Vascular disease

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The article covers vascular disease, i.e. diseases of blood vessels. Vasculitides are covered in a separate article called vasculitides.

Normal blood vessels

Comparing arteries and veins:[1]

Feature Artery Vein
Internal elastic lamina prominent/thick, usu. complete thin & incomplete
External elastic lamina present, thick absent
Shape circular / lumen wide open collapsed
Wall thickness thick thin

Great vessels

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

Atherosclerosis

General

Clinical risk factors:

  • Age.
  • Blood pressure - modifiable (antihypertensives).
  • Cholesterol - modifiable (statins, diet).
  • Diabetes mellitus - modifiable (hypoglycemic medications, diet, lifestyle).
  • Smoking - modifiable (cessation).
  • Family history.

Microscopic

Features:

  • Intimal hyperplasia.
  • Lipid deposition.
  • Foamy macrophages within intima & media.
  • Cholesterol clefts
  • Luminal narrowing.

Image:

Notes:

  • Considered "complex" if any of the following are present:[2]
    • Calcifications.
    • Thrombosis.
    • Haemorrhage.

Aortic dissection

General

Associations

Heritable:[3]

Others:

Classification

Two classification exist:

  • DeBakey.
  • Stanford.

Stanford dissection classification:[5]

  • Type A - aortic root to the left subclavian artery.
    • Considered a surgical emergency.
  • Type B - distal to (left) subclavian artery.
    • Generally, treated conservatively.

Microscopic

See: cystic medial degeneration.

Images:

Cystic medial degeneration

General

  • AKA cystic medial necrosis.[6]
    • Often not cystic and not necrotic.

Microscopic

Features:[7][8]

  • Basophilic ground substance in the media (seen on Movat's stain).
  • Disruption of the elastic lamina (seen on elastic trichrome stain).
  • +/-Focal necrosis.

Images:

Medial calcific sclerosis

  • AKA Moenckeberg medial calcific sclerosis, calcific medial sclerosis of Monckeberg, and Monckeberg's arteriosclerosis.

General

  • Usually of no clinical consequence.

Microscopic

Features:[9]

  • Medial calcification (purple irregular stuff -- calcium phosphate).

Note:

  • Lumen unaffected.

Images:

Hyperplastic arteriolosclerosis

General

Microscopic

Features:[9]

  • Onion-skin appearance of intima & media due to:
    • Intimal hyperplasia.
    • Smooth muscle hyperplasia.

Image: Hyperplastic arteriolosclerosis (utah.edu).

Fibromuscular dysplasia

  • Abbreviated FMD.

General

Etiology:

  • Unknown, possibly genetic.

Gender:

  • Women > men.
  • May be seen in virtually any artery.
  • Reported as a cause of sudden death with involvement of the artery supplying the AV node.[11]

Gross/radiologic

  • Segmental - thinning and thickening.[12]

Classical locations:[12]

Microscopic

Features:[12]

  • Smooth muscle hyperplasia - key feature.
  • Elastic fibre fragmentation.
  • Luminal narrowing.

Images:

Stains

Thromboangiitis obliterans

General

  • Strong association with smoking.[13]
  • Small and medium-sized vessels of the extremities.

Diagnosis - clinical:

  • Corkscrew vessels on angiography.[14]

Treatment:

  • Stop smoking.

Microscopic

Features:[15]

  • Acute inflammation:
    • Endarteritis - inner layers of blood vessels.
    • Periarteritis.

Thrombosis

See also: Cerebral venous thrombosis.

General

Definition:

  • Blood clot formation within a vessel.

Complications:

Risk factors:

  • The classic pimping question is what "Virchow's triad?"
    • Stasis, hypercoagulability, endothelial injury.
  • A long list is found in: risk factors for VTE.

Gross

See: Pulmonary embolism - gross features.

Microscopic

Features:

  • Lines of Zahn.
  • Fibrin - pink acellular stuff on a H&E stain.

Image:

Cholesterol embolism

  • Abbreviated CE.

General

  • Strong association with atherosclerosis - found in ~3% of individuals in an autopsy series of 267 older individuals (mean age ~65 years).[16]
  • Significant CEs are often iatrogenic.
    • Known complication of coronary catherization (incidence ~ 1%).[17]
    • May complicate any vascular surgery, CABG.

Microscopic

Features:[18]

  • Intravascular cholesterol clefts (biconvex white spaces) - key feature.
    • Typically ~ 100-500 micrometers (long axis) x 50-100 micrometers (short axis). (?)
  • +/-Macrophages and giant cells.
  • +/-Eosinophils.

Note:

  • May be associated with ischemic changes and necrosis.
  • Usually in the context of severe atherosclerosis.

Note (trivia):

  • Cholesterol crystals dissolve with routine processing (paraffin embedding); this is why one talks of "cholesterol clefts".

Images:

See also

References

  1. ↑ URL: http://www.lab.anhb.uwa.edu.au/mb140/corepages/vascular/vascular.htm. Accessed on: 13 January 2011.
  2. ↑ Klatt, Edward C. (2006). Robbins and Cotran Atlas of Pathology (1st ed.). Saunders. pp. 4. ISBN 978-1416002741.
  3. ↑ 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.
  4. ↑ 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.
  5. ↑ Finkelmeier BA (September 1997). "Dissection of the aorta: a clinical update". J Vasc Nurs 15 (3): 88-93. PMID 9362838.
  6. ↑ URL: http://emedicine.medscape.com/article/756835-overview. Accessed on: 12 August 2010.
  7. ↑ URL: http://emedicine.medscape.com/article/756835-overview. Accessed on: 12 August 2010.
  8. ↑ Ha HI, Seo JB, Lee SH, et al. (2007). "Imaging of Marfan syndrome: multisystemic manifestations". Radiographics 27 (4): 989–1004. doi:10.1148/rg.274065171. PMID 17620463. http://radiographics.rsna.org/content/27/4/989.full.
  9. ↑ 9.0 9.1 Klatt, Edward C. (2006). Robbins and Cotran Atlas of Pathology (1st ed.). Saunders. pp. 7. ISBN 978-1416002741.
  10. ↑ URL: http://library.med.utah.edu/WebPath/IMMHTML/IMM028.html. Accessed on: 11 May 2011.
  11. ↑ 11.0 11.1 Lee, S.; Chae, J.; Cho, Y. (Dec 2006). "Causes of sudden death related to sexual activity: results of a medicolegal postmortem study from 2001 to 2005.". J Korean Med Sci 21 (6): 995-9. PMID 17179675.
  12. ↑ 12.0 12.1 12.2 Hata, D. (Sep 2001). "Fibromuscular dysplasia.". Intern Med 40 (9): 978-9. PMID 11579971.
  13. ↑ Highlander, P.; Southerland, CC.; VonHerbulis, E.; Gonzalez, A. (Jan 2011). "Buerger disease (thromboangiitis obliterans): a clinical diagnosis.". Adv Skin Wound Care 24 (1): 15-7. doi:10.1097/01.ASW.0000392923.37852.43. PMID 21173586.
  14. ↑ Fujii, Y.; Soga, J.; Nakamura, S.; Hidaka, T.; Hata, T.; Idei, N.; Fujimura, N.; Nishioka, K. et al. (Aug 2010). "Classification of corkscrew collaterals in thromboangiitis obliterans (Buerger's disease): relationship between corkscrew type and prevalence of ischemic ulcers.". Circ J 74 (8): 1684-8. PMID 20534945.
  15. ↑ Kurata, A.; Schulz, A.; Franke, FE. (2004). "Reappraisal of thromboangiitis obliterans--a pathological contribution.". Verh Dtsch Ges Pathol 88: 231-6. PMID 16892557.
  16. ↑ Flory CM (1945). "Arterial occlusions produced by emboli from eroded aortic atheromatous plaques". Am J Pathol 21 (3): 549–565. PMC 1934118. PMID 19970827. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1934118/.
  17. ↑ Fukumoto Y, Tsutsui H, Tsuchihashi M, Masumoto A, Takeshita A (July 2003). "The incidence and risk factors of cholesterol embolization syndrome, a complication of cardiac catheterization: a prospective study". J. Am. Coll. Cardiol. 42 (2): 211–6. doi:10.1016/S0735-1097(03)00579-5. PMID 12875753. http://linkinghub.elsevier.com/retrieve/pii/S0735109703005795.
  18. ↑ Mills, Stacey E; Carter, Darryl; Greenson, Joel K; Reuter, Victor E; Stoler, Mark H (2009). Sternberg's Diagnostic Surgical Pathology (5th ed.). Lippincott Williams & Wilkins. pp. 1735-6. ISBN 978-0781779425.
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