Thrombosis pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-In-Chief: Aida Javanbakht, M.D.

## Overview

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Irreversible formation of the blood clot is called thrombosis. This process can happen in the artery and vein [1].

## Pathophysiology

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Rudolf Virchow noted several factors affecting the clot formation, which are as follows:

1) Alterations in blood flow (stasis): Blood flows throughout the circulatory system, without significantly stopping or slowing any where. In certain pathological conditions where the blood flow slows down or stops, it causes:

* Increase in platelet to endothelium contact
* Decrease the dilution of clotting factors

This increases the risk of clot formation and form microthrombi, which further grow and propagate.

2) Injury to the vascular endothelium: Intrinsic or secondary to external trauma (eg, catheterization) can cause intimal damage and stimulates clot formation. See Coagulation.

3) Alterations in the constitution of blood (hypercoagulability): It is the propensity to develop thrombosis due to an abnormality in the system of coagulation.

These three conditions are collectively known as Virchow's triad and lead to intravascular coagulation, forming a mass of red blood cells, leukocytes, and fibrin.

Shown below is a table depicting the elements of Virchow's triad and their modern counterparts.

Virchow's[2] | Modern  | Notes

|
|

Phenomena of interrupted blood-flow  | "Stasis" or "venous stasis"[3] | The first category, alterations in normal blood flow, refers to several situations. These include turbulence, stasis, mitral stenosis, and varicose veins. The equivalence of Virchow's version and the modern version has been disputed.[4]
Phenomena associated with irritation of the vessel and its vicinity  | "Endothelial injury" or "vessel wall injury"  | The second category, injuries and/or trauma to endothelium includes damage to the veins arising from shear stress or hypertension.
Phenomena of blood-coagulation | "Hypercoagulability"  | The last category, alterations in the constitution of blood,[5] has numerous possible risk factors such as hyperviscosity, deficiency of antithrombin III, nephrotic syndrome, changes after severe trauma or burn, disseminated cancer, late pregnancy and delivery, race, age, whether the patient is a smoker, and obesity. All of these risk factors lead to hypercoagulability.

### Thrombus Formation

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* Usually there is a balance between the coagulation and fibrinolysis systems in order to not having abnormal thrombosis in the body.
* Factors that increase the risk for a homeostatic imbalance include:

> Thrombophilia

> Immobilization

> Trauma

* An insult to homeostatic balance can expose the sub-endothelium and lead to the collection of various coagulation factors. Accumulation of coagulation factors can lead to the formation of a thrombus of red blood cells, leukocytes, and fibrin.
* A thrombus is characteristically found to first develop in the calf veins and progressively grow in the direction of blood flow (leading to the heart).
* An exceedingly extensive thrombosis in deep veins can extend well into the iliac veins or the inferior vena cava.
* Atherosclerosis is a miss balance between lipids and the hemostasis system which caused clot in arteries. By occluding the artery myocardial infarction, stroke could happen [6].
* Thrombosis can happen in both Bare Metal Stent (BMS) and Drug Eluting Stent (DES).

Factors that serve as nidus for development stent thrombosis are:

> Delayed endothelialization[7][8][9].

> Inflammatory response to the stent material[10][11].

> Hypersensitivity reaction around the stent material in DES serving as nidus for ST[12][13][14][15][16].

* Pregnancy increases risk of having thrombosis in both veins and arteries because of hypercoagulate state [17].
* Acquired risk factors for thrombosis are:

Oral contraceptive use,

Hormone replacement therapy

Advanced age

Surgery

Prolonged immobilization like hospitalization [18].

This video explains the process of thrombosis:

{{#ev:youtube|X_POCRsy7i4}}

## Genetics

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Genetic factors that play roles in causing thrombosis [19]:

* Non-O blood groups
* Factor V Leiden mutation
* Prothrombin G20210A gene variants
* Polymorphisms in factors IX17 or XI [20]

## Gross Pathology

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* Dull appearance.
* Zahn line from platelets and fibrin with layers of RBCs in pulmonary venous thromboembolism.
* Gross picture of thrombosis is different in live and dead person.

In live person it is gray and firm.

In dead person it is dark purple or yellow elastic called "chicken fat".

## Microscopic Pathology

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* lamination
* Zahn line

## References

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1. ↑ Asakura H (July 2014). "[Pathophysiology and classification of thrombosis]". Nippon Rinsho (in Japanese). 72 (7): 1184–90. PMID 25163306.CS1 maint: Unrecognized language (link)
2. ↑ Agutter, Paul S. (2008). The Aetiology of Deep Venous Thrombosis: A Critical, Historical and Epistemological Survey. Berlin: Springer. p. 84\. ISBN 1-4020-6649-X.
3. ↑ Lowe GD (2003). "Virchow's triad revisited: abnormal flow". Pathophysiol. Haemost. Thromb. 33 (5–6): 455–7. doi:10.1159/000083845. PMID 15692260.
4. ↑ "Further reflections on Virchow's triad. - Free Online Library". Retrieved 2009-02-10.
5. ↑ Chung I, Lip GY (2003). "Virchow's triad revisited: blood constituents". Pathophysiol. Haemost. Thromb. 33 (5–6): 449–54. doi:10.1159/000083844. PMID 15692259.
6. ↑ Prentice CR (1990). "Pathogenesis of thrombosis". Haemostasis. 20 Suppl 1: 50–9. doi:10.1159/000216161. PMID 2083873.
7. ↑ Camenzind E, Steg PG, Wijns W (2007). "Stent thrombosis late after implantation of first-generation drug-eluting stents: a cause for concern". Circulation. 115 (11): 1440–55, discussion 1455. doi:10.1161/CIRCULATIONAHA.106.666800. PMID 17344324.CS1 maint: Multiple names: authors list (link)
8. ↑ Awata M, Kotani J, Uematsu M, Morozumi T, Watanabe T, Onishi T; et al. (2007). "Serial angioscopic evidence of incomplete neointimal coverage after sirolimus-eluting stent implantation: comparison with bare-metal stents". Circulation. 116 (8): 910–6. doi:10.1161/CIRCULATIONAHA.105.609057. PMID 17684153.CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link)
9. ↑ Kotani J, Awata M, Nanto S, Uematsu M, Oshima F, Minamiguchi H; et al. (2006). "Incomplete neointimal coverage of sirolimus-eluting stents: angioscopic findings". J Am Coll Cardiol. 47 (10): 2108–11. doi:10.1016/j.jacc.2005.11.092. PMID 16697331.CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link)
10. ↑ Leon MB, Abizaid A, Moses JW. Subgroup analysis from the Cypher clinical trials. In: The Cypher Stent: A New Gold Standard in the Treatment of Coronary Artery Disease. New York, NY: Cardiovascular Research Foundation; 2003:54–57.
11. ↑ Tanabe K, Serruys PW, Degertekin M, Grube E, Guagliumi G, Urbaszek W; et al. (2005). "Incomplete stent apposition after implantation of paclitaxel-eluting stents or bare metal stents: insights from the randomized TAXUS II trial". Circulation. 111 (7): 900–5. doi:10.1161/01.CIR.0000155607.54922.16. PMID 15710761.CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link)
12. ↑ Virmani R, Guagliumi G, Farb A, Musumeci G, Grieco N, Motta T; et al. (2004). "Localized hypersensitivity and late coronary thrombosis secondary to a sirolimus-eluting stent: should we be cautious?". Circulation. 109 (6): 701–5. doi:10.1161/01.CIR.0000116202.41966.D4. PMID 14744976.CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link)
13. ↑ Nebeker JR, Virmani R, Bennett CL, Hoffman JM, Samore MH, Alvarez J; et al. (2006). "Hypersensitivity cases associated with drug-eluting coronary stents: a review of available cases from the Research on Adverse Drug Events and Reports (RADAR) project". J Am Coll Cardiol. 47 (1): 175–81. doi:10.1016/j.jacc.2005.07.071. PMID 16386683.CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link)
14. ↑ Joner M, Finn AV, Farb A, Mont EK, Kolodgie FD, Ladich E; et al. (2006). "Pathology of drug-eluting stents in humans: delayed healing and late thrombotic risk". J Am Coll Cardiol. 48 (1): 193–202. doi:10.1016/j.jacc.2006.03.042. PMID 16814667.CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link)
15. ↑ Ong AT, McFadden EP, Regar E, de Jaegere PP, van Domburg RT, Serruys PW (2005). "Late angiographic stent thrombosis (LAST) events with drug-eluting stents". J Am Coll Cardiol. 45 (12): 2088–92. doi:10.1016/j.jacc.2005.02.086. PMID 15963413.CS1 maint: Multiple names: authors list (link)
16. ↑ Grube E, Lansky A, Hauptmann KE, Di Mario C, Di Sciascio G, Colombo A; et al. (2004). "High-dose 7-hexanoyltaxol-eluting stent with polymer sleeves for coronary revascularization: one-year results from the SCORE randomized trial". J Am Coll Cardiol. 44 (7): 1368–72. doi:10.1016/j.jacc.2004.06.054. PMID 15464315.CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link)
17. ↑ James AH (September 2015). "Thrombosis in pregnancy and maternal outcomes". Birth Defects Res. C Embryo Today. 105 (3): 159–66. doi:10.1002/bdrc.21106. PMID 26383185.
18. ↑ Wolberg AS, Rosendaal FR, Weitz JI, Jaffer IH, Agnelli G, Baglin T, Mackman N (May 2015). "Venous thrombosis". Nat Rev Dis Primers. 1: 15006. doi:10.1038/nrdp.2015.6. PMID 27189130.
19. ↑ Rosendaal FR, Reitsma PH (July 2009). "Genetics of venous thrombosis". J. Thromb. Haemost. 7 Suppl 1: 301–4. doi:10.1111/j.1538-7836.2009.03394.x. PMID 19630821.
20. ↑ Austin H, De Staercke C, Lally C, Bezemer ID, Rosendaal FR, Hooper WC (March 2011). "New gene variants associated with venous thrombosis: a replication study in White and Black Americans". J. Thromb. Haemost. 9 (3): 489–95. doi:10.1111/j.1538-7836.2011.04185.x. PMC 4532311. PMID 21232005.

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