Editing Thrombus (section)

==Classification==
Thrombi are classified into two major groups depending on their location and the relative amount of platelets and red blood cells.<ref name=":3">{{cite web |title=Thrombus Formation – Virchow's triad & Types of Thrombi |url=https://www.thrombosisadviser.com/en/professionals/knowledge-base/essentials/thrombus-formation |access-date=20 March 2020 |website=Thrombosis Adviser |publisher=Bayer AG}}</ref> The two major groups are:
# [[Arterial]] or white thrombi (characterized by predominance of platelets)
# [[Venous]] or red thrombi (characterized by predominance of red blood cells).

===Microclots===
In the [[microcirculation]] consisting of the very small and smallest blood vessels, the [[capillaries]], tiny thrombi (microthrombi)<ref>{{cite web |title=Medical Definition of micro thrombus |url=https://www.merriam-webster.com/medical/microthrombus |website=www.merriam-webster.com |access-date=22 February 2023 |language=en}}</ref> known as microclots can obstruct the flow of blood in the capillaries. Microclots are small clumps of blood that form within the circulation, possibly as a result of a larger thrombus breaking down into smaller pieces or more likely by accretion. 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 [[ischemia|ischemic events]].<ref>{{cite journal |last1=Kell |first1=DB |last2=Laubscher |first2=GJ |last3=Pretorius |first3=E |title=A central role for amyloid fibrin microclots in long COVID/PASC: origins and therapeutic implications. |journal=Biochem J |date=2022 |volume=479 |pages=537-559 |url=https://portlandpress.com/biochemj/article/479/4/537/230829/A-central-role-for-amyloid-fibrin-microclots-in}}</ref> This can in turn lead to a form of chronic ischaemia-reperfusion injury<ref>{{cite journal |last1=Kell |first1=DB |last2=Pretorius |first2=E |title=The potential role of ischaemia-reperfusion injury in chronic, relapsing diseases such as rheumatoid arthritis, long COVID and ME/CFS: evidence, mechanisms, and therapeutic implications |journal=Biochem J |date=2022 |volume=479 |pages=1653-1709 |url=https://portlandpress.com/biochemj/article/479/16/1653/231696/The-potential-role-of-ischaemia-reperfusion-injury/}}</ref> and to the generation of autoantibodies.<ref>{{cite journal |last1=Kell |first1=DB |last2=Pretorius |first2=E |title=Are fibrinaloid microclots a cause of autoimmunity in Long Covid and other post-infection diseases? |journal=Biochem J |date=2023 |volume=480 |pages=1217-1240 |url=https://portlandpress.com/biochemj/article/480/15/1217/233389/Are-fibrinaloid-microclots-a-cause-of-autoimmunity}}</ref> Because of their amyloid nature<ref>{{cite journal |last1=Pretorius |first1=E |last2=Mbotwe |first2=S |last3=Bester |first3=J |last4=Robinson |first4=C |last5=Kell |first5=DB |title=Acute induction of anomalous and amyloidogenic blood clotting by molecular amplification of highly substoichiometric levels of bacterial lipopolysaccharide. |journal=J R Soc Interf |date=2016 |pages=20160539 |url=http://rsif.royalsocietypublishing.org/content/13/122/20160539}}</ref><ref>{{cite journal |last1=Kell |first1=DB |last2=Pretorius |first2=E |title=Proteins behaving badly. Substoichiometric molecular control and amplification of the initiation and nature of amyloid fibril formation: lessons from and for blood clotting. |journal=Progr Biophys Mol Biol |date=2017 |volume=123 |pages=15-41 |pmid=27554450 |url=http://www.sciencedirect.com/science/article/pii/S0079610716300499}}</ref> they are somewhat resistant to thrombolytic agents, which,<ref>{{cite journal |last1=Kell |first1=DB |last2=Pretorius |first2=E |title=Proteomic evidence for amyloidogenic cross-seeding in fibrinaloid microclots. |journal=Int J Mol Sci |date=2024 |volume=25 |pages=10809 |url=https://www.mdpi.com/1422-0067/25/19/10809}}</ref> along with the presence of certain other proteins,<ref>{{cite journal |last1=Pretorius |first1=E |last2=Vlok |first2=M |last3=Venter |first3=C |last4=Bezuidenhout |first4=J |last5=Laubscher |first5=GJ |last6=Steenkamp |first6=J |last7=Kell |first7=DB |title=Persistent clotting protein pathology in Long COVID/ Post-Acute Sequelae of COVID-19 (PASC) is accompanied by increased levels of antiplasmin. |journal=Cardiovasc Diabetol |date=2021 |volume=20 |pages=172 |URL=https://cardiab.biomedcentral.com/articles/10.1186/s12933-021-01359-7|pmid=34425843}}</ref> explains their persistence. Evidence based on the proteomes of such microclots implies<ref>{{cite journal |last1=Kell |first1=DB |last2=Pretorius |first2=E |title=The proteome content of blood clots observed under different conditions: successful role in predicting clot amyloid(ogenicity). |journal=Molecules |date=2025 |volume=30 |pages=668 |url=https://www.mdpi.com/1420-3049/30/3/668}}</ref> that the macroclots formed in other diseases should also be amyloid in character; this has been shown<ref>{{cite journal |last1=Grixti |first1=JM |last2=Chandran |first2=A |last3=Pretorius |first3=J |last4=Walker |first4=M |last5=Sekhar |first5=A |last6=Pretorius |first6=E |last7=Kell |first7=DB |title=The clots removed from ischaemic stroke patients by mechanical thrombectomy are amyloid in nature. |journal=medRxiv |date=2024 |pages=2024:10.1101/2024.1111.1101.24316555v24316551 |url=https://www.medrxiv.org/content/10.1101/2024.11.01.24316555v1}}</ref> for [[ischaemic stroke]].

Microclots can cause a number of problems particularly affecting the [[pulmonary alveolus|alveoli]] in the [[lung]]s of the [[respiratory system]], resulting from reduced oxygen supply. Microclots have been found to be a characteristic feature in severe cases of [[COVID-19]], and in [[long COVID]].<ref>{{cite journal |last1=Pretorius |first1=E |last2=Venter |first2=C |last3=Laubscher |first3=GJ |last4=Kotze |first4=MJ |last5=Oladejo |first5=S |last6=Watson |first6=LR |last7=Rajaratnam |first7=K |last8=Watson |first8=BW |last9=Kell |first9=DB |title=Prevalence of symptoms, comorbidities, fibrin amyloid microclots and platelet pathology in individuals with Long COVID/ Post-Acute Sequelae of COVID-19 (PASC) |journal=Cardiovasc Diabetol |date=2022 |volume=21 |pages=148 |url=https://cardiab.biomedcentral.com/articles/10.1186/s12933-022-01579-5}}</ref><ref name="Pretorius" /><ref name="Chen">{{cite journal |vauthors=Chen W, Pan JY |title=Anatomical and Pathological Observation and Analysis of SARS and COVID-19: Microthrombosis Is the Main Cause of Death |journal= Biological Procedures Online|volume= 23|issue=1 |pages=4 |date=January 2021 |pmid= 33472576|doi=10.1186/s12575-021-00142-y |s2cid=255608747 |url=|pmc=7816139 |doi-access=free }}</ref><ref>{{cite web |title="Long COVID and the role of fibrin amyloid (fibrinaloid) microclots" |url=http://dbkgroup.org/longcovid/}}</ref><ref>{{cite journal |last1=Dalton |first1=CF |last2=de Oliveira |first2=MIR |last3=Stafford |first3=P |last4=Peake |first4=N |last5=Kane |first5=B |last6=Higham |first6=A |last7=Singh |first7=D |last8=Jackson |first8=N |last9=Davies |first9=H |last10=Price |first10=D |last11=Duncan |first11=R |last12=Tattersall |first12=N |last13=Barnes |first13=A |last14=Smith |first14=DP |title=Increased fibrinaloid microclot counts in platelet-poor plasma are associated with Long COVID |journal=medRxiv |date=2024 |pages=2024.04.04.24305318 |url=https://www.medrxiv.org/content/medrxiv/early/2024/04/05/2024.04.04.24305318.full.pdf}}</ref> Fibrinaloid microclots can be induced directly via the addition of [[SARS-CoV-2]] [[spike protein]] to 'healthy' plasma,<ref>{{cite journal |last1=Grobbelaar |first1=LM |last2=Venter |first2=C |last3=Vlok |first3=M |last4=Ngoepe |first4=M |last5=Laubscher |first5=GJ |last6=Lourens |first6=PJ |last7=Steenkamp |first7=J |last8=Kell |first8=DB |last9=Pretorius |first9=E |title=SARS-CoV-2 spike protein S1 induces fibrin(ogen) resistant to fibrinolysis: implications for microclot formation in COVID-19 |journal=Biosci Rep |date=2021 |volume=41 |issue=8 |pages=BSR20210611 |url=https://portlandpress.com/bioscirep/article/41/8/BSR20210611/229418/SARS-CoV-2-spike-protein-S1-induces-fibrin-ogen}}</ref> and the fact that the amyloidogenic potential of the spike variant is related to its virulence<ref>{{cite journal |last1=Grobbelaar |first1=LM |last2=Kruger |first2=A |last3=Venter |first3=C |last4=Burger |first4=EM |last5=Laubscher |first5=GJ |last6=Maponga |first6=TG |last7=Kotze |first7=MJ |last8=Kwaan |first8=HC |last9=Miller |first9=JB |last10=Fulkerson |first10=D |last11=Huff |first11=W |last12=Chang |first12=E |last13=Wiarda |first13=G |last14=Bunch |first14=CM |last15=Walsh |first15=MM |last16=Raza |first16=S |last17=Zamlut |first17=M |last18=Moore |first18=HB |last19=Moore |first19=EE |last20=Neal |first20=M |last21=Kell |first21=DB |last22=Pretorius |first22=E |title=Relative hypercoagulopathy of the SARS-CoV-2 Beta and Delta variants when compared to the less severe Omicron variants is related to TEG parameters, the extent of fibrin amyloid microclots, and the severity of clinical illness |journal=Semin Thromb Hemost |date=2022 |volume=48 |pages=858-868 |url=https://www.thieme-connect.de/products/ejournals/abstract/10.1055/s-0042-1756306}}</ref> provides a strong indication that the microclots are on the [[aetiological]] pathway of [[Long Covid]].

The fibrinaloid microclots also provide a ready explanation for other phenomena such as Postural Orthostatic Tachycardia Syndrome (POTS),<ref>{{cite journal |last1=Kell |first1=DB |last2=Khan |first2=MA |last3=Kane |first3=B |last4=Lip |first4=GYH |last5=Pretorius |first5=E |title=The role of fibrinaloid microclots in Postural Orthostatic Tachycardia Syndrome (POTS): focus on Long COVID. |journal=J Personalized Med |date=2024 |volume=14 |pages=170 |url=https://www.mdpi.com/2075-4426/14/2/170}}</ref> atrial fibrillation,<ref>{{cite journal |last1=Kell |first1=DB |last2=Lip |first2=GYH |last3=Pretorius |first3=E |title=Fibrinaloid Microclots and Atrial Fibrillation. |journal=Biomedicines |date=2024 |volume=12 |pages=891 |url=https://www.mdpi.com/2227-9059/12/4/891}}</ref> and fibromyalgia.<ref>{{cite journal |last1=Kell |first1=DB |last2=Pretorius |first2=E |title=Potential roles of fibrinaloid microclots in fibromyalgia syndrome |journal=OSF |date=2024 |pages=9e2y5 |url=https://osf.io/9e2y5/}}</ref>

Fibrinaloid microclots are easily measured using techniques such as fluorescence microscopy<ref>{{cite journal |last1=Grixti |first1=JM |last2=Theron |first2=CW |last3=Salcedo-Sora |first3=JE |last4=Pretorius |first4=E |last5=Kell |first5=DB |title=Automated microscopic measurement of fibrinaloid microclots and their degradation by nattokinase, the main natto protease. |journal=J Exp Clin App Chin Med |date=2024 |volume=5 |pages=30-55 |url=https://ojs.exploverpub.com/index.php/jecacm/article/view/201}}</ref> and flow cytometry<ref>{{cite journal |last1=Turner |first1=S |last2=Laubscher |first2=GJ |last3=Khan |first3=MA |last4=Kell |first4=DB |last5=Pretorius |first5=E |title=Accelerating discovery: A novel flow cytometric method for detecting fibrin(ogen) amyloid microclots using long COVID as a model. |journal=Heliyon |date=2023 |volume=9 |pages=e19605 |url=https://www.cell.com/heliyon/pdf/S2405-8440(23)06813-5.pdf}}</ref> ('flow clotometry'<ref>{{cite journal |last1=Pretorius |first1=E |last2=Nunes |first2=M |last3=Pretorius |first3=J |last4=Kell |first4=DB |title=Flow Clotometry: Measuring Amyloid Microclots in ME/CFS, Long COVID, and Healthy Samples with Imaging Flow Cytometry. |journal=Research Square |pages=https://www.researchsquare.com/article/rs-4507472/v4507471 |url=https://www.researchsquare.com/article/rs-4507472/v1}}</ref>).

===Mural thrombi===
{{Further|Left ventricular thrombus}}
Mural thrombi form and adhere on the inner wall of a large [[blood vessel]] or [[heart chamber]], often as a result of blood stasis.<ref name="Singh" /> They are most commonly found in the [[aorta]], the largest [[artery]] in the body, more often in the [[descending aorta]], and less often in the [[aortic arch]] or [[abdominal aorta]].<ref name="Singh"/> They can restrict blood flow but usually do not block it entirely. Mural thrombi are usually found in vessels already damaged by [[atherosclerosis]].<ref name="Karaolanis"/>

A mural thrombus can affect any heart chamber. When found in the [[left ventricle]] 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.<ref name="Singh"/> They appear grey-red with alternating light and dark lines (known as [[lines of Zahn]]) which represent bands of white blood cells and red blood cells (darker) entrapped in layers of [[fibrin]].{{citation needed|date=September 2022}}