Heart

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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 throught 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

  • 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.

Standard sections

Minimalist approach (Cybulsky):

  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 (Butany):

  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[4]

  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.[5]
    • Cannot be identified grossly.
    • Artery of the SA (branch of RCA) may be a clue to where it lies.

Submitting the SA Node:[5]

  • 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[6] 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:

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).[7]
    • 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.[8]
      • 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[9] 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

  • AKA bread and butter pericarditis.

General

Etiology:

  • Radiation.[11]
  • Uremia.

Gross

  • Pericardium with a shaggy rough appearance.
    • Described as "buttered bread dropped-on-the-floor look".[12]

Image:

Microscopic

Features:

  • Fibrin - pink amorphous material.

Images:

Myocardial infarction

  • Abbreviated MI.
  • AKA myocardial infarct.

Clinical

  • Usually diagnosed clinically - with blood work (troponin, CK-MB) or EKG.
  • MI may be precipitated by cocaine use... and further exacerbated by treatment with a beta-blocker.[14]
  • Acute myocardial infarction (abbreviated AMI) = MI < 6 hours old.[15]
    • Usually no PMN infiltrate.

Classic symptoms:

  • Retrosternal chest pain +/- with radiation down the arms.
  • Nausea & vomiting.
  • Diaphoresis.

Enzymatic tests:[16]

  • CK: peaks at day 1, resolves after 2-3 days.
  • AST: peaks close to day 2, resolves after 4-5 days.
  • LDH: peaks day 2, resolves after ~6 days.

Complications of MI:[17]

  • Contractile dysfunction.
  • Cardiac arrhythmia.
  • Aneurysm formation, e.g. left ventricular aneurysm.
  • Ventricular rupture:
    • Ventricular free wall rupture.
    • Ventricular septal rupture.
  • Fibrinous pericarditis.
    • Dressler's syndrome AKA postmyocardial infarction syndrome[18]; pericarditis post-myocardial infarction +/- pericardial effusion (clinically tamponade).
  • Mural thrombosis.
  • Extension of MI.

Pathologic

Gross

Sequence:[19]

  • 18-24 hours - myocardial pallor.
  • 1-3 days - pallor, moderate hyperemia (redness due to congestion with blood).
  • 3-7 days - yellow lesion with hyperemic border.
  • 10-21 days - maximally yellow.
  • 6 weeks - white (fibrosis).

Microscopic

Sequence:[20]

  • 1-3 hours - Wavy (myocardial) fibers
  • 4-12 hours - Coagulative necrosis & loss of cross striations, contraction bands, edema, hemorrhage, PMN infiltrate.
  • 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.

Images:

Contraction band necrosis

General:

  • Mediated by catecholamines.[21]
  • Thought to arise in reperfusion from hypercontraction.

Microscopic:

  • Thick intensely eosinophilic staining bands (on H&E) ~ typically 4-5 micrometres wide
    • Span the short axis of myocyte.
    • Can be thought of bunched-up striae.

Notes:

  • Better seen with special stains (Masson or Gomori trichrome).[22]

Images:

Coronary artery atherosclerosis

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

General

  • Greater than 75% (diameter) stenosis - considered significant.[23]
  • Leading cause of morbidity and mortality, esp. in the elderly.
  • Left main coronary artery (LMCA) disease is particularly fatal.[24]

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.

Stenosis definition

Definition (as per NASCET):[25]

With a bit of allegbra 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.[26][27]
  • Thickness criteria.

Rules of thumb:[28]

  • >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:[29]

  • 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:

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

Congential heart disease... a domain of paediatric 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 insolation or part of systemic sarcoidosis.[30]
  • May mimic hypertrophic cardiomyopathy clinically.[31]
  • Clinical: associated with heart block.[30]

Gross

  • Ventricular septum base - most common site of involvement.[30]

Distribution by autopsy findings:[32]

Notes:

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

Microscopic

Features:[32]

  • 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.[32]

Myocarditis

Work-up

  • Requires 10 sections to exclude;[33] sections should include RV and LV.
    • It is often missed with five.[34]

Classification[35]

  • Eosinophilic - hypersensitivity myocarditis - most common.
    • May be assoc. with peripheral blood eosinophilia.[36]
  • Lymphocytic - viral, autoimmune.
  • Granulomatous - infectious, idiopathic.
  • Neutrophilic.
  • Reperfusion (associated with myocardial infarction).

Images:

Idiopathic granulomatous myocarditis

  • AKA giant cell myocarditis[35] and less ambiguously idiopathic giant cell myocarditis.

General

  • Unknown etiology.[37]

Microscopic

Features:[32]

Note:

  • Eosinophils and myocyte necrosis differentiate this entity from cardiac sarcoidosis.
    • Granulomas in sarcoidosis are well formed and also involve the fat.[37]

DDx:

Images:

Stains

Chagas disease

  • AKA American trypanosomiasis.

General

  • Essentially a South American disease.
  • Etiology: protozoa Trypanosoma cruzi - transmitted by reduvid bugs,[38] also known as kissing bug.[39]

Clinical:[40]

  • Depends on phase of infection.
  • Arrhythmias (late).

Dx:[41]

  • Usually serology.
  • Thin blood smear.

Tx:

  • Antimicrobials: benznidazole, nifurtimox.[38]

Microscopic

Features:

  • Inflammation - main finding.[40]
  • Intramuscular organisms (without an inflammatory response).
  • Neuronal loss in atrial ganglia.[42]

DDx:

Images:

IHC

  • Anti–T cruzi immunoperoxidase.[42]

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.[45]
  • Thioflavin-T stain[46]

Images (amyloidosis cardiac):

Images (amyloidosis - non-cardiac):

Notes:

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

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. ↑ KC. 1 October 2010.
  5. ↑ 5.0 5.1 Virmani et al. Cardiovascular Pathology. 2nd Ed. 2001. P.16.
  6. ↑ 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.
  7. ↑ PF. August 21, 2009.
  8. ↑ Virmani et al. Cardiovascular Pathology. 2nd Ed. 2001. P.18.
  9. ↑ Virmani et al. Cardiovascular Pathology. 2nd Ed. 2001. P.17.
  10. ↑ 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.
  11. ↑ Schneider, JS.; Edwards, JE. (May 1979). "Irradiation-induced pericarditis.". Chest 75 (5): 560-4. PMID 436483.
  12. ↑ Cohen, MB.; Laennec, RT. (Feb 2004). "Cross your heart: Some historical comments about fibrinous pericarditis.". Hum Pathol 35 (2): 147-9. PMID 14991530.
  13. ↑ URL: http://autopsy.stanford.edu/fellowships.html. Accessed on: 21 January 2012.
  14. ↑ Mohamad T, Kondur A, Vaitkevicius P, Bachour K, Thatai D, Afonso L (2008). "Cocaine-induced chest pain and beta-blockade: an inner city experience". Am J Ther 15 (6): 531-5. doi:10.1097/MJT.0b013e3181758cfc. PMID 19127137.
  15. ↑ Senter, S.; Francis, GS. (Mar 2009). "A new, precise definition of acute myocardial infarction.". Cleve Clin J Med 76 (3): 159-66. doi:10.3949/ccjm.75a.08092. PMID 19258462.
  16. ↑ URL: http://pro2services.com/Lectures/Fall/CardEnz/a6mienz.gif. Accessed on: 27 April 2012.
  17. ↑ 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.
  18. ↑ Hutchcroft BJ (July 1972). "Dressler's syndrome". Br Med J 3 (5817): 49. PMC 1788531. PMID 5039567. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1788531/.
  19. ↑ http://library.med.utah.edu/WebPath/TUTORIAL/MYOCARD/MYOCARD.html
  20. ↑ http://library.med.utah.edu/WebPath/TUTORIAL/MYOCARD/MYOCARD.html
  21. ↑ Hopster DJ, Milroy CM, Burns J, Roberts NB (May 1996). "Necropsy study of the association between sudden cardiac death, cardiac isoenzymes and contraction band necrosis". J. Clin. Pathol. 49 (5): 403–6. PMC 500481. PMID 8707956. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC500481/.
  22. ↑ Hopster DJ, Milroy CM, Burns J, Roberts NB (May 1996). "Necropsy study of the association between sudden cardiac death, cardiac isoenzymes and contraction band necrosis". J. Clin. Pathol. 49 (5): 403–6. PMC 500481. PMID 8707956. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC500481/.
  23. ↑ Chamberlain, D. March 7, 2008.
  24. ↑ 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.
  25. ↑ 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.
  26. ↑ 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.
  27. ↑ 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.
  28. ↑ KC. 14 October 2010.
  29. ↑ 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.
  30. ↑ 30.0 30.1 30.2 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.
  31. ↑ 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.
  32. ↑ 32.0 32.1 32.2 32.3 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.
  33. ↑ KC. 1 October 2010.
  34. ↑ Kubo, N.; Morimoto, S.; Hiramitsu, S.; Uemura, A.; Kimura, K.; Shimizu, K.; Hishida, H. (1997). "Feasibility of diagnosing chronic myocarditis by endomyocardial biopsy.". Heart Vessels 12 (4): 167-70. PMID 9559966.
  35. ↑ 35.0 35.1 http://emedicine.medscape.com/article/1612533-overview
  36. ↑ 36.0 36.1 Amini R, Nielsen C (2010). "Eosinophilic myocarditis mimicking acute coronary syndrome secondary to idiopathic hypereosinophilic syndrome: a case report". J Med Case Reports 4: 40. doi:10.1186/1752-1947-4-40. PMC 2830978. PMID 20181108. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2830978/.
  37. ↑ 37.0 37.1 URL: http://path.upmc.edu/cases/case175/dx.html. Accessed on: 8 January 2012.
  38. ↑ 38.0 38.1 URL: http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0002348/. Accessed on: 4 December 2011.
  39. ↑ URL: http://www.who.int/topics/chagas_disease/en/. Accessed on: 1 December 2011.
  40. ↑ 40.0 40.1 Teixeira, AR.; Nascimento, RJ.; Sturm, NR. (Aug 2006). "Evolution and pathology in chagas disease--a review.". Mem Inst Oswaldo Cruz 101 (5): 463-91. PMID 17072450.
  41. ↑ URL: http://www.cdc.gov/parasites/chagas/diagnosis.html. Accessed on: 4 December 2011.
  42. ↑ 42.0 42.1 Marin-Neto, JA.; Cunha-Neto, E.; Maciel, BC.; Simões, MV. (Mar 2007). "Pathogenesis of chronic Chagas heart disease.". Circulation 115 (9): 1109-23. doi:10.1161/CIRCULATIONAHA.106.624296. PMID 17339569.
  43. ↑ URL: http://path.upmc.edu/cases/case160/micro.html. Accessed on: 8 January 2012.
  44. ↑ Higuchi, Mde L.; Benvenuti, LA.; Martins Reis, M.; Metzger, M. (Oct 2003). "Pathophysiology of the heart in Chagas' disease: current status and new developments.". Cardiovasc Res 60 (1): 96-107. PMID 14522411.
  45. ↑ 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.
  46. ↑ 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.
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