Heart transplant pathology

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Heart transplant pathology is a niche in cardiac pathology.

Overview - table

Types of rejection[1]

Type (grade) Description Details Image
antibody-mediated rejection (acute vascular) edema, dilated small vessels scant inflammation acute
normal (0R) normal no extravascular monocytes
acute cellular (1R) (perivascular) inflammatory infiltrate, myocyte damage scant interstitial infiltrate (lymphoplasmacytic), scant damage mild cellular
acute cellular (2R) (perivascular) inflammatory space-occupying lesion diffuse interstitial infiltrate displaces parenchyma (lymphoplasmacytic), obvious damage (myocyte eosinophilia or drop-out) mod. cellular, mod. cellular resolving
acute cellular (3R) disruption of normal arch. diffuse interstitial infiltrate disrupts parenchyma (lymphoplasmic & PMNs), fibre loss/damage
chronic concentric intimal thicking internal elastic lamina preserved (unlike atherosclerosis) chronic, chronic

Pitfalls[1]

Name Description Details Image
Quilty effect endocardial/subendocardial B-lymphocytes (in clusters) may extend into myocardium, not assoc. with blood vessels +/-myocyte damage; benign behaviour clinically Quilty effect, Quilty effect
Old biopsy site hemosiderin-laden macrophages fibrosis/myocyte replacement old Bx site

Mimics

Biopsy site reaction

General

  • Can be confused for rejection.

Microscopic

Features:

  • Hemosiderin-laden macrophages.
  • +/-Fibrosis/myofibre loss-replacement.
  • +/-Scant inflammatory infiltration.

Image: Biopsy site (pathconsultddx.com).

Quilty effect

  • AKA endocardial lymphocytic infiltrate.[2]

General

  • Can be confused for rejection.
  • Benign behaviour.

Trivia:

  • The name Quilty comes from the patient in which this was first recognized.

Microscopic

Features:[3]

  • Lymphocytes in clusters (B cells and T cells).
    • Associated with the endocardium ("endothelium of the heart"), i.e. on the surface - key feature.
    • Often have capillaries in centre; usu. not associated with large blood vessels.
    • Lymphocytes separated by collagen.

Notes:

  • No longer subclassified.[2]
    • Traditional classification (by location):
      • Quilty A: Endocardial/subendocardial.
      • Quilty B: Endocardial/subendocardial + myocardium.
        • +/-Myocyte damage.[4]

Images:

IHC

Mix of T cell and B cells:[3]

  • CD3 +ve.
  • CD20 +ve.

Notes:

  • ACR is T cells.[3]

Coronary atherosclerosis (ischemic injury)

General

  • Usu. early - related to atherosclerosis in the donor heart.
  • Not typically biopsied. (???)

Microscopic

Features:

Rejection

It comes in different flavours:[5]

  • Antibody-mediate rejection (acute vascular rejection).
  • Acute cellular rejection.
  • Chronic rejection.

Antibody-mediated rejection

  • Abbreviated as AMR.

General

  • AKA acute vascular rejection, hyperacute rejection, humoral rejection.[2][6]

Microscopic

Features:[7]

  • Edema.
  • Dilated small vessels.
  • Scant inflammatory infiltrate.
    • Macrophage margination.[8] (???)

Image:

IHC

Features:[2]

  • C4d.
  • C3d.

Acute cellular rejection

General

  • Common form of rejection.

Microscopic

Features:

  • Perivascular lymphocytic infiltrate, usu. deep.
  • Reactive endothelium.
  • +/-Myocardial eosinophilia.
  • +/-Expansion of perivascular space.

Notes:

  • The main DDx is a Quilty lesion - these are attached to the surface and are typically not associated with a blood vessel.

Grading - comparison

Grading scheme 2004/1990:[9]

Grade 2004 Grade 1990 Description Details Image
0R 0 normal no extravascular monocytes
1R 1A infiltrate, myocyte damage scant interstitial infiltrate (lymphoplasmic), scant damage mild
1R 1B infiltrate, myocyte damage diffuse interstitial infiltrate (lymphoplasmic), focal damage
1R 2 infiltrate, myocyte damage diffuse interstitial infiltrate (lymphoplasmic), obvious damage
2R 3A space-occupying lesion diffuse interstitial infiltrate displaces parenchyma (lymphoplasmic), obvious damage mod., mod. resolving
3R 3B disruption of normal arch. diffuse interstitial infiltrate disrupts parenchyma (lymphoplasmic & PMNs), obvious damage
3R 4 disruption of normal arch. diffuse interstitial infiltrate disrupts parenchyma (lymphoplasmic & PMNs), fibre loss

Chronic rejection

General

  • AKA transplant arteriopathy or cardiac allograft vasculopathy.
  • Thought to be a form of accelerated atherosclerosis.[10]

Microscopic

Features:[11]

  • Concentric intimal thickening.
  • Preservation of internal elastic lamina.

Images:

Notes:

  • Morphologically vaguely similar to atherosclerosis.

Other

Post-transplant lymphoproliferative disorder

Main article: Post-transplant lymphoproliferative disorder
  • Abbreviated PTLD.

General

Microscopic

Features:

  • Large cell lymphoma - see DLBCL.

See also

References

  1. ↑ 1.0 1.1 Humphrey, Peter A; Dehner, Louis P; Pfeifer, John D (2008). The Washington Manual of Surgical Pathology (1st ed.). Lippincott Williams & Wilkins. pp. 136-7. ISBN 978-0781765275.
  2. ↑ 2.0 2.1 2.2 2.3 Tan CD, Baldwin WM, Rodriguez ER (August 2007). "Update on cardiac transplantation pathology". Arch. Pathol. Lab. Med. 131 (8): 1169–91. PMID 17683180.
  3. ↑ 3.0 3.1 3.2 URL: http://emedicine.medscape.com/article/1612493-overview. Accessed on: 8 March 2011.
  4. ↑ Winters GL (March 1997). "The challenge of endomyocardial biopsy interpretation in assessing cardiac allograft rejection". Curr. Opin. Cardiol. 12 (2): 146–52. PMID 9192483.
  5. ↑ URL: http://emedicine.medscape.com/article/1612493-overview. Accessed on: 9 Febraury 2011.
  6. ↑ Olsen SL, Wagoner LE, Hammond EH, et al. (1993). "Vascular rejection in heart transplantation: clinical correlation, treatment options, and future considerations". J. Heart Lung Transplant. 12 (2): S135–42. PMID 8476883.
  7. ↑ URL: http://www.pathconsultddx.com/pathCon/largeImage?pii=S1559-8675%2806%2970592-7&figureId=fig4. Accessed on: 7 January 2011.
  8. ↑ Lee CY, Lotfi-Emran S, Erdinc M, et al. (November 2007). "The involvement of FcR mechanisms in antibody-mediated rejection". Transplantation 84 (10): 1324–34. doi:10.1097/01.tp.0000287457.54761.53. PMID 18049118.
  9. ↑ Humphrey, Peter A; Dehner, Louis P; Pfeifer, John D (2008). The Washington Manual of Surgical Pathology (1st ed.). Lippincott Williams & Wilkins. pp. 136. ISBN 978-0781765275.
  10. ↑ Humphrey, Peter A; Dehner, Louis P; Pfeifer, John D (2008). The Washington Manual of Surgical Pathology (1st ed.). Lippincott Williams & Wilkins. pp. 137. ISBN 978-0781765275.
  11. ↑ URL: http://www.pathconsultddx.com/pathCon/largeImage?pii=S1559-8675%2806%2970592-7&figureId=fig5. Accessed on: 7 January 2011.
  12. ↑ URL: http://newsroom.ucla.edu/portal/ucla/ucla-team-uncovers-mechanism-behind-179330.aspx. Accessed on: 7 January 2011.
  13. ↑ URL: http://emedicine.medscape.com/article/431364-overview. Accessed on: 10 February 2011.

External links

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