Arterial and venous thrombosis differences and similarities: Difference between revisions

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! Parameter !! Arterial !! Venous
! Parameter !! Arterial !! Venous
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|Contributing Modern factor of[[Virchow's triad]]  
|Contributing Modern factor of [[Virchow's triad]]  
|Endothelial wall defect, (+ some [[Hypercoagulability]])
|Endothelial wall defect, (+ some [[Hypercoagulability]])
|Stasis, Endothelial wall defect, [[Hypercoagulability]]  
|Stasis, Endothelial wall defect, [[Hypercoagulability]]  

Revision as of 05:06, 27 August 2018

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

More than a century ago, Virchow postulated that a triad of conditions (later called virchow's triad) leads to thrombus formation. Venous thrombosis has been associated with red blood cell and fibrin rich red clot while arterial thrombosis occur on atherosclerotic lesions with active inflammation, and are rich in platelets and give an appearance of white clot.[1] Furthermore certain studies have indicated the role of platelet in Venous thrombosis.[2] Thus, traditionally, venous thrombosis and arterial thrombosis has been described as distinct diseases with different risk factors, pathology and treatment. However, recent studies have shown an association between them.

Similarities

The two vascular complications, venous and arterial thrombosis, share many risk factors, most of which are associated with increaased risk of atherosclerosis and endothelial wall injury due to the nature of arterial thrombosis development; these risk factors include:

Furthermore there are many diseases that causes both arterial and venous thrombosis, such as:

  • Antiphospholipid antibody syndrome
  • Hyperhomocysteinemia
  • Malignancies
  • Infections
  • Nephrotic syndrome[3]
  • Hormonal treatment
  • Bechet's disease
  • Poplitial artery aneurysm (Large aneurysm can compress the poplitial vein and cause DVT)

Although arterial and venous thrombosis are being treated as separate entities due to the pathophysiological point of view; recent studies have emphasized the strong correlation between atherothrombotic events risk and VTE risk. The discovered shared risks of arterial and venous thrombotic events are to the extent that it is suggested to treat the whole thrombotic risk of an individual as a single entity rather than categorize it.

Differences

Arterial thrombosis occur at places of arterial plaque rupture where the shear rate is higher, in contrast vein thrombosis occur at places where the vein wall is normal and blood flow and shear rate is low.

Parameter Arterial Venous
Contributing Modern factor of Virchow's triad Endothelial wall defect, (+ some Hypercoagulability) Stasis, Endothelial wall defect, Hypercoagulability
Inherit property of the vessel Firm, thick walled, high pressure and rapid flow Floppy, thin walled, low pressure and slow flow.
Location of the thrombus formation Arterial plaque rupture Normal vein wall
Duration from initial insult to thrombus formation Takes a long time, often decades to happen Occur rapidly
Shear rate High Low
Microscopic appearance of clot Excess platelet and less fibrin, thus called white clot Less platelet and more fibrin, thus termed red clot
Complication More chances of distal thrombosis Can cause pulmonary embolism
Approach to treatment Risk factor modification (eg, smoking cessation, diabetes control, obesity management) plus anti-platelet drugs Prophylaxis against venous stasis and blood thinners.
Example MI, Stroke, Peripheral artery diseases Deep vein thrombosis

References

  1. Jerjes-Sanchez C (2005). "Venous and arterial thrombosis: a continuous spectrum of the same disease?". Eur Heart J. 26 (1): 3–4. doi:10.1093/eurheartj/ehi041. PMID 15615791.
  2. Sobieszczyk P, Fishbein MC, Goldhaber SZ (2002). "Acute pulmonary embolism: don't ignore the platelet". Circulation. 106 (14): 1748–9. PMID 12356622.
  3. Mahmoodi BK, ten Kate MK, Waanders F, Veeger NJ, Brouwer JL, Vogt L; et al. (2008). "High absolute risks and predictors of venous and arterial thromboembolic events in patients with nephrotic syndrome: results from a large retrospective cohort study". Circulation. 117 (2): 224–30. doi:10.1161/CIRCULATIONAHA.107.716951. PMID 18158362.

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