Coronary artery thrombus
Coronary Angiography | |
General Principles | |
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Anatomy & Projection Angles | |
Normal Anatomy | |
Anatomic Variants | |
Projection Angles | |
Epicardial Flow & Myocardial Perfusion | |
Epicardial Flow | |
Myocardial Perfusion | |
Lesion Complexity | |
ACC/AHA Lesion-Specific Classification of the Primary Target Stenosis | |
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
Arterial thrombosis is typically associated with athero- sclerotic plaque rupture. This pathogenic process results in exposure or release of subendothelial cells and procoagu- lant material (e.g., TF, collagen) from within the plaque and activation and aggregation of platelets. The growing thrombus increases the degree of stenosis, which can result in extremely high shear rates (up to 70,000 s 1 ) within the stenotic region.53 In some cases, depending on stenosis geometry and location in the vasculature, turbulent flow may develop downstream of the stenosis. Ultimately, plate- let accumulation and fibrin deposition produces an occlu- sive platelet-rich intravascular thrombus. [2] [3]
Interplay between abnormali- ties in blood components, the vascula- ture, and blood flow contribute to the development of arterial thrombosis. Arte- rial thrombosis involves the formation of platelet-rich “white clots” that form after rupture of atherosclerotic plaques and exposure of procoagulant material such as lipid-rich macrophages (foam cells), collagen, tissue factor, and/or endothe- lial breach, in a high shear environment.[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
References
- ↑ 1.0 1.1 "http://www.cts.usc.edu/zglossary-thrombosis.html". Retrieved 14 November 2013. External link in
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(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
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ignored (help) - ↑ 3.0 3.1 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
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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
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ignored (help)