Difference between revisions of "Heart"

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Heart (view source)

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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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*Hypertrophic [[cardiomyopathy]] (usually eccentric).
*Hypertrophic [[cardiomyopathy]] (usually eccentric).


==Cardiomyopathy==
<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. 


==Congenital heart disease==
It includes discussion of ''dilated cardiomyopathy'', ''hypertrophic cardiomyopathy'' and ''arrhythmogenic right ventricular cardiomyopathy''.
 
===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==
Michael
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