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Arterial Thrombosis

Arterial thrombosis is a blood clot in an artery, which can be very serious because it can either slow or stop blood reaching important organs. Arteries are blood vessels that carry blood from the heart to the body and the heart muscle. Blood clots do not usually cause symptoms until they blocks the flow of blood to part of the body. This can cause several serious medical issues, including:

  • heart attack, when blood flow to the heart muscle is suddenly blocked, causing chest painshortness of breath and dizziness

  • stroke, when blood flow to the brain is cut off; the main symptoms are one side of the face dropping, weakness in one side of the body and slurred speech

  • transient ischaemic attack (TIA) or "mini-stroke", when blood flow to the brain is temporarily blocked, causing short-lived stroke symptoms

  • critical limb ischaemia (a complication of peripheral arterial disease), when the blood supply to a limb is blocked, causing it to become painful, discoloured (either pale or blue) and cold


Arterial thrombosis typically affects people with atherosclerotic plaques (fatty deposits) in their arteries. These deposits cause the arteries to harden and narrow over time and can rupture and increase the risk of blood clots (thrombi). Myocardial infarction and stroke, the most common causes of morbidity and mortality in middle-aged Americans, are consequences of arterial thrombosis. The clinical manifestation of myocardial infarction and strokes are different, but they are the result of the same pathogenic process, formation of a thrombus over an atherosclerotic plaque in the environment of high flow and high shear arterial circulation. The thrombus typically overlies a ruptured plaque or an intact plaque with surface endothelial erosion. Plaque composition rather than plaque size or severity of stenosis dictates plaque rupture and subsequent thrombosis. Exposure of blood cells to the procoagulant materials in the ruptured plaque promotes thrombosis. Catalytically active tissue factor is present in the atherosclerotic plaque and seems to play a major role in the triggering of thrombosis following rupture. Under shear stresses in the artery, only platelets are capable of adhesion to the damaged vessel wall. Several adhesion molecules and platelet activators are present in the plaque such as collagen, and oxidized lipids. In contrast to venous thrombosis, activation of coagulation factors does not appear to play a major role in arterial thrombosis as these factors are likely to be removed by the high flow in the arterial system. Vessel wall damage due to atherosclerosis, hypertension, or vascular anomalies is a major risk factor for arterial thrombosis, by inducing turbulence and altered blood flow, which allows platelet adhesion. Consequently, hyperactivity of platelets also plays a role in the pathogenesis. Antiplatelet therapy such as aspirin is used to prevent vascular events in arterial thrombosis while they are of limited value in preventing venous thrombosis (adapted from Additional information on Thrombosis can be found from the NHS (

1. Amsterdam EA, Wenger NK, Brindis RG, Casey DE, Jr., Ganiats TG, Holmes DR, Jr., et al. 2014 AHA/ACC guideline for the management of patients with non-ST-elevation acute coronary syndromes: executive summary: a Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation. 2014;130(25):2354-94.
2. Mauri L, Kereiakes DJ, Yeh RW, Driscoll-Shempp P, Cutlip DE, Steg PG, et al. Twelve or 30 months of dual antiplatelet therapy after drug-eluting stents. N Engl J Med. 2014;371(23):2155-66.
3. Angiolillo DJ, Fernandez-Ortiz A, Bernardo E, Ramirez C, Sabate M, Jimenez-Quevedo P, et al. Platelet function profiles in patients with type 2 diabetes and coronary artery disease on combined aspirin and clopidogrel treatment. Diabetes. 2005;54(8):2430-5.
4. Andersson C, Lyngbaek S, Nguyen CD, Nielsen M, Gislason GH, Kober L, et al. Association of clopidogrel treatment with risk of mortality and cardiovascular events following myocardial infarction in patients with and without diabetes. JAMA. 2012;308(9):882-9.
5. Angiolillo DJ, Jakubowski JA, Ferreiro JL, Tello-Montoliu A, Rollini F, Franchi F, et al. Impaired responsiveness to the platelet P2Y12 receptor antagonist clopidogrel in patients with type 2 diabetes and coronary artery disease. J Am Coll Cardiol. 2014;64(10):1005-14.
6. Alexopoulos D, Xanthopoulou I, Gkizas V, Kassimis G, Theodoropoulos KC, Makris G, et al. Randomized assessment of ticagrelor versus prasugrel antiplatelet effects in patients with ST-segment-elevation myocardial infarction. Circ Cardiovasc interv. 2012;5(6):797-804.
7. Parodi G, Valenti R, Bellandi B, Migliorini A, Marcucci R, Comito V, et al. Comparison of prasugrel and ticagrelor loading doses in ST-segment elevation myocardial infarction patients: RAPID (Rapid Activity of Platelet Inhibitor Drugs) primary PCI study. J Am Coll Cardiol. 2013;61(15):1601-6.
8. Wiviott SD, Braunwald E, McCabe CH, Montalescot G, Ruzyllo W, Gottlieb S, et al. Prasugrel versus clopidogrel in patients with acute coronary syndromes. N Engl J Med. 2007;357(20):2001-15.
9. Price MJ. Diabetes mellitus and clopidogrel response variability. J Am Coll Cardiol. 2014;64(10):1015-8.
10. Verheugt FW. Drug interactions with good old clopidogrel: Case closed. JACC Cardiovasc Interv. 2013;6(12):1282-3.
11. Serebruany VL, Dinicolantonio JJ, Can MM, Pershukov IV, Kuliczkowski W. Gastrointestinal adverse events after dual antiplatelet therapy: clopidogrel is safer than ticagrelor, but prasugrel data are lacking or inconclusive. Cardiology. 2013;126(1):35-40.
12. Zhu Y, Zhou J. Identification of the significant involvement and mechanistic role of CYP3A4/5 in clopidogrel bioactivation. ACS Med Chem Lett. 2012;3:844-9.
13. Zhang H, Hollenberg PF. From mechanism to therapeutics: overcoming inter-individual varibility in clopidogrel therapy. In: Alesci JP, Victorino A, editors. Clopidogrel: Pharmacology, Clinical Uses and Adverse Effects. New York: Nova Scientific Publisher; 2014.p. 121-47.
14. Shuldiner AR, O'Connell JR, Bliden KP, Gandhi A, Ryan K, Horenstein RB, et al. Association of cytochrome P450 2C19 genotype with the antiplatelet effect and clinical efficacy of clopidogrel therapy. JAMA. 2009;302(8):849-57.
15.Simon T, Verstuyft C, Mary-Krause M, Quteineh L, Drouet E, Meneveau N, et al. Genetic determinants of response to clopidogrel and cardiovascular events. N Engl J Med. 2009;360(4):363-75.
16. Mega JL, Close SL, Wiviott SD, Shen L, Hockett RD, Brandt JT, et al. Cytochrome P-450 polymorphisms and response to clopidogrel. N Engl J Med. 2009;360(4):354-62.
17. Zhang H, Lauver DA, Hollenberg PF. CYP-independent inhibition of platelet aggregation in rabbits by a mixed disulfide conjugate of clopidogrel. Thromb Haemost. 2014 Dec;112(6):1304-11.
​18. Zhang H, Lauver DA, Wang H, Sun D, Hollenberg PF, Chen YE, Osawa Y, Eitzman DT. Significant Improvement of Antithrombotic Responses to Clopidogrel by Use of a Novel Conjugate as Revealed in an Arterial Model of Thrombosis. J Pharmacol Exp Ther. 2016 Oct;359(1):11-7.

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