Difference between revisions of "Heart valves"
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**Myxomatous change? | **Myxomatous change? | ||
=Normal | =Normal morphology= | ||
==Aortic valve== | |||
General | ===General=== | ||
*Covered by endothelium. | *Covered by endothelium. | ||
*Mostly avascular (nutrients supplied by diffusion). | *Mostly avascular (nutrients supplied by diffusion). | ||
===Gross=== | |||
Terminology: | Terminology: | ||
*Base - closest to the aortic wall. | *Base - closest to the aortic wall. | ||
*Free edge - closest to the centre of the valve/interacts with other valve cusps. | *Free edge - closest to the centre of the valve/interacts with other valve cusps. | ||
Cusps: | |||
*Left - has LMCA ostium. | |||
*Right - has RCA ostium. | |||
*Posterior (non-coronary cusp). | |||
===Microscopic=== | |||
Three layers (from proximal (ventricular side) to distal (valsalva side)):<ref name=Ref_PBoD558>{{Ref PBoD|558}}</ref> | Three layers (from proximal (ventricular side) to distal (valsalva side)):<ref name=Ref_PBoD558>{{Ref PBoD|558}}</ref> | ||
#Ventricularis. | #Ventricularis. | ||
| Line 58: | Line 65: | ||
*The loading of the ventricular aspect is tensile and the valsalva side compressive. Thus, it makes sense that the tissue on the ventricular aspect is good in tensile loading and the tissue on the valsalva side good in compression. The elastic tissue can be thought of as [http://en.wikipedia.org/wiki/Rebar rebar]... the collagen as concrete. | *The loading of the ventricular aspect is tensile and the valsalva side compressive. Thus, it makes sense that the tissue on the ventricular aspect is good in tensile loading and the tissue on the valsalva side good in compression. The elastic tissue can be thought of as [http://en.wikipedia.org/wiki/Rebar rebar]... the collagen as concrete. | ||
==Mitral valve== | |||
===Gross=== | ===Gross=== | ||
*Cordae tendinae. | *Cordae tendinae. | ||
| Line 64: | Line 71: | ||
**No fusion. | **No fusion. | ||
=== | ===Microscopic=== | ||
Similar to the aortic valve - layers: | |||
#Atrialis. | |||
#Spongiosa. | |||
#Fibrosa. | |||
=Degenerative conditions= | =Degenerative conditions= | ||
Revision as of 14:01, 27 April 2012
Heart valves are the domain of the cardiac surgeon and their bread & butter.
Clinical
General
- Insufficiency (regurgitant flow) - murmur in diastole.
- Stenosis (decreased flow area) - murmur in systole.
Pathology
Which valves cause the most trouble?
- Mostly those on the left side (subjected to higher pressures), i.e. mitral valve (or left atrioventricular v.) and aortic valve.
Aortic stenosis - cause?
- Mostly "calcific aortic stenosis".
Quick approach to valves
Gross
- Calcification?
- Consider calcific stenosis.
- Vegetations?
- Consider infective endocarditis.
- Thin (see-through)?
- Consider myxomatous change.
Microscopic
- Inflammation?
- Consider endocarditis.
- Anitschkow's cells (caterpillar cells)?
- Rheumatic heart disease.
- Aschoff bodies?
- Rheumatic heart disease.
- Thickening of spongiosa (layer)?
- Myxomatous change?
Normal morphology
Aortic valve
General
- Covered by endothelium.
- Mostly avascular (nutrients supplied by diffusion).
Gross
Terminology:
- Base - closest to the aortic wall.
- Free edge - closest to the centre of the valve/interacts with other valve cusps.
Cusps:
- Left - has LMCA ostium.
- Right - has RCA ostium.
- Posterior (non-coronary cusp).
Microscopic
Three layers (from proximal (ventricular side) to distal (valsalva side)):[1]
- Ventricularis.
- Elastic tissue.
- Spongiosa.
- Loose connective tissue.
- Fibrosa.
- Mostly collagen, thickest part in a normal valve.
Notes:
- The loading of the ventricular aspect is tensile and the valsalva side compressive. Thus, it makes sense that the tissue on the ventricular aspect is good in tensile loading and the tissue on the valsalva side good in compression. The elastic tissue can be thought of as rebar... the collagen as concrete.
Mitral valve
Gross
- Cordae tendinae.
- Should be thin.
- No fusion.
Microscopic
Similar to the aortic valve - layers:
- Atrialis.
- Spongiosa.
- Fibrosa.
Degenerative conditions
Calcific aortic stenosis
General
- Somewhat similar to atherosclerosis; however, considered a separate entity.[2]
- Mitral valve is usually normal.
- Most common cause of aortic stenosis.
DDx of aortic stenosis:
- Calcific aortic stenosis.
- Bicuspid aortic valve with calcific aortic stenosis.
- Rheumatic heart disease.
Clinical (mnemonic SAD):
- Syncope.
- Angina.
- Dyspnea (shortness of breath) - first symptom.
Microscopic
Features:[3]
- Affects the valsalva side of the valve.
- It affects the fibrosa.
- Primarily at the base of the valve, i.e. there is relative sparing the free edge.
Localized dystrophic heart valve amyloidosis
General
- Common:
- ~75[4]-100%[5] of valves with calcific degeneration, i.e. calcific aortic stenosis.
- ~50% of valves with post-rheumatic sclerosis.[6]
- Not seen in acute disease and healed endocarditis.[6]
Hypothesis:
- Amyloid deposition in the aortic valve is the precursor lesion of calcific aortic stenosis.[5]
Microscopic
Features:[6]
- Pink amorphous material - key feature.
- Usually around the calcific foci.
DDx:
- Systemic amyloidosis, e.g. senile systemic amyloidosis, AL-amyloidosis.
Stains
- Congo red +ve.
Dystrophic amyloid:[6]
- Alcian blue -ve.
- Periodic acid-Schiff -ve.
Myxomatous degeneration
General
- Usually affects the mitral valve.
- Female > male,[7] disputed by Toronto data.[8]
- Associated with Marfan's syndrome and Turner syndrome (Monosomy X).[9]
Gross
Features:[10]
- No commissural fusion.
- Commissural fusion typical of rheumatic heart disease.
- Thickened.
- Rubbery consistency.
- Reactive/secondary changes.
- Fibrosis due to prolapse/abnormal contact of valve with other structures.
- Clots/organized thrombus - due to stasis.
Microscopic
- Thinning of fibrosa layer.
- Thickening of spongiosa layer with mucoid (myxomatous) material. (key feature).
- +/-Secondary changes (due to valvular dysfunction): thrombi, fibrosis.
Staining
- Movat stain.
Interpretation of Movat stain:[12]
- Black = nuclei and elastic fibers.
- Yellow = collagen and reticular fibers.
- Blue = mucin, ground substance.
- Red (intense) = fibrin.
- Red = muscle.
Image:
Infective conditions
Rheumatic heart disease
General
- Classically leads to mitral valve stenosis.
- Disease less frequent today - as streptococcal pharynigits is treated.
Gross
- "Fish-mouth appearance".
- Slit-like morphology; elliptical cross-sectional flow area (mitral valve) has an abnormally small semi-minor axis[15] axis due to valve thickening.
- Image: Fish-mouth appearance - pipe (principia-eng.com).
- Significant valvular thickening.
- Thickening of the cordae tendinae.
- Images:
Microscopic
Features:[16]
- Caterpillar cells (AKA Anitschkow cells)
- Abundant eosinophilic cytoplasm.
- Moderately-poorly defined cell border.
- Well-defined central ovoid nucleus with a prominent wavy ribbon-like chromatin -- looks vaguely like a caterpillar with some imagination.
- Pathognomonic for rheumatic fever.
- Aschoff bodies - usually in the heart itself:
- Jumbled collagen, eosinophilic.
- Surrounded by lymphocytes (T cells) +/- plasma cells.
Notes:
- Anitschkow cells are thought to be histocytes and Aschoff bodies are thought to be granulomas.[17]
- This is disputed.[18]
Images:
IHC
Features (Aschoff bodies & Anitschkow cells):[17]
- S100 -ve.
- Muscle specific actin -ve.
- Desmin -ve.
- NF -ve.
- Vimentin +ve.
- CD45 +ve (weak).
Infective endocarditis
- Abbreviated IE.
General
- Infection of the endocardium - often involves the valves (which are covered by endocardium).
- Before the time of antibiotics -- 100% fatal.
Organisms
Most common organism overall:
- Staphylococcus aureus.[19]
Organisms associated with particular clinical scenarios:
- IV drug users / normal valves = Staphylococcus aureus.[20]
- Previously damaged valve = Streptococcus viridans.
- Prosthetic valves = Staphylococcus epidermidis.[21]
Organisms that less commonly cause IE are known as the HASEK group:[20]
- Haemophilus (Haemophilus parainfluenzae, Haemophilus aphrophilus, Haemophilus paraphrophilus).
- Actinobacillus (Actinobacillus actinomycetemcomitans, Aggregatibacter aphrophilus).
- Cardiobacterium hominis.
- Eikenella corrodens. †
- Kingella (Kingella kingae).
Notes:
- † Enterococci are not included in this list but are lumped with the HACEK organisms.[20]
Clinical
- Diagnosed (clinically) using the Duke criteria.[22][23]
- Positive blood cultures.
- Cardiac involvement - vegetation.
- +/-Febrile.
Subdivided into:
- Acute IE.
- Classically due to Staphylococcus aureus.
- Subacute IE.
- Classically due to Streptococcus viridans.
Gross
- Location - left-sided involvement (mitral, aortic) more common than right-sided involvement (pulmonic, tricuspid).
- +/-Valvular destruction.
- More common in acute IE.
- +/-Distant emboli.
- More common in acute IE.
- +/-Valvular vegetations.
- Irregular ball of loosely adherent tissue - dull, irregular surface.
- On the ventricular aspect in aortic valve IE.
- Larger in acute IE.
Image:
Microscopic
- Inflammatory infiltrate (key feature @ low power):
- +/-Plasma cells.
- +/-Neutrophils.
- Microorganisms - key feature (diagnostic).
- Hard to see (even at high power).
Stains
- GMS stain (Gomori Methenamine-silver stain).
- Look for fungi.
- Gram stain.
- Look for bacteria.
Non-infective conditions
Nonbacterial thrombotic endocarditis
General
- Abbreviated NBTE.
- May be associated with catheterization.
Microscopic
Features:
- No inflammation.
- No organisms.
Libman-Sacks endocarditis
General
- Associated with systemic lupus erythematosus - seen in approximately in 1/10 cases by echocardiography.[25]
Gross
- Vegetations anywhere on the valve surface.[25]
Microscopic
Features:
- Hematoxylin bodies. (???)
Biscupid aortic valve
General
- Aortic valve usually tricuspid.
- Most common congenital heart defect.[26]
- Inherited in autosomal dominant pattern.
- NOTCH1 gene - implicated.[29]
Significance:
- Associated with ascending aortic aneurysms - x10 risk of aortic dissection vs. normal population.[27]
- 30% develop serious morbidity.[27]
- Associated with early development of calcific aortic stenosis.
Gross
Features - either:
Note:
- Raphe ~ suture or seam.[32]
Images:
Microscopic
Features - section through raphe:
- "No evidence of fusion."[30]
- Elastic fibres through-out (not interrupted by fibrous tissue). (???)
Heart valve tumours
Main article: Cardiac tumours
Papillary fibroelastomas are the most common tumour of the valve.
See also
References
- ↑ 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. 558. ISBN 0-7216-0187-1.
- ↑ Otto CM (September 2008). "Calcific aortic stenosis--time to look more closely at the valve". N. Engl. J. Med. 359 (13): 1395-8. doi:10.1056/NEJMe0807001. PMID 18815402.
- ↑ 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. 590. ISBN 0-7216-0187-1.
- ↑ Kristen, AV.; Schnabel, PA.; Winter, B.; Helmke, BM.; Longerich, T.; Hardt, S.; Koch, A.; Sack, FU. et al. "High prevalence of amyloid in 150 surgically removed heart valves--a comparison of histological and clinical data reveals a correlation to atheroinflammatory conditions.". Cardiovasc Pathol 19 (4): 228-35. doi:10.1016/j.carpath.2009.04.005. PMID 19502085.
- ↑ 5.0 5.1 Falk, E.; Ladefoged, C.; Christensen, HE. (Jan 1981). "Amyloid deposits in calcified aortic valves.". Acta Pathol Microbiol Scand A 89 (1): 23-6. PMID 7223424.
- ↑ 6.0 6.1 6.2 6.3 Cooper, JH. (Jul 1983). "Localized dystrophic amyloidosis of heart valves.". Hum Pathol 14 (7): 649-53. PMID 6190729.
- ↑ URL: http://emedicine.medscape.com/article/759004-overview. Accessed on: 8 June 2010.
- ↑ Leong SW, Soor GS, Butany J, Henry J, Thangaroopan M, Leask RL (October 2006). "Morphological findings in 192 surgically excised native mitral valves". Can J Cardiol 22 (12): 1055-61. PMID 17036100.
- ↑ Wigle ED, Rakowski H, Ranganathan N, Silver MC (1976). "Mitral valve prolapse". Annu. Rev. Med. 27: 165–80. doi:10.1146/annurev.me.27.020176.001121. PMID 779595.
- ↑ 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. 591. ISBN 0-7216-0187-1.
- ↑ URL: http://www.mayomedicallaboratories.com/test-catalog/Overview/9832. Accessed on: 8 June 2010.
- ↑ 12.0 12.1 Modified Movat's Pentachrome Stain. University Penn Medicine. URL: http://www.med.upenn.edu/mcrc/histology_core/movat.shtml. Accessed on: January 29, 2009.
- ↑ 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. 594. ISBN 0-7216-0187-1.
- ↑ Chopra, P.; Gulwani, H. (Oct 2007). "Pathology and pathogenesis of rheumatic heart disease.". Indian J Pathol Microbiol 50 (4): 685-97. PMID 18306530.
- ↑ URL: http://en.wikipedia.org/wiki/Ellipse. Accessed on: 13 November 2010.
- ↑ 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. 593. ISBN 0-7216-0187-1.
- ↑ 17.0 17.1 Love, GL.; Restrepo, C. (Jul 1988). "Aschoff bodies of rheumatic carditis are granulomatous lesions of histiocytic origin.". Mod Pathol 1 (4): 256-61. PMID 3070554.
- ↑ Stehbens, WE.; Zuccollo, JM. (May 1999). "Anitschkow myocytes or cardiac histiocytes in human hearts.". Pathology 31 (2): 98-101. PMID 10399163.
- ↑ Petti, CA.; Fowler, VG. (Jun 2002). "Staphylococcus aureus bacteremia and endocarditis.". Infect Dis Clin North Am 16 (2): 413-35, x-xi. PMID 12092480.
- ↑ 20.0 20.1 20.2 20.3 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. 298. ISBN 978-1416054542.
- ↑ Alonso-Valle, H.; Fariñas-Alvarez, C.; García-Palomo, JD.; Bernal, JM.; Martín-Durán, R.; Gutiérrez Díez, JF.; Revuelta, JM.; Fariñas, MC. (Apr 2010). "Clinical course and predictors of death in prosthetic valve endocarditis over a 20-year period.". J Thorac Cardiovasc Surg 139 (4): 887-93. doi:10.1016/j.jtcvs.2009.05.042. PMID 19660339.
- ↑ http://www.medcalc.com/endocarditis.html
- ↑ Durack DT, Lukes AS, Bright DK (March 1994). "New criteria for diagnosis of infective endocarditis: utilization of specific echocardiographic findings. Duke Endocarditis Service". Am. J. Med. 96 (3): 200-9. PMID 8154507.
- ↑ Mathura, KC.; Thapa, N.; Rauniyar, A.; Magar, A.; Gurubacharya, DL.; Karki, DB.. "Injection drug use and tricuspid valve endocarditis.". Kathmandu Univ Med J (KUMJ) 3 (1): 84-6. PMID 16401952.
- ↑ 25.0 25.1 Plastiras, SC.; Pamboucas, CA.; Tektonidou, M.; Toumanidis, ST. (Mar 2010). "Real-time three-dimensional echocardiography in evaluating Libman-Sacks vegetations.". Eur J Echocardiogr 11 (2): 184-5. doi:10.1093/ejechocard/jep172. PMID 19946116.
- ↑ Siu SC, Silversides CK (June 2010). "Bicuspid aortic valve disease". J. Am. Coll. Cardiol. 55 (25): 2789–800. doi:10.1016/j.jacc.2009.12.068. PMID 20579534.
- ↑ 27.0 27.1 27.2 Vallely MP, Semsarian C, Bannon PG (October 2008). "Management of the ascending aorta in patients with bicuspid aortic valve disease". Heart Lung Circ 17 (5): 357-63. doi:10.1016/j.hlc.2008.01.007. PMID 18514024.
- ↑ Tzemos, N.; Therrien, J.; Yip, J.; Thanassoulis, G.; Tremblay, S.; Jamorski, MT.; Webb, GD.; Siu, SC. (Sep 2008). "Outcomes in adults with bicuspid aortic valves.". JAMA 300 (11): 1317-25. doi:10.1001/jama.300.11.1317. PMID 18799444.
- ↑ Garg, V.; Muth, AN.; Ransom, JF.; Schluterman, MK.; Barnes, R.; King, IN.; Grossfeld, PD.; Srivastava, D. (Sep 2005). "Mutations in NOTCH1 cause aortic valve disease.". Nature 437 (7056): 270-4. doi:10.1038/nature03940. PMID 16025100.
- ↑ 30.0 30.1 Rose, Alan G. (2008). Atlas of Gross Pathology with Histologic Correlation (1st ed.). Cambridge University Press. pp. 2. ISBN 978-0521868792.
- ↑ Sabet, HY.; Edwards, WD.; Tazelaar, HD.; Daly, RC. (Jan 1999). "Congenitally bicuspid aortic valves: a surgical pathology study of 542 cases (1991 through 1996) and a literature review of 2,715 additional cases.". Mayo Clin Proc 74 (1): 14-26. doi:10.4065/74.1.14. PMID 9987528.
- ↑ URL: http://dictionary.reference.com/browse/raphe. Accessed on: 25 February 2012.
- ↑ Fedak, PW.; Verma, S.; David, TE.; Leask, RL.; Weisel, RD.; Butany, J. (Aug 2002). "Clinical and pathophysiological implications of a bicuspid aortic valve.". Circulation 106 (8): 900-4. PMID 12186790.