Heart valves

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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 histology

Aortic valve

General:

  • Covered by endothelium.
  • Mostly avascular (nutrients supplied by diffusion).

Terminology:

  • Base - closest to the aortic wall.
  • Free edge - closest to the centre of the valve/interacts with other valve cusps.

Three layers (from proximal (ventricular side) to distal (valsalva side)):[1]

  1. Ventricularis.
    • Elastic tissue.
  2. Spongiosa.
    • Loose connective tissue.
  3. Fibrosa.
    • Mostly collagen, thickest part in a normal valve.

Mitral valve

Gross

  • Cordae tendinae.

Histology

  • Similar to the aortic valve.

Calcific aortic stenosis

General

  • Somewhat similar to atherosclerosis; however, considered a separate entity[2]
  • Mitral valve is usually normal.

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.

Myxomatous degeneration

General

Gross

Features:[7]

  • 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.
    • Acid fuchsin, alcian blue, crocein scarlet, elastic hematoxylin, pathology consultation, and saffron.[8][9]

Interpretation of Movat stain:[9]

  • Black = nuclei and elastic fibers.
  • Yellow = collagen and reticular fibers.
  • Blue = mucin, ground substance.
  • Red (intense) = fibrin.
  • Red = muscle.

Image:

Rheumatic heart disease

General

  • Classically leads to mitral valve stenosis.
    • Rheumatic fever accounts for 99% of mitral stenosis.[10]
  • Disease less frequent today - as streptococcal pharynigits is treated.

Gross

  • "Fish-mouth appearance".
    • Slit-like morphology; ellipical cross-sectional flow area (mitral valve) has an abnormally small semi-minor axis[11] axis due to valve thickening.
    • Image: Fish-mouth appearance (pipe) - principia-eng.com.
  • Significant valvular thickening.
  • Thickening of the cordae tendinae.

Microscopic

Features:[12]

  • Caterpillar cell (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 immagination.
    • Pathognomonic for rheumatic fever.
  • Aschoff bodies:
    • Usually in the heart itself,
    • Jumbled collagen, eosinophilic, and
    • Surrounded by lymphocytes (T cells) +/- plasma cells.

Images:

Endocarditis

General

  • Infection of the endocardium - often involves the valves (which are covered by endocardium).
  • Before the time of antibiotics -- 100% fatal.

Clinical

  • Diagnosed (clinically) using the Duke criteria.[13][14]
    • positive blood cultures.
    • cardiac involvement - vegetation.
    • +/-febrile.

Microscopic

  • Inflammatory infiltrate (key feature @ low power)
    • +/-Plasma cells,
    • +/-Neutrophils.
  • Microorganisms (key feature - diagnostic)
    • Hard to see (even at high power).

Stains

  • GMS (Gomori Methenamine-silver stain)
    • Look for fungi.
  • Gram stain
    • Look for bacteria.

Biscupid aortic valve

General

  • Aortic valve usually tricuspid.
  • 1-2% of general population.[15]
  • Inherited in autosomal dominant pattern.

Significance

  • Associated with ascending aortic aneurysms - x10 risk of dissection vs. normal population[15]
  • 30% develop serious morbidity.[15]
  • Associated with early development of calcific aortic stenosis.

Tumours

Main article: Cardiac tumours

Papillary fibroelastomas are the most common tumour of the valve.

See also

References

  1. ↑ 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.
  2. ↑ 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.
  3. ↑ 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.
  4. ↑ URL: http://emedicine.medscape.com/article/759004-overview. Accessed on: 8 June 2010.
  5. ↑ 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.
  6. ↑ 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.
  7. ↑ 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.
  8. ↑ URL: http://www.mayomedicallaboratories.com/test-catalog/Overview/9832. Accessed on: 8 June 2010.
  9. ↑ 9.0 9.1 Modified Movat's Pentachrome Stain. University Penn Medicine. URL: http://www.med.upenn.edu/mcrc/histology_core/movat.shtml. Accessed on: January 29, 2009.
  10. ↑ 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.
  11. ↑ http://en.wikipedia.org/wiki/Ellipse
  12. ↑ 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.
  13. ↑ http://www.medcalc.com/endocarditis.html
  14. ↑ 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.
  15. ↑ 15.0 15.1 15.2 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.
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