
  2. Fibrous (old).

Identifying hardware

  • Defibrillator - thick wires.
  • Pacer - thin wires.

General rule

  • Open along the lines of flow.

Note:

  • Do not open right atrium (RA) SVC to IVC.
    • Why? A.: You cut through the territory of the SA node.

Coronary arteries

  • These are often done first, i.e. before the heart is opened.
  • They should be sectioned (axially) at ~2 mm intervals.
    • Longitudinally opening the coronaries does not allow accurate assessment of luminal stenosis.[1]
  • A significant stenosis (defined by diameter narrowing) is 70-75%.[2]

Notes:

  • If calcified:
    • Dissect off the coronary tree + decal.

Right atrium

  • Open anteriorly ~ 1 cm above the tricuspid valve annulus.
    • Open right auricle at the same time.

Examination of apex

  • Slice apex (perpendicular to the long axis of the heart), such that both ventricles can be seen.

Right ventricle

  • Make cut through the apex (transverse/biventicular section).
  • Open along lateral edge (from RA cut).

Right ventricular outflow tract

  • Cut along pulmonary artery.

Left atrium

  • Isolate the four pulmonary veins - cut 'em so they are long on the heart.
  • Join the pulmonary veins on the right with a cut.
  • Join the pulmonary veins on the left with a cut.
  • Open the posterior aspect of the LA by joining the two previous cuts.
  • Open the left auricle (to look for thrombus).

Left ventricle

  • Open on the lateral aspect with a long knife.

Left ventricular outflow tract

  • Open LVOT with cut(s) from LV; stay close to intraventricular septum.[3]
    • Avoid cutting the pulmonary artery.
    • With luck you end-up between the left coronary cusp and right coronary cusp.
      • Check whether the aortic valve and coronary ostia are normal.

Slicing

  • After the heart is opened it should be sliced at 5-10 mm intervals to the semilunar valves.

Standard measures of the heart

  • Mass (weight).
  • Left ventricle (LV) - 2 cm below the MV.
  • Right ventricle (RV) - 2 cm below the TV.
  • Aortic valve (AV) circumference.
  • Mitral valve (MV) circumference.
  • Pulmonic valve (PV) circumference.
  • Tricuspid valve (TV) circumference.

Normal measures

Younger adults (20-60 years)

Based on Ludwig:[4]

Measure Men Women
Aortic valve 6.7 (6.0-7.4) 6.3 (5.7-6.9)
Pulmonary valve 6.6 (6.1-7.1) 6.2 (5.7-6.7)
Mitral valve 9.6 (9.4-9.9) 8.6 (8.2-9.1)
Tricuspid valve 11.4 (11.2-11.7) 10.6 (10.2-10.9)

Based on Ludwig:[4]

Feature Measure
Left ventricle 1.25 (1.00-1.50)
Right ventricle 0.4 (0.25-0.50)

Older adults (>60 years)

Based on Ludwig:[4]

Measure Men Women
Aortic valve 8.3 (8.1-8.5) 7.6 (7.3-7.9)
Pulmonary valve 7.3 (7.2-7.5) 7.1 (6.8-7.4)
Mitral valve 9.5 (9.2-9.8) 8.6 (8.2-9.0)
Tricuspid valve 11.6 (11.4-11.8) 10.5 (10.0-11.1)

Based on Ludwig:[4]

Feature Measure
Left ventricle 1.15 (1.05-1.25)
Right ventricle 0.38 (0.35-0.40)

Standard sections

Minimalist approach (Dr. C.):

  1. LV and PPM (left ventricle and posterior papillary muscle).
  2. LV and APM (left ventricle and anterior papillary muscle).

Compromise approach:

  1. LV and PPM.
  2. LV and APM.
  3. LV lateral wall.
  4. Intraventricular septum.
  5. RV.

Make the lab work hard approach (Dr. B.):

  1. PRV (post. RV) with tricuspid valve.
  2. ARV (ant. RV) with pulm. valve.
  3. PLV (post. LV) with mitral valve.
  4. ALV (ant. LV) with aortic valve.
  5. Lat. LV.
  6. LV and PPM.
  7. Post. septum.
  8. Mid. septum.
  9. Ant. septum.
  10. Ant. LV wall.
  11. LV and APM.
  12. RCA.
  13. LAD.
  14. LCx.

Stock

  • One slice (close to apex).
  • +/-Region of SA node.
  • +/-Region of AV node.

Conducting system

Indications for examining the conducting system[5]

  1. History of syncope.
  2. History of arrhythmia.
  3. Negative autopsy.

Sinoatrial node

  • Sinoatrial (SA) node is at the lateral aspect of sulcus terminalis; lateral aspect of the superior vena cava and right atrium junction.[6]
    • Cannot be identified grossly.
    • Artery of the SA (branch of RCA) may be a clue to where it lies.

Submitting the SA Node:[6]

  • Submit all of lateral sulcus terminalis -- serially section perpendicular to the sulcus terminalis, i.e. cuts are in the axis of the SVC (superior to inferior).

Notes: Gulino[7] has a good description and good pictures.

SA node histology

The SA node is best identified by it location:

  • The SA Node is superficial to cardiac muscle, i.e. distant to the RA relative to the cardiac muscle.
    • The SA nodal tissue abuts cardiac muscle.
  • It sits around the sinoatrial node artery - which should be seen on its lumen if the sections were taken properly.
  • The SA node is deep to adipose tissue that covers that epicardial aspect of the heart.
  • Nerve fibres (from the vagus nerve) are typically found between that adipose tissue and SA nodal tissue.

Histologic characteristics:

  • Spindle cell morphology + wavy nucleus.
  • Cytoplasm stains lighter with eosin than cardiac muscle.
  • +/-Vacuoles.
Images

  • SA node - low mag. - vignetting (WC)

  • SA node - low mag. (WC)

  • SA node - high mag.(WC)

Atrioventricular node

Approach 1 (Peter method):

  • Open the LVOT - if it hasn't been opened yet.
  • Cut a section of that includes the right coronary cusp (of the aortic valve) and about 1.5 cm below it (this has the membranous septum and the superior muscular septum).[8]
    • This section should then be serially sectioned in the axis of the VLOT.

Approach 2 (Virmani method):

  1. View from right atrium: AV node is between the coronary sinus and membranous septum.
  2. View from LVOT: Inferior to the posterior (non-coronary) cusp of the aortic valve.
    • One should cut a (coronal) section of that includes the posterior (non-coronary) cusp and about 1.5 cm below it (this has the membranous septum and the superior muscular septum) -- see: Figure 1-15 in Virmani et al.[9]
      • This section should then be serially sectioned in the axis of the VLOT.

Approach 3 (Location by triangle of Koch):

  • Atrioventicular (AV) node is in the triangle of Koch.

Triangle of Koch according to Virmani[10] is the floor of the RA and:

  • Tendon of Todaro = "superior".
  • Tricuspid valve annulus = "inferior".
  • Coronary sinus = "posterior".

Images:

Tamponade

  • Tamponade is a clinical diagnosis (classically: elevated JVP, low BP). It cannot be made at autopsy.

The pathologist (like radiologists) can say...

Image: Pericardial effusion - CT scan (wikipedia.org).

Fibrinous pericarditis

General

Etiology:

Note:

  • Roberts suggests that pericardial heart disease may be a better term for this, as this isn't really an inflammatory process.[14]

Gross

  • Pericardium with a shaggy rough appearance.
    • Described as "buttered bread dropped-on-the-floor look".[15]

Image:

Microscopic

Features:

  • Fibrin - pink amorphous material.

Note:

  • Inflammation is not a strict requirement for the diagnosis.[14]

Images:

  • Fibrinous pericarditis. (WC)

Sign out

Pericardium, Excision:
- Fibrinous pericardial heart disease.

Myocardial infarction

  • Abbreviated MI.
  • AKA myocardial infarct.
Main article: Myocardial infarction

Coronary artery atherosclerosis

Main article: Atherosclerosis
  • AKA coronary artery disease, abbreviated CAD.
  • AKA atherosclerotic heart disease, abbreviated ASHD.
  • AKA atherosclerotic coronary artery disease.

General

  • Greater than 75% (diameter) stenosis - considered significant.[17]
  • Leading cause of morbidity and mortality, esp. in the elderly.
  • Left main coronary artery (LMCA) disease is particularly fatal.[18]

Clinical presentations:

Note:

  • Coronary artery atherosclerosis is not the only type of coronary artery disease... but it is by far the most common; thus, CAD is generally considered synonymous with coronary artery atherosclerosis.

Treatment:

  • Medical management (blood pressure control (antihypertensives), cholesterol control (e.g. statins, exercise), diabetes control, smoking cessation).
  • Coronary artery bypass surgery (CABG).
  • Percutaneous coronary intervention (PCI).

Stenosis definition

Definition (as per NASCET):[19]

With a bit of algebra one can show:

Where:

  • x = 1 - (percent diameter reduction/100).
  • Ao = the initial area.
  • Ax = the area with diameter x.

If one applies the above equation:

  • A 50% diameter reduction results in a 75% area reduction.
  • A 75% diameter reduction results in a 93.75% area reduction.
  • A 90% diameter reduction results in a 99% area reduction.

Microscopic

See Atherosclerosis.

Abnormal hearts

Cardiac hypertrophy

Can be by:

  • Mass criteria described in a couple of articles from the Mayo Clinic Proceedings.[20][21]
  • Thickness criteria.

Rules of thumb:[22]

  • >400 g is often abnormal.
  • >500 g is abnormal.
  • >1.5 cm left ventricle thickness.
  • >0.5 cm right ventricle thickness.

Common patterns

Dilated hearts

Dilated pattern DDx:[23]

  • Hypertensive heart disease.
  • Hypertrophic cardiomyopathy.
  • Amyloidosis.

Concentric left ventricular hypertrophy

Concentric left ventricular hypertrophy is a common gross pathologic finding.

The main DDx is:

Other considerations:

  • Concentric LVH. (WC)

Eccentric left ventricular hypertrophy

Detail articles

Cardiomyopathy

Main article: Cardiomyopathy

In the land of cardiology... there is a thing called cardiomyopathy. This article deals with it.

It includes discussion of dilated cardiomyopathy, hypertrophic cardiomyopathy and arrhythmogenic right ventricular cardiomyopathy.

Congenital heart disease

Main article: Congenital heart disease

Congenital heart disease... a domain of pediatric cardiac surgery and occasionally adult cardiac surgery.

The article covers shunts, both left-to-right and right-to-left.

Tumours

Main article: Tumours of the heart

These are rare buggers.

Valvular disease

Main article: Valvular heart disease

This is the domain of cardiac surgery... only seen in hospitals with cardiac surgery.

Endocarditis

Main article: Infective endocarditis

Cardiac sarcoidosis

Main article: Sarcoidosis

General

  • Can be in isolation or part of systemic sarcoidosis.[24]
  • May mimic hypertrophic cardiomyopathy clinically.[25]
  • Clinical: associated with heart block.[24]

Gross

  • Ventricular septum base - most common site of involvement.[24]

Distribution by autopsy findings:[26]

Notes:

  • Advanced lesions are fibrotic and may mimic old infarcts (grossly) due to coronary artery atherosclerosis.

Microscopic

Features:[26]

  • Non-caseating granulomas.
  • Subepicardial predominance.
  • +/-Fibrosis - old lesions are fibrotic.

Negatives:

  • Significant number of eosinophils.
  • Myocyte necrosis.

Notes:

  • Myocyte necrosis and eosinophils are features of granulomatous myocarditis.[26]

Myocarditis

Main article: Myocarditis

Idiopathic granulomatous myocarditis

  • AKA giant cell myocarditis[27] and less ambiguously idiopathic giant cell myocarditis.

General

  • Unknown etiology.[28]

Microscopic

Features:[26]

Note:

  • Eosinophils and myocyte necrosis differentiate this entity from cardiac sarcoidosis.
    • Granulomas in sarcoidosis are well formed and also involve the fat.[28]

DDx:

Images:

Stains

Chagas disease

  • AKA American trypanosomiasis.
Main article: Chagas disease

Cardiac amyloidosis

Main article: Amyloidosis

General

Microscopic

Features (H&E stain):

  • Acellular fluffy pink material.

Special stains:

  • Congo red stain - red (normal light), apple-green in polarized light.[29]
  • Thioflavin-T stain[30]

Images (amyloidosis cardiac):

Images (amyloidosis - non-cardiac):

Notes:

  • ABCs of pink on H&E = amyloid, blood (fibrin), collagen, smooth muscle.

Mesothelial/monocytic incidental cardiac excrescence

  • AKA Cardiac MICE.

General

  • Very rare.
  • Benign.
  • May be confused with a tumour.[31]

Microscopic

Features:[31]

  • Mesothelial cells.

Cocaine toxicity

Main article: Cocaine toxicity

No distinctive pathologic findings. May appear older than one would expect, e.g. advanced atherosclerosis in a young man.

Heart transplant pathology

Main article: Heart transplant pathology

Comes in different flavours... cellular, acute vascular chronic.

See also

References

  1. ↑ URL: http://www.histopathology-india.net/CAEx.htm. Accessed on: 7 July 2011.
  2. ↑ Burton, Julian L.; Rutty, Guy N. (2010). The Hospital Autopsy A Manual of Fundamental Autopsy Practice (3rd ed.). Oxford University Press. pp. 147. ISBN 978-0340965146.
  3. ↑ {{Ref HospAuto|
  4. ↑ 4.0 4.1 4.2 4.3 Ludwig, Jurgen (2002). Handbook of Autopsy Practice (3rd ed.). Humana Press. pp. 569. ISBN 978-1588291691.
  5. ↑ KC. 1 October 2010.
  6. ↑ 6.0 6.1 Virmani et al. Cardiovascular Pathology. 2nd Ed. 2001. P.16.
  7. ↑ Gulino SP (September 2003). "Examination of the cardiac conduction system: forensic application in cases of sudden cardiac death". Am J Forensic Med Pathol 24 (3): 227–38. doi:10.1097/01.paf.0000083453.43318.74. PMID 12960658.
  8. ↑ PF. August 21, 2009.
  9. ↑ Virmani et al. Cardiovascular Pathology. 2nd Ed. 2001. P.18.
  10. ↑ Virmani et al. Cardiovascular Pathology. 2nd Ed. 2001. P.17.
  11. ↑ Macedo, PG.; Patel, SM.; Bisco, SE.; Asirvatham, SJ. (2010). "Septal accessory pathway: anatomy, causes for difficulty, and an approach to ablation.". Indian Pacing Electrophysiol J 10 (7): 292-309. PMID 20680108.
  12. ↑ 12.0 12.1 Mitchell, Richard; Kumar, Vinay; Fausto, Nelson; Abbas, Abul K.; Aster, Jon (2011). Pocket Companion to Robbins & Cotran Pathologic Basis of Disease (8th ed.). Elsevier Saunders. pp. 293. ISBN 978-1416054542.
  13. ↑ Schneider, JS.; Edwards, JE. (May 1979). "Irradiation-induced pericarditis.". Chest 75 (5): 560-4. PMID 436483.
  14. ↑ 14.0 14.1 Roberts, WC. (Jan 2005). "Pericardial heart disease: its morphologic features and its causes.". Proc (Bayl Univ Med Cent) 18 (1): 38-55. PMID 16200146.
  15. ↑ Cohen, MB.; Laennec, RT. (Feb 2004). "Cross your heart: Some historical comments about fibrinous pericarditis.". Hum Pathol 35 (2): 147-9. PMID 14991530.
  16. ↑ URL: http://autopsy.stanford.edu/fellowships.html. Accessed on: 21 January 2012.
  17. ↑ Chamberlain, D. March 7, 2008.
  18. ↑ Kanjwal, MY.; Carlson, DE.; Schwartz, JS. (Nov 1999). "Chronic/subacute total occlusion of the left main coronary artery--a case report and review of literature.". Angiology 50 (11): 937-45. PMID 10580359.
  19. ↑ Barnett HJ, Taylor DW, Eliasziw M, et al. (November 1998). "Benefit of carotid endarterectomy in patients with symptomatic moderate or severe stenosis. North American Symptomatic Carotid Endarterectomy Trial Collaborators". The New England Journal of Medicine 339 (20): 1415–25. PMID 9811916. http://content.nejm.org/cgi/pmidlookup?view=short&pmid=9811916&promo=ONFLNS19.
  20. ↑ Scholz DG, Kitzman DW, Hagen PT, Ilstrup DM, Edwards WD (February 1988). "Age-related changes in normal human hearts during the first 10 decades of life. Part I (Growth): A quantitative anatomic study of 200 specimens from subjects from birth to 19 years old". Mayo Clin. Proc. 63 (2): 126–36. PMID 3276973.
  21. ↑ Kitzman DW, Scholz DG, Hagen PT, Ilstrup DM, Edwards WD (February 1988). "Age-related changes in normal human hearts during the first 10 decades of life. Part II (Maturity): A quantitative anatomic study of 765 specimens from subjects 20 to 99 years old". Mayo Clin. Proc. 63 (2): 137–46. PMID 3276974.
  22. ↑ KC. 14 October 2010.
  23. ↑ Cotran, Ramzi S.; Kumar, Vinay; Fausto, Nelson; Nelso Fausto; Robbins, Stanley L.; Abbas, Abul K. (2005). Robbins and Cotran pathologic basis of disease (7th ed.). St. Louis, Mo: Elsevier Saunders. pp. 602. ISBN 0-7216-0187-1.
  24. ↑ 24.0 24.1 24.2 Veinot JP, Johnston B (May 1998). "Cardiac sarcoidosis--an occult cause of sudden death: a case report and literature review". J. Forensic Sci. 43 (3): 715–7. PMID 9608713.
  25. ↑ Matsumori A, Hara M, Nagai S, et al. (September 2000). "Hypertrophic cardiomyopathy as a manifestation of cardiac sarcoidosis". Jpn. Circ. J. 64 (9): 679–83. PMID 10981852.
  26. ↑ 26.0 26.1 26.2 26.3 Tavora F, Cresswell N, Li L, Ripple M, Solomon C, Burke A (August 2009). "Comparison of necropsy findings in patients with sarcoidosis dying suddenly from cardiac sarcoidosis versus dying suddenly from other causes". Am. J. Cardiol. 104 (4): 571–7. doi:10.1016/j.amjcard.2009.03.068. PMID 19660614.
  27. ↑ http://emedicine.medscape.com/article/1612533-overview
  28. ↑ 28.0 28.1 URL: http://path.upmc.edu/cases/case175/dx.html. Accessed on: 8 January 2012.
  29. ↑ Ebert EC, Nagar M (March 2008). "Gastrointestinal manifestations of amyloidosis". Am. J. Gastroenterol. 103 (3): 776-87. doi:10.1111/j.1572-0241.2007.01669.x. PMID 18076735.
  30. ↑ Nishi S, Alchi B, Imai N, Gejyo F (April 2008). "New advances in renal amyloidosis". Clin. Exp. Nephrol. 12 (2): 93-101. doi:10.1007/s10157-007-0008-3. PMID 18175051.
  31. ↑ 31.0 31.1 de Gouveia, RH.; Ramos, S.; Ribeiro, MA.; Ferreira, M.; Martins, AP. (Apr 2003). "Cardiac MICE--tumor or thrombus?". Rev Port Cardiol 22 (4): 523-9. PMID 12879644.
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