Coronary artery thrombus: Difference between revisions
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==Pathophysiology== | ==Pathophysiology== | ||
The pathogenic process of arterial thrombosis involves the formation of platelet-rich “white clots” after the rupture of atherosclerotic plaques and exposure of procoagulant material such as lipid-rich macrophages (foam cells), collagen, tissue factor, and/or endothelial breach, in a high shear environment. The exposed material come from within the plaque and also from the activation and aggregation of platelets. Platelet accumulation and fibrin deposition cause an occlusive platelet-rich intravascular thrombus. The growing thrombus increases the degree of narrowing, which may result in extremely high shear rates within the stenotic region. This phenomenum is responsible for a turbulent flow which is developed downstream of the stenosis depending on stenosis geometry and location in the vasculature.<ref name="Bark-2010">{{Cite journal | last1 = Bark | first1 = DL. | last2 = Ku | first2 = DN. | title = Wall shear over high degree stenoses pertinent to atherothrombosis. | journal = J Biomech | volume = 43 | issue = 15 | pages = 2970-7 | month = Nov | year = 2010 | doi = 10.1016/j.jbiomech.2010.07.011 | PMID = 20728892 }}</ref> | The pathogenic process of arterial thrombosis involves the formation of platelet-rich “white clots” after the rupture of atherosclerotic plaques and exposure of procoagulant material such as lipid-rich macrophages (foam cells), collagen, tissue factor, and/or endothelial breach, in a high shear environment. The exposed material come from within the plaque and also from the activation and aggregation of platelets. Platelet accumulation and fibrin deposition cause an occlusive platelet-rich intravascular thrombus. The growing thrombus increases the degree of narrowing, which may result in extremely high shear rates within the stenotic region. This phenomenum is responsible for a turbulent flow which is developed downstream of the stenosis depending on stenosis geometry and location in the vasculature.<ref name="Bark-2010">{{Cite journal | last1 = Bark | first1 = DL. | last2 = Ku | first2 = DN. | title = Wall shear over high degree stenoses pertinent to atherothrombosis. | journal = J Biomech | volume = 43 | issue = 15 | pages = 2970-7 | month = Nov | year = 2010 | doi = 10.1016/j.jbiomech.2010.07.011 | PMID = 20728892 }}</ref><ref name="Wolberg-2012">{{Cite journal | last1 = Wolberg | first1 = AS. | last2 = Aleman | first2 = MM. | last3 = Leiderman | first3 = K. | last4 = Machlus | first4 = KR. | title = Procoagulant activity in hemostasis and thrombosis: Virchow's triad revisited. | journal = Anesth Analg | volume = 114 | issue = 2 | pages = 275-85 | month = Feb | year = 2012 | doi = 10.1213/ANE.0b013e31823a088c | PMID = 22104070 }}</ref> | ||
<ref name="Wolberg-2012">{{Cite journal | last1 = Wolberg | first1 = AS. | last2 = Aleman | first2 = MM. | last3 = Leiderman | first3 = K. | last4 = Machlus | first4 = KR. | title = Procoagulant activity in hemostasis and thrombosis: Virchow's triad revisited. | journal = Anesth Analg | volume = 114 | issue = 2 | pages = 275-85 | month = Feb | year = 2012 | doi = 10.1213/ANE.0b013e31823a088c | PMID = 22104070 }}</ref> | |||
==Clinical Significance== | ==Clinical Significance== | ||
Revision as of 19:48, 14 November 2013
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Coronary Angiography | |
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General Principles | |
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Anatomy & Projection Angles | |
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Normal Anatomy | |
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Anatomic Variants | |
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Projection Angles | |
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Epicardial Flow & Myocardial Perfusion | |
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Epicardial Flow | |
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Myocardial Perfusion | |
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Lesion Complexity | |
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ACC/AHA Lesion-Specific Classification of the Primary Target Stenosis | |
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Lesion Morphology | |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: ; Vanessa Cherniauskas, M.D. [2]
Synonyms and keywords: Coronary thrombosis
Overview
The Thrombus of coronary arteries occurs when the lumen, of the artery starts becoming smaller and creates a narrowed segment in which the blood flow clots slowly in the artery. This phenomenum in coronary artery decreases the perfusion and may cause necrosis which may lead to a heart attack if not treated.[1]
Definition
The coronary artery thrombus may be defined as an occlusion or blockage of blood flow within a vessel due to a clot.[1]
Pathophysiology
The pathogenic process of arterial thrombosis involves the formation of platelet-rich “white clots” after the rupture of atherosclerotic plaques and exposure of procoagulant material such as lipid-rich macrophages (foam cells), collagen, tissue factor, and/or endothelial breach, in a high shear environment. The exposed material come from within the plaque and also from the activation and aggregation of platelets. Platelet accumulation and fibrin deposition cause an occlusive platelet-rich intravascular thrombus. The growing thrombus increases the degree of narrowing, which may result in extremely high shear rates within the stenotic region. This phenomenum is responsible for a turbulent flow which is developed downstream of the stenosis depending on stenosis geometry and location in the vasculature.[2][3]
Clinical Significance
- The location of the thrombosis is clinically relevant once the infarction may be subclinical or not.[4]
- Coronary thrombosis may be a complication related to drug-eluting stents.[4]
TIMI Thrombus Grade
Treatment
Examples
References
- ↑ 1.0 1.1 "http://www.cts.usc.edu/zglossary-thrombosis.html". Retrieved 14 November 2013. External link in
|title=(help) - ↑ Bark, DL.; Ku, DN. (2010). "Wall shear over high degree stenoses pertinent to atherothrombosis". J Biomech. 43 (15): 2970–7. doi:10.1016/j.jbiomech.2010.07.011. PMID 20728892. Unknown parameter
|month=ignored (help) - ↑ Wolberg, AS.; Aleman, MM.; Leiderman, K.; Machlus, KR. (2012). "Procoagulant activity in hemostasis and thrombosis: Virchow's triad revisited". Anesth Analg. 114 (2): 275–85. doi:10.1213/ANE.0b013e31823a088c. PMID 22104070. Unknown parameter
|month=ignored (help) - ↑ 4.0 4.1 Lüscher, TF.; Steffel, J.; Eberli, FR.; Joner, M.; Nakazawa, G.; Tanner, FC.; Virmani, R. (2007). "Drug-eluting stent and coronary thrombosis: biological mechanisms and clinical implications". Circulation. 115 (8): 1051–8. doi:10.1161/CIRCULATIONAHA.106.675934. PMID 17325255. Unknown parameter
|month=ignored (help)