Clinical utility of cardiac troponin measurement in COVID-19 infection.
Identifieur interne : 000380 ( Main/Corpus ); précédent : 000379; suivant : 000381Clinical utility of cardiac troponin measurement in COVID-19 infection.
Auteurs : David C. GazeSource :
- Annals of clinical biochemistry [ 1758-1001 ] ; 2020.
English descriptors
- KwdEn :
- MESH :
- chemical , blood : Biomarkers, Troponin.
- diagnosis : Coronavirus Infections, Pneumonia, Viral.
- Betacoronavirus, Humans, Pandemics.
Abstract
The novel coronavirus SARS-CoV-2 causes the disease COVID-19, a severe acute respiratory syndrome. COVID-19 is now a global pandemic and public health emergency due to rapid human-to-human transmission. The impact is far-reaching, with enforced social distancing and isolation, detrimental effects on individual physical activity and mental wellbeing, education in the young and economic impact to business. Whilst most COVID-19 patients demonstrate mild-to-moderate symptoms, those with severe disease progression are at a higher risk of mortality. As more is learnt about this novel disease, it is becoming evident that comorbid cardiovascular disease is associated with a greater severity and increased mortality. Many patients positive for COVID-19 demonstrate increased concentrations of cardiac troponin, creating confusion in clinical interpretation. While myocardial infarction is associated with acute infectious respiratory disease, the majority of COVID-19 patients demonstrate stable cTn rather than the dynamically changing values indicative of an acute coronary syndrome. Although full understanding of the mechanism of cTn release in COVID-19 is currently lacking, this mini-review assesses the limited published literature with a view to offering insight to pathophysiological mechanisms and reported treatment regimens.
DOI: 10.1177/0004563220921888
PubMed: 32255359
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pubmed:32255359Le document en format XML
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<affiliation><nlm:affiliation>Clinical Blood Sciences, South West London Pathology, St George's Healthcare NHS Foundation Trust, London, UK.</nlm:affiliation>
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<series><title level="j">Annals of clinical biochemistry</title>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Betacoronavirus (MeSH)</term>
<term>Biomarkers (blood)</term>
<term>Coronavirus Infections (diagnosis)</term>
<term>Humans (MeSH)</term>
<term>Pandemics (MeSH)</term>
<term>Pneumonia, Viral (diagnosis)</term>
<term>Troponin (blood)</term>
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<term>Troponin</term>
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<front><div type="abstract" xml:lang="en">The novel coronavirus SARS-CoV-2 causes the disease COVID-19, a severe acute respiratory syndrome. COVID-19 is now a global pandemic and public health emergency due to rapid human-to-human transmission. The impact is far-reaching, with enforced social distancing and isolation, detrimental effects on individual physical activity and mental wellbeing, education in the young and economic impact to business. Whilst most COVID-19 patients demonstrate mild-to-moderate symptoms, those with severe disease progression are at a higher risk of mortality. As more is learnt about this novel disease, it is becoming evident that comorbid cardiovascular disease is associated with a greater severity and increased mortality. Many patients positive for COVID-19 demonstrate increased concentrations of cardiac troponin, creating confusion in clinical interpretation. While myocardial infarction is associated with acute infectious respiratory disease, the majority of COVID-19 patients demonstrate stable cTn rather than the dynamically changing values indicative of an acute coronary syndrome. Although full understanding of the mechanism of cTn release in COVID-19 is currently lacking, this mini-review assesses the limited published literature with a view to offering insight to pathophysiological mechanisms and reported treatment regimens.</div>
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<Abstract><AbstractText>The novel coronavirus SARS-CoV-2 causes the disease COVID-19, a severe acute respiratory syndrome. COVID-19 is now a global pandemic and public health emergency due to rapid human-to-human transmission. The impact is far-reaching, with enforced social distancing and isolation, detrimental effects on individual physical activity and mental wellbeing, education in the young and economic impact to business. Whilst most COVID-19 patients demonstrate mild-to-moderate symptoms, those with severe disease progression are at a higher risk of mortality. As more is learnt about this novel disease, it is becoming evident that comorbid cardiovascular disease is associated with a greater severity and increased mortality. Many patients positive for COVID-19 demonstrate increased concentrations of cardiac troponin, creating confusion in clinical interpretation. While myocardial infarction is associated with acute infectious respiratory disease, the majority of COVID-19 patients demonstrate stable cTn rather than the dynamically changing values indicative of an acute coronary syndrome. Although full understanding of the mechanism of cTn release in COVID-19 is currently lacking, this mini-review assesses the limited published literature with a view to offering insight to pathophysiological mechanisms and reported treatment regimens.</AbstractText>
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<Keyword MajorTopicYN="Y">Troponin</Keyword>
<Keyword MajorTopicYN="Y">analytes</Keyword>
<Keyword MajorTopicYN="Y">cardiac troponin I</Keyword>
<Keyword MajorTopicYN="Y">cardiac troponin T</Keyword>
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