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Thrombus
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<h2 id="classification">Classification</h2> <p>Thrombi are classified into two major groups depending on their location and the relative amount of platelets and red blood cells.<a class="footnote-ref" id="fnref:7" href="#fn:7"><sup>7</sup></a> The two major groups are: </p> <ol><li><a href="/facts/Arterial/Y1Yj0jat">Arterial</a> or white thrombi (characterized by predominance of platelets)</li> <li><a href="/facts/Venous/I6ycr6gF">Venous</a> or red thrombi (characterized by predominance of red blood cells).</li></ol> <h3>Microclots</h3> <p>In the <a href="/facts/Microcirculation/EecoBYyz">microcirculation</a> consisting of the very small and smallest blood vessels, the <a href="/facts/Capillaries/4BIzKJAe">capillaries</a>, tiny thrombi (microthrombi)<a class="footnote-ref" id="fnref:8" href="#fn:8"><sup>8</sup></a> known as microclots can obstruct the flow of blood in the capillaries. Microclots are small clumps of blood that form within the circulation, usually as a result of a larger thrombus breaking down into smaller pieces. They can be a cause for concern as they can lead to blockages in small vessels and restrict blood flow, leading to tissue damage and potentially causing <a href="/facts/Ischemia/ySL9xbCl">ischemic events</a>. </p><p>Microclots can cause a number of problems particularly affecting the <a href="/facts/Pulmonary_alveolus/aEHP1ATT">alveoli</a> in the <a href="/facts/Lung/gTWXI6Fj">lungs</a> of the <a href="/facts/Respiratory_system/IG8v5JEr">respiratory system</a>, resulting from reduced oxygen supply. Microclots have been found to be a characteristic feature in severe cases of <a href="/facts/COVID-19/YsUgvsaX">COVID-19</a>, and in <a href="/facts/Long_COVID/9YQdUEE2">long COVID</a>.<a class="footnote-ref" id="fnref:9" href="#fn:9"><sup>9</sup></a><a class="footnote-ref" id="fnref:10" href="#fn:10"><sup>10</sup></a> </p> <h3>Mural thrombi</h3> <p class="note">Further information: <a href="/facts/Left_ventricular_thrombus/pnaUBcUc">Left ventricular thrombus</a></p> <p>Mural thrombi form and adhere on the inner wall of a large <a href="/facts/Blood_vessel/FG3GjPNW">blood vessel</a> or <a href="/facts/Heart_chamber/fF4KSGdk">heart chamber</a>, often as a result of blood stasis.<a class="footnote-ref" id="fnref:11" href="#fn:11"><sup>11</sup></a> They are most commonly found in the <a href="/facts/Aorta/ov2Gp9h4">aorta</a>, the largest <a href="/facts/Artery/Y1Yj0jat">artery</a> in the body, more often in the <a href="/facts/Descending_aorta/6twrDNKW">descending aorta</a>, and less often in the <a href="/facts/Aortic_arch/JvSt61eK">aortic arch</a> or <a href="/facts/Abdominal_aorta/W0hEwh5X">abdominal aorta</a>.<a class="footnote-ref" id="fnref:12" href="#fn:12"><sup>12</sup></a> They can restrict blood flow but usually do not block it entirely. Mural thrombi are usually found in vessels already damaged by <a href="/facts/Atherosclerosis/WIS8QQ6v">atherosclerosis</a>.<a class="footnote-ref" id="fnref:13" href="#fn:13"><sup>13</sup></a> </p><p>A mural thrombus can affect any heart chamber. When found in the <a href="/facts/Left_ventricle/FCzV1xm7">left ventricle</a> it is often a result of a heart attack complication. The thrombus in this case can separate from the chamber, be carried through arteries and block a blood vessel.<a class="footnote-ref" id="fnref:14" href="#fn:14"><sup>14</sup></a> They appear grey-red with alternating light and dark lines (known as <a href="/facts/Lines_of_Zahn/Sc63Cvk6">lines of Zahn</a>) which represent bands of white blood cells and red blood cells (darker) entrapped in layers of <a href="/facts/Fibrin/BFar47y5">fibrin</a>. </p> <h2 id="cause">Cause</h2> <p>It was suggested over 150 years ago that thrombus formation is a result of abnormalities in blood flow, vessel wall, and blood components. This concept is now known as <a href="/facts/Virchow%27s_triad/CYEINs1P">Virchow's triad</a>. The three factors have been further refined to include circulatory stasis, vascular wall injury, and hypercoagulable state, all of which contribute to increased risk for venous thromboembolism and other cardiovascular diseases.<a class="footnote-ref" id="fnref:15" href="#fn:15"><sup>15</sup></a> </p><p><a href="/facts/Virchow%27s_triad/CYEINs1P">Virchow's triad</a> describes the <a href="/facts/Pathogenesis/o9kHHK0U">pathogenesis</a> of thrombus formation:<a class="footnote-ref" id="fnref:16" href="#fn:16"><sup>16</sup></a><a class="footnote-ref" id="fnref:17" href="#fn:17"><sup>17</sup></a> </p> <ol><li>Endothelial injury: Injury to the <a href="/facts/Endothelium/L4ENFVnw">endothelium</a> (interior surface of blood vessel), causing platelet activation and aggregation; <ul><li>Common causes include: <a href="/facts/Injury/PJ7CbnMQ">trauma</a>, <a href="/facts/Health_effects_of_tobacco/J4WdbVWz">smoking</a>, <a href="/facts/Hypertension/wlAvBfcf">hypertension</a>, <a href="/facts/Atheroma/cMw1I9rt">atheroma</a>.</li></ul></li> <li><a href="/facts/Hemodynamics/HzubzJpn">Hemodynamic</a> changes (stasis, turbulence): Blood stasis promotes greater contact between platelets/coagulative factors with vascular endothelium. If rapid blood circulation (e.g., because of <a href="/facts/Tachycardia/ycmyzP7q">tachycardia</a>) occurs within vessels that have endothelial injuries, that creates disordered flow (turbulence) that can lead to the formation of thrombosis;<a class="footnote-ref" id="fnref:18" href="#fn:18"><sup>18</sup></a> <ul><li>Common causes of stasis include anything that leads to prolonged immobility and reduced blood flow such as: <a href="/facts/Injury/PJ7CbnMQ">trauma</a>/<a href="/facts/Bone_fracture/faEv3Ve5">broken bones</a> and extended <a href="/facts/Air_travel/unbhGQTk">air travel</a>.</li></ul></li> <li>Hypercoagulability (also called <a href="/facts/Thrombophilia/C0Bho8NB">thrombophilia</a>; any disorder of the blood that predisposes to thrombosis);<a class="footnote-ref" id="fnref:19" href="#fn:19"><sup>19</sup></a> <ul><li>Common causes include: cancer (<a href="/facts/Leukaemia/WpEfW0Qh">leukaemia</a>), <a href="/facts/Factor_V/auQHWp12">factor V</a> mutation (<a href="/facts/Factor_V_Leiden/LDvd8h9Q">Leiden</a>) – prevents Factor V inactivation leading to increased coagulability.</li></ul></li></ol> <p><a href="/facts/Disseminated_intravascular_coagulation/CuWaSKQW">Disseminated intravascular coagulation</a> (DIC) involves widespread microthrombi formation throughout the majority of the blood vessels. This is due to excessive consumption of coagulation factors and subsequent activation of <a href="/facts/Fibrinolysis/moYzJ5Gx">fibrinolysis</a> using all of the body's available <a href="/facts/Platelets/I0xrDVGa">platelets</a> and clotting factors. The result is hemorrhaging and ischemic necrosis of tissue/organs. Causes are <a href="/facts/Septicaemia/n52bkffJ">septicaemia</a>, acute <a href="/facts/Leukaemia/WpEfW0Qh">leukaemia</a>, <a href="/facts/Shock_(circulatory)/aIKGDS0e">shock</a>, snake bites, <a href="/facts/Fat_embolism/8JbwPzSy">fat emboli</a> from broken bones, or other severe traumas. DIC may also be seen in <a href="/facts/Pregnancy/vEKYGpep">pregnant females</a>. Treatment involves the use of <a href="/facts/Fresh_frozen_plasma/QRs8fF4y">fresh frozen plasma</a> to restore the level of clotting factors in the blood, as well as platelets and heparin to prevent further thrombi formation. </p> <h2 id="pathophysiology">Pathophysiology</h2> <p>A thrombus occurs when the hemostatic process, which normally occurs in response to injury, becomes activated in an uninjured or slightly injured vessel. A thrombus in a large blood vessel will decrease blood flow through that vessel (termed a mural thrombus). In a small blood vessel, blood flow may be completely cut off (termed an occlusive thrombus), resulting in death of tissue supplied by that vessel. If a thrombus dislodges and becomes free-floating, it is considered an <a href="/facts/Embolism/A8BD4RoI">embolus</a>. If an embolus becomes trapped within a blood vessel, it blocks blood flow and is termed as an embolism. Embolisms, depending on their specific location, can cause more significant effects like strokes, heart attacks, or even death.<a class="footnote-ref" id="fnref:20" href="#fn:20"><sup>20</sup></a> </p> <p>Some of the conditions which increase the risk of blood clots developing include <a href="/facts/Atrial_fibrillation/Rzkq1tmN">atrial fibrillation</a> (a form of <a href="/facts/Cardiac_arrhythmia/ooEpr46Q">cardiac arrhythmia</a>), heart valve replacement, a recent <a href="/facts/Myocardial_infarction/xoGw0qcG">heart attack</a> (also known as a <a href="/facts/Myocardial_infarction/xoGw0qcG">myocardial infarction</a>), extended periods of inactivity (see <a href="/facts/Deep_venous_thrombosis/vX7cGv8J">deep venous thrombosis</a>), and genetic or disease-related deficiencies in the blood's clotting abilities. </p> <h3>Formation</h3> <p>Platelet activation occurs through injuries that damage the <a href="/facts/Endothelium/L4ENFVnw">endothelium</a> of the blood vessels, exposing the enzyme called <a href="/facts/Factor_VII/cAFLoqTS">factor VII</a>, a protein normally circulating within the vessels, to the <a href="/facts/Tissue_factor/8qSycULo">tissue factor</a>, which is a protein encoded by the F3 gene. The platelet activation can potentially cause a cascade, eventually leading to the formation of the thrombus.<a class="footnote-ref" id="fnref:21" href="#fn:21"><sup>21</sup></a> This process is regulated through <a href="/facts/Thromboregulation/bygAe6fp">thromboregulation</a>. </p> <h2 id="prevention">Prevention</h2> <p class="note">Main articles: <a href="/facts/Thrombolysis/6hUSmL3G">Thrombolysis</a>, <a href="/facts/Thrombosis_prophylaxis/XcYbKGSY">Thrombosis prophylaxis</a>, and <a href="/facts/Reperfusion_therapy/Wr2JCXYt">Reperfusion therapy</a></p> <p><a href="/facts/Anticoagulant/cARpjm0G">Anticoagulants</a> are drugs used to prevent the formation of blood clots, reducing the risk of <a href="/facts/Stroke/DwpjdzY0">stroke</a>, <a href="/facts/Myocardial_infarction/xoGw0qcG">heart attack</a> and <a href="/facts/Pulmonary_embolism/LPjKCPba">pulmonary embolism</a>. <a href="/facts/Heparin/4lxSm2pB">Heparin</a> and <a href="/facts/Warfarin/kMnH6tb0">warfarin</a> are used to inhibit the formation and growth of existing thrombi, with the former used for acute anticoagulation while the latter is used for long-term anticoagulation.<a class="footnote-ref" id="fnref:22" href="#fn:22"><sup>22</sup></a> The mechanism of action of heparin and warfarin are different as they work on different pathways of the <a href="/facts/Coagulation/vnfEevM0">coagulation cascade</a>.<a class="footnote-ref" id="fnref:23" href="#fn:23"><sup>23</sup></a> </p><p>Heparin works by binding to and activating the enzyme inhibitor <a href="/facts/Antithrombin/k5pbgBct">antithrombin III</a>, an enzyme that acts by inactivating thrombin and factor Xa.<a class="footnote-ref" id="fnref:24" href="#fn:24"><sup>24</sup></a> In contrast, warfarin works by inhibiting <a href="/facts/Vitamin_K_epoxide_reductase/xmgCx8u5">vitamin K epoxide reductase</a>, an enzyme needed to synthesize vitamin K dependent clotting factors II, VII, IX, and X.<a class="footnote-ref" id="fnref:25" href="#fn:25"><sup>25</sup></a><a class="footnote-ref" id="fnref:26" href="#fn:26"><sup>26</sup></a> Bleeding time with heparin and warfarin therapy can be measured with the partial thromboplastin time (PTT) and <a href="/facts/Prothrombin_time/pkLRGqcY">prothrombin time</a> (PT), respectively.<a class="footnote-ref" id="fnref:27" href="#fn:27"><sup>27</sup></a> </p> <h2 id="treatment">Treatment</h2> <p>Once clots have formed, other drugs can be used to promote <a href="/facts/Thrombolysis/6hUSmL3G">thrombolysis</a> or clot breakdown. <a href="/facts/Streptokinase/mAxd0GSK">Streptokinase</a>, an enzyme produced by <a href="/facts/Streptococcus/Fx8lJ0nz">streptococcal bacteria</a>, is one of the oldest thrombolytic drugs.<a class="footnote-ref" id="fnref:28" href="#fn:28"><sup>28</sup></a> This drug can be administered <a href="/facts/Intravenous_therapy/AwwuD3Nu">intravenously</a> to dissolve blood clots in <a href="/facts/Coronary_circulation/SJhPVTgM">coronary vessels</a>. However, streptokinase causes systemic fibrinolytic state and can lead to bleeding problems. <a href="/facts/Tissue_plasminogen_activator/CQ94BqkJ">Tissue plasminogen activator</a> (tPA) is a different enzyme that promotes the degradation of fibrin in clots but not free fibrinogen.<a class="footnote-ref" id="fnref:29" href="#fn:29"><sup>29</sup></a> This drug is made by transgenic bacteria and converts plasminogen into the clot-dissolving enzyme, <a href="/facts/Plasmin/bfLCyyPt">plasmin</a>.<a class="footnote-ref" id="fnref:30" href="#fn:30"><sup>30</sup></a> Recent research indicates that tPA could have toxic effects in the central nervous system. In cases of severe stroke, tPA can cross the <a href="/facts/Blood%E2%80%93brain_barrier/xYzvVwdu">blood–brain barrier</a> and enter interstitial fluid, where it then increases excitotoxicity, potentially affecting permeability of the blood–brain barrier,<a class="footnote-ref" id="fnref:31" href="#fn:31"><sup>31</sup></a> and causing cerebral hemorrhage.<a class="footnote-ref" id="fnref:32" href="#fn:32"><sup>32</sup></a> </p><p>There are also some anticoagulants that come from animals that work by dissolving <a href="/facts/Fibrin/BFar47y5">fibrin</a>. For example, <i><a href="/facts/Haementeria_ghilianii/hfbfwlJd">Haementeria ghilianii</a></i>, an <a href="/facts/Amazon_rainforest/MGVatclX">Amazon</a> <a href="/facts/Leech/eYSMx97F">leech</a>, produces an enzyme called <a href="/facts/Hementin/DI7cATSY">hementin</a> from its <a href="/facts/Salivary_gland/VtteDtH0">salivary glands</a>.<a class="footnote-ref" id="fnref:33" href="#fn:33"><sup>33</sup></a> </p> <h2 id="prognosis">Prognosis</h2> <p>Thrombus formation can have one of four outcomes: propagation, embolization, dissolution, and organization and recanalization.<a class="footnote-ref" id="fnref:34" href="#fn:34"><sup>34</sup></a> </p> <ol><li>Propagation of a thrombus occurs towards the direction of the heart and involves the accumulation of additional platelets and fibrin. This means that it is anterograde in veins or retrograde in arteries.</li> <li><a href="/facts/Embolization/zPNry9cY">Embolization</a> occurs when the thrombus breaks free from the vascular wall and becomes mobile, thereby traveling to other sites in the vasculature. A venous embolus (mostly from <a href="/facts/Deep_vein_thrombosis/vX7cGv8J">deep vein thrombosis</a> in the <a href="/facts/Human_leg/sjU6X2E3">lower limbs</a>) will travel through the systemic circulation, reach the right side of the heart, and travel through the pulmonary artery, resulting in a pulmonary embolism. Arterial thrombosis resulting from hypertension or atherosclerosis can become mobile and the resulting emboli can occlude any artery or arteriole downstream of the thrombus formation. This means that cerebral stroke, myocardial infarction, or any other organ can be affected.</li> <li>Dissolution occurs when the <a href="/facts/Fibrinolysis/moYzJ5Gx">fibrinolytic mechanisms</a> break up the thrombus and blood flow is restored to the vessel. This may be aided by fibrinolytic drugs such as Tissue Plasminogen Activator (tPA) in instances of coronary artery occlusion. The best response to fibrinolytic drugs is within a couple of hours, before the fibrin meshwork of the thrombus has been fully developed.</li> <li>Organization and recanalization involves the ingrowth of <a href="/facts/Smooth_muscle/mpcpTsHp">smooth muscle</a> cells, <a href="/facts/Fibroblast/n08KsFll">fibroblasts</a> and <a href="/facts/Endothelium/L4ENFVnw">endothelium</a> into the <a href="/facts/Fibrin/BFar47y5">fibrin</a>-rich thrombus. If recanalization proceeds it provides capillary-sized channels through the thrombus for continuity of blood flow through the entire thrombus but may not restore sufficient blood flow for the metabolic needs of the downstream tissue.<a class="footnote-ref" id="fnref:35" href="#fn:35"><sup>35</sup></a></li></ol> <h2 id="see-also">See also</h2> <ul><li><a href="/facts/Thrombogenicity/Y20nAh5S">Thrombogenicity</a> (the tendency to clot)</li> <li><a href="/facts/National_Blood_Clot_Alliance/Np2DILFU">National Blood Clot Alliance</a></li> <li><a href="/facts/Hemorrhoid/wlInkR8T">Hemorrhoid</a></li></ul> <h2 id="external-links">External links</h2> Look up <i>thrombus</i> or <i>clot</i> in Wiktionary, the free dictionary. <ul><li><a href="http://www.medicalnewstoday.com/articles/87699.php">Muscle Relaxing Drugs Can Reduce Lethal Blood Clots</a> <a href="https://web.archive.org/web/20090204115537/http://www.medicalnewstoday.com/articles/87699.php">Archived</a> 2009-02-04 at the <a href="/facts/Wayback_Machine/nmQ3a6JC">Wayback Machine</a></li> <li><a href="https://web.archive.org/web/20070925112008/http://www.planetark.com/dailynewsstory.cfm/newsid/44436/story.htm">Air Pollution Triggers Blood Clots – US Study</a>[usurped].</li></ul> <h2 id="references">References</h2> <ol> <li id="fn:1"><p>Bang, Nils U.; Beller, Fritz K.; Deutsch, Erwin; Mammen, Eberhard F., eds. (1971-01-01), "Thrombosis", Thrombosis and Bleeding Disorders, Academic Press, pp. 488–534, ISBN 978-0-12-077750-1, retrieved 2025-02-27 <a href="978-0-12-077750-1" target="_blank">978-0-12-077750-1</a> <a href="#fnref:1" class="footnote-back-ref">↩</a></p></li> <li id="fn:2"><p>Rubin, Emanuel; Reisner, Howard M. (2009). Essentials of Rubin's Pathology. Lippincott Williams & Wilkins. ISBN 978-0-7817-7324-9. <a href="978-0-7817-7324-9" target="_blank">978-0-7817-7324-9</a> <a href="#fnref:2" class="footnote-back-ref">↩</a></p></li> <li id="fn:3"><p>Pretorius E, Vlok M, Venter C, Bezuidenhout JA, Laubscher GJ, Steenkamp J, Kell DB (August 2021). "Persistent clotting protein pathology in Long COVID/Post-Acute Sequelae of COVID-19 (PASC) is accompanied by increased levels of antiplasmin". Cardiovasc Diabetol. 20 (1): 172. doi:10.1186/s12933-021-01359-7. PMC 8381139. PMID 34425843. <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8381139" target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8381139</a> <a href="#fnref:3" class="footnote-back-ref">↩</a></p></li> <li id="fn:4"><p>Singh, Davinder P.; Basit, Hajira; Malik, Ahmad; Mahajan, Kunal (5 November 2021). "Mural Thrombi". PMID 30484999. Retrieved 11 February 2022. <a href="https://www.ncbi.nlm.nih.gov/books/NBK534294/" target="_blank">https://www.ncbi.nlm.nih.gov/books/NBK534294/</a> <a href="#fnref:4" class="footnote-back-ref">↩</a></p></li> <li id="fn:5"><p>Singh, Davinder P.; Basit, Hajira; Malik, Ahmad; Mahajan, Kunal (5 November 2021). "Mural Thrombi". PMID 30484999. Retrieved 11 February 2022. <a href="https://www.ncbi.nlm.nih.gov/books/NBK534294/" target="_blank">https://www.ncbi.nlm.nih.gov/books/NBK534294/</a> <a href="#fnref:5" class="footnote-back-ref">↩</a></p></li> <li id="fn:6"><p>Karaolanis G, Moris D, Bakoyiannis C, Tsilimigras DI, Palla VV, Spartalis E, Schizas D, Georgopoulos S (August 2017). "A critical reappraisal of the treatment modalities of normal appearing thoracic aorta mural thrombi". Ann Transl Med. 5 (15): 306. doi:10.21037/atm.2017.05.15. PMC 5555985. PMID 28856146. <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5555985" target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5555985</a> <a href="#fnref:6" class="footnote-back-ref">↩</a></p></li> <li id="fn:7"><p>"Thrombus Formation – Virchow's triad & Types of Thrombi". Thrombosis Adviser. Bayer AG. Retrieved 20 March 2020. <a href="https://www.thrombosisadviser.com/en/professionals/knowledge-base/essentials/thrombus-formation" target="_blank">https://www.thrombosisadviser.com/en/professionals/knowledge-base/essentials/thrombus-formation</a> <a href="#fnref:7" class="footnote-back-ref">↩</a></p></li> <li id="fn:8"><p>"Medical Definition of micro thrombus". www.merriam-webster.com. Retrieved 22 February 2023. <a href="https://www.merriam-webster.com/medical/microthrombus" target="_blank">https://www.merriam-webster.com/medical/microthrombus</a> <a href="#fnref:8" class="footnote-back-ref">↩</a></p></li> <li id="fn:9"><p>Pretorius E, Vlok M, Venter C, Bezuidenhout JA, Laubscher GJ, Steenkamp J, Kell DB (August 2021). "Persistent clotting protein pathology in Long COVID/Post-Acute Sequelae of COVID-19 (PASC) is accompanied by increased levels of antiplasmin". Cardiovasc Diabetol. 20 (1): 172. doi:10.1186/s12933-021-01359-7. PMC 8381139. PMID 34425843. <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8381139" target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8381139</a> <a href="#fnref:9" class="footnote-back-ref">↩</a></p></li> <li id="fn:10"><p>Chen W, Pan JY (January 2021). "Anatomical and Pathological Observation and Analysis of SARS and COVID-19: Microthrombosis Is the Main Cause of Death". Biological Procedures Online. 23 (1): 4. doi:10.1186/s12575-021-00142-y. PMC 7816139. PMID 33472576. S2CID 255608747. <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7816139" target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7816139</a> <a href="#fnref:10" class="footnote-back-ref">↩</a></p></li> <li id="fn:11"><p>Singh, Davinder P.; Basit, Hajira; Malik, Ahmad; Mahajan, Kunal (5 November 2021). "Mural Thrombi". PMID 30484999. Retrieved 11 February 2022. <a href="https://www.ncbi.nlm.nih.gov/books/NBK534294/" target="_blank">https://www.ncbi.nlm.nih.gov/books/NBK534294/</a> <a href="#fnref:11" class="footnote-back-ref">↩</a></p></li> <li id="fn:12"><p>Singh, Davinder P.; Basit, Hajira; Malik, Ahmad; Mahajan, Kunal (5 November 2021). "Mural Thrombi". PMID 30484999. Retrieved 11 February 2022. <a href="https://www.ncbi.nlm.nih.gov/books/NBK534294/" target="_blank">https://www.ncbi.nlm.nih.gov/books/NBK534294/</a> <a href="#fnref:12" class="footnote-back-ref">↩</a></p></li> <li id="fn:13"><p>Karaolanis G, Moris D, Bakoyiannis C, Tsilimigras DI, Palla VV, Spartalis E, Schizas D, Georgopoulos S (August 2017). "A critical reappraisal of the treatment modalities of normal appearing thoracic aorta mural thrombi". Ann Transl Med. 5 (15): 306. doi:10.21037/atm.2017.05.15. PMC 5555985. 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