Difference between revisions of "Heart"

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==Cardiac amyloidosis==
==Cardiac amyloidosis==
{{main|amyloidosis}}
{{main|amyloidosis}}
===General===
*Amyloid in the heart.
*Amyloid in the heart.
*Rare.
*Rare.
Line 303: Line 304:
===Histology===
===Histology===
Features (H&E stain):
Features (H&E stain):
*Fluffy pink material.
*Acellular fluffy pink material.


Special stains:
Special stains:
Line 312: Line 313:
*[http://en.wikipedia.org/wiki/File:Small_bowel_duodenum_with_amyloid_deposition_congo_red_10X.jpg Amyloid - congo red stain] - wikipedia.org.
*[http://en.wikipedia.org/wiki/File:Small_bowel_duodenum_with_amyloid_deposition_congo_red_10X.jpg Amyloid - congo red stain] - wikipedia.org.
*[http://commons.wikimedia.org/wiki/File:Small_bowel_duodenum_with_amyloid_deposition_20X.jpg Amyloid - H&E stain] - wikimedia.org.
*[http://commons.wikimedia.org/wiki/File:Small_bowel_duodenum_with_amyloid_deposition_20X.jpg Amyloid - H&E stain] - wikimedia.org.
Notes:
*ABCs of pink on H&E = '''a'''myloid, '''b'''lood (fibrin), '''c'''ollagen, '''s'''mooth muscle.


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

Revision as of 12:08, 12 August 2010

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.

Heart dissection

General rule

  • Open along the lines of flow.

Note:

  • Don't open RA SVC to IVC - Why? A.: You cut through the territory of the SA node.

Right atrium

  • Open along crista terminalis (where the pectinate muscles end).
    • Open right auricle at the same time.

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

  • Cut the aorta.
    • Avoid cutting the pulmonary artery.
    • Go between the left coronary cusp and right coronary cusp. (???)

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:

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

Make the lab work hard approach:

  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.

Conducting system

Sinoatrial node

  • Sinoatrial (SA) node is at the lateral aspect of sulcus terminalis; lateral aspect of the superior vena cava and right atrium junction).[1]
    • CANNOT be identified grossly.
    • Artery of the SA (branch of RCA) may be a clue to where it lies.

Submitting the SA Node:[1]

  • 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[2] 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 section 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.

A picture is worth many words: SA node - low mag. micrograph (Wikicommons).

Histologic characteristics:

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

Image: SA node - high mag. micrograph (Wikicommons).

Atrioventricular node

Approach 1:

  • 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).[3]
    • This section should then be serially sectioned in the axis of the VLOT.

Approach 2:

  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.[4]
      • This section should then be serially sectioned in the axis of the VLOT.

Approach 3:

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

Triangle of Koch according to Virmani[5] is the floor of the RA and:

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

Notes (Approach 3):

  • The above makes little sense to me.

Notes:

Tamponade

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

The pathologist (like radiologists) can say...

  • Pericardial effusion.
    • Hemopericardium.

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

Myocardial infarction

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.[6]

Classic symptoms:

  • Chest pain (with radiation down the arms).
  • Nausea & vomiting.
  • Diaphoresis.

Enzymatic tests[7][8]

  • 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.

Pathologic

Microscopic

Sequence:[9]

  • 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.

Gross

Sequence:[10]

  • 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).

Coronary artery atherosclerosis

  • Greater than 75% (diameter) stenosis - considered significant.[11]

Stenosis definition (as per NASCET):[12]

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.

Abnormal hearts

Dilated pattern DDx:[13]

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

Cardiomyopathy

Main article: Cardiomyopathy

In the land of cardiology... there is a thing called cardiomyopathy.

Congenital heart disease

Main article: Congenital heart disease

Congential heart disease... a domain of paediatric cardiac surgery and occasionally adult cardiac surgery.

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

See Valvular heart disease.

Great vessels

When things go wrong here, you see a cardiac surgeon.

Aortic dissection

Associations

Heritable:[14]

  • Marfan's syndrome.
  • Loeys-Dietz syndrome.[15]
    • Marfan-like syndrome.
  • Ehlers-Danlos syndrome.
  • Bicuspid aortic valve.

Others:

  • Tertiary syphilis.

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:[16]

  • 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:[17]

  • 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

General

  • Can be in insolation or part of systemic sarcoidosis.[18]
  • May mimic hypertrophic cardiomyopathy clinically.[19]
  • Clinical: associated with heart block.[18]

Gross

  • Ventricular septum base - most common site of involvement.[18]

Distribution by autopsy findings:[20]

  • Septum - 31.5%.
  • Posterior LV - 24.6%.
  • Anterior LV - 18.0%.
  • RV - 17.9%.
    • RV involvement may lead to confusion with arrhythmogenic right ventricular cardiomyopathy (ARVC).
  • Lateral LV - 14.1%.

Notes:

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

Histology

Features:[20]

  • 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.[20]

Myocarditis

Histologic classification:[21]

  • Eosinophilic - hypersensitivity myocarditis - most common.
  • Lymphocytic - viral, autoimmune.
  • Granulomatous.
  • Neutrophilic.
  • Reperfusion (associated with myocardial infarction).

Granulomatous myocarditis

General

  • AKA giant cell myocarditis.[21]

Histology

Features:[20]

  • Granulomas.
  • Myocyte necrosis.
  • Eosinophils.

Note:

  • Eosinophils and myocyte necrosis differentiate this entity from cardiac sarcoidosis.

Cardiac amyloidosis

Main article: amyloidosis

General

  • Amyloid in the heart.
  • Rare.

Histology

Features (H&E stain):

  • Acellular fluffy pink material.

Special stains:

  • Congo red stain - red (normal light), apple-green in polarized light.[22]
  • Thioflavin-T stain[23]

Images (amyloidosis - non-cardiac):

Notes:

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

See also

References

  1. ↑ 1.0 1.1 Virmani et al. Cardiovascular Pathology. 2nd Ed. 2001. P.16.
  2. ↑ 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.
  3. ↑ PF. August 21, 2009.
  4. ↑ Virmani et al. Cardiovascular Pathology. 2nd Ed. 2001. P.18.
  5. ↑ Virmani et al. Cardiovascular Pathology. 2nd Ed. 2001. P.17.
  6. ↑ 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.
  7. ↑ http://pro2services.com/Lectures/Fall/CardEnz/a6mienz.gif
  8. ↑ http://www.hope-academic.org.uk/biochem/pbl/IMG00030.GIF
  9. ↑ http://library.med.utah.edu/WebPath/TUTORIAL/MYOCARD/MYOCARD.html
  10. ↑ http://library.med.utah.edu/WebPath/TUTORIAL/MYOCARD/MYOCARD.html
  11. ↑ Chamberlain. March 7, 2008.
  12. ↑ 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.
  13. ↑ 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.
  14. ↑ Gleason TG (2005). "Heritable disorders predisposing to aortic dissection". Semin. Thorac. Cardiovasc. Surg. 17 (3): 274-81. doi:10.1053/j.semtcvs.2005.06.001. PMID 16253833.
  15. ↑ Loeys BL, Schwarze U, Holm T, et al (August 2006). "Aneurysm syndromes caused by mutations in the TGF-beta receptor". N. Engl. J. Med. 355 (8): 788-98. doi:10.1056/NEJMoa055695. PMID 16928994. http://content.nejm.org/cgi/content/full/355/8/788.
  16. ↑ 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. 566. ISBN 0-7216-0187-1.
  17. ↑ 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. 568. ISBN 0-7216-0187-1.
  18. ↑ 18.0 18.1 18.2 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.
  19. ↑ 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.
  20. ↑ 20.0 20.1 20.2 20.3 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.
  21. ↑ 21.0 21.1 http://emedicine.medscape.com/article/1612533-overview
  22. ↑ 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.
  23. ↑ 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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