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dc.contributor.advisorMorelli, Vânia Maris
dc.contributor.advisorBrækkan, Sigrid Kufaas
dc.contributor.advisorHansen, John-Bjarne
dc.contributor.authorEdvardsen, Magnus Sandvik
dc.date.accessioned2024-05-31T12:22:15Z
dc.date.available2024-05-31T12:22:15Z
dc.date.issued2022-05-31en
dc.description.abstractBackground: Myocardial infarction (MI) is the most common cause of death worldwide. Important modifiable risk factors have been unraveled and preventive measures established, but the disease burden remains substantial. Von Willebrand Factor (VWF) is a protein involved in hemostasis known to have platelet-recruiting ability according to molecular size. A disintegrin and metalloprotease with thrombospondin motif 13 (ADAMTS13) is responsible for the cleavage of VWF multimers, making it an important regulator of VWF thrombogenicity. As severe deficiency of ADAMTS13 is known to cause thrombosis in microvessels, it has been hypothesized that a slight to moderate decrease in ADAMTS13 levels leads to increased risk of MI. Aim: To perform a literature review of existing case-control and cohort studies assessing the association between ADAMTS13 and MI. Methods: The PubMed database was used to perform a literature search designed to retrieve all case-control and cohort studies on the association between ADAMTS13 and MI. Only studies that investigated ADAMTS13 as exposure and MI as outcome were included. Results: Twelve studies were included, 10 case-control studies and 2 cohort studies. In the acute phase of MI, the vast majority of studies reported lower antigen or activity levels of ADAMTS13 in MI cases compared with control subjects. Findings were somewhat controversial when ADAMTS13 was measured several months/years after MI. A large prospective population-based cohort study found that individuals with low ADAMTS13 activity at baseline had increased risk of MI during 10 years of follow-up. Conclusion: Existing literature suggests an association between ADAMTS13 and MI. In the acute phase of MI, patients have lower levels of ADAMTS13 compared with control subjects. ADAMTS13 activity also appears to be reduced in the years prior to the MI event. However, further research using a prospective study design (e.g., cohorts) is necessary to confirm the association between ADAMTS13 and risk of future MI.en_US
dc.identifier.urihttps://hdl.handle.net/10037/33665
dc.language.isoengen_US
dc.publisherUiT Norges arktiske universitetno
dc.publisherUiT The Arctic University of Norwayen
dc.rights.holderCopyright 2022 The Author(s)
dc.rights.urihttps://creativecommons.org/licenses/by-nc-sa/4.0en_US
dc.rightsAttribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0)en_US
dc.subject.courseIDMED-3950
dc.subjectVDP::Medisinske Fag: 700::Klinisk medisinske fag: 750::Kardiologi: 771en_US
dc.subjectVDP::Medical disciplines: 700::Clinical medical disciplines: 750::Cardiology: 771en_US
dc.subjectVDP::Medisinske Fag: 700::Klinisk medisinske fag: 750::Hematologi: 775en_US
dc.subjectVDP::Medical disciplines: 700::Clinical medical disciplines: 750::Hematology: 775en_US
dc.subjectMyocardial Infarctionen_US
dc.subjectADAMTS13en_US
dc.titleADAMTS13 and Myocardial Infarction: A Literature Reviewen_US
dc.typeMaster thesisen
dc.typeMastergradsoppgaveno


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Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0)
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