Arterial and venous thrombosis differences and similarities: Difference between revisions
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{{ | ==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.<ref name="pmid15615791">{{cite journal| author=Jerjes-Sanchez C| title=Venous and arterial thrombosis: a continuous spectrum of the same disease? | journal=Eur Heart J | year= 2005 | volume= 26 | issue= 1 | pages= 3-4 | pmid=15615791 | doi=10.1093/eurheartj/ehi041 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15615791 }} </ref> Furthermore certain studies have indicated the role of platelet in Venous thrombosis.<ref name="pmid12356622">{{cite journal| author=Sobieszczyk P, Fishbein MC, Goldhaber SZ| title=Acute pulmonary embolism: don't ignore the platelet. | journal=Circulation | year= 2002 | volume= 106 | issue= 14 | pages= 1748-9 | pmid=12356622 | doi= | pmc= | url= }} </ref> 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 | 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: | ||
*[[Obesity]] | |||
*[[Hypertension]] | |||
*Tobacco use | |||
*[[Dyslipidemia]] | |||
*[[Diabetes mellitus]] | |||
*[[Metabolic syndrome]] | |||
*Diet | |||
*Age | *Age | ||
* | *Hormonal replacement/contraceptive therapy | ||
Furthermore there are many diseases that causes both arterial and venous thrombosis, such as: | Furthermore there are many diseases that causes both arterial and venous thrombosis, such as: | ||
*Antiphospholipid antibody syndrome | *Antiphospholipid antibody syndrome | ||
*Hyperhomocysteinemia | *Hyperhomocysteinemia | ||
*Malignancies | *Malignancies | ||
*Infections, | *Infections | ||
*Hormonal treatment. | *Nephrotic syndrome<ref name="pmid18158362">{{cite journal| author=Mahmoodi BK, ten Kate MK, Waanders F, Veeger NJ, Brouwer JL, Vogt L et al.| title=High absolute risks and predictors of venous and arterial thromboembolic events in patients with nephrotic syndrome: results from a large retrospective cohort study. | journal=Circulation | year= 2008 | volume= 117 | issue= 2 | pages= 224-30 | pmid=18158362 | doi=10.1161/CIRCULATIONAHA.107.716951 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18158362 }} </ref> | ||
*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<ref name="pmidhttps://doi.org/10.1024/0301-1526/a000695">{{cite journal| author=Schmoldt A, Benthe HF, Haberland G| title=Digitoxin metabolism by rat liver microsomes. | journal=Biochem Pharmacol | year= 1975 | volume= 24 | issue= 17 | pages= 1639-41 | pmid=https://doi.org/10.1024/0301-1526/a000695 | doi= | pmc=5922622 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10 }}</ref><ref name="pmid225603802" /><ref name="pmid15615791" />. 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<ref name="pmid225603802">{{cite journal| author=Franchini M, Mannucci PM| title=Association between venous and arterial thrombosis: clinical implications. | journal=Eur J Intern Med | year= 2012 | volume= 23 | issue= 4 | pages= 333-7 | pmid=22560380 | doi=10.1016/j.ejim.2012.02.008 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22560380 }}</ref>. | |||
==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. | |||
{| border="1" | |||
|+ | |||
! 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 occlusive disease|Peripheral artery diseases]] | |||
| [[Deep vein thrombosis]] | |||
|} | |||
==References== | |||
{{reflist|2}} | |||
[[de:Virchow-Trias]] | |||
[[pl:Triada Virchowa]] | |||
[[pt:Tríade de Virchow]] | |||
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[[Category:Pulmonology]] | |||
Latest revision as of 09:03, 29 January 2019
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Vahid Eidkhani, M.D.
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:
- Obesity
- Hypertension
- Tobacco use
- Dyslipidemia
- Diabetes mellitus
- Metabolic syndrome
- Diet
- Age
- Hormonal replacement/contraceptive therapy
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[4][5][1]. 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[5].
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
- ↑ 1.0 1.1 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.
- ↑ Sobieszczyk P, Fishbein MC, Goldhaber SZ (2002). "Acute pulmonary embolism: don't ignore the platelet". Circulation. 106 (14): 1748–9. PMID 12356622.
- ↑ 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.
- ↑ Schmoldt A, Benthe HF, Haberland G (1975). "Digitoxin metabolism by rat liver microsomes". Biochem Pharmacol. 24 (17): 1639–41. PMC 5922622. PMID https://doi.org/10.1024/0301-1526/a000695 Check
|pmid=value (help). - ↑ 5.0 5.1 Franchini M, Mannucci PM (2012). "Association between venous and arterial thrombosis: clinical implications". Eur J Intern Med. 23 (4): 333–7. doi:10.1016/j.ejim.2012.02.008. PMID 22560380.