Atteintes myocardiques au cours de la maladie à coronavirus 19 (Covid-19) : principaux mécanismes physiopathologiques et utilité clinique des biomarqueurs cardiaques (notice n° 420285)

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Personal name Kamel, Said
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Title Atteintes myocardiques au cours de la maladie à coronavirus 19 (Covid-19) : principaux mécanismes physiopathologiques et utilité clinique des biomarqueurs cardiaques
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Date of publication, distribution, etc. 2021.<br/>
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General note 30
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Summary, etc. RésuméLa Covid-19 est fréquemment responsable d’une atteinte myocardique aggravant la maladie. Les mécanismes physiopathologiques complexes impliquent des effets directs du virus après pénétration dans les myocytes et des effets indirects secondaires aux manifestations cliniques de l’infection virale. Les cardiomyocytes expriment fortement le récepteur de l’enzyme de conversion de l’angiotensine II favorisant la pénétration du virus et la survenue de myocardite, d’altérations morphologiques du myocarde ventriculaire et plus rarement d’infarctus du myocarde. Les manifestations cardiaques peuvent également être secondaires au syndrome inflammatoire généralisé et à l’état d’hypercoagulabilité dû à l’infection virale pulmonaire. L’existence d’un axe cardio-intestinal, avec une altération du métabolisme entérocytaire du tryptophane, provoquant une colite puis une inflammation généralisée, a également été évoquée pour expliquer les atteintes cardiaques. L’atteinte myocardique s’accompagne d’une augmentation des concentrations sanguines de troponine et des peptides natriurétiques dont le dosage s’est avéré très utile sur le plan diagnostique, pronostique et pour stratifier le risque cardiovasculaire du patient infecté. Les données de la littérature démontrent qu’environ 20 % des patients à l’admission ont des concentrations élevées de troponine et/ou de BNP et qu’une concentration de troponine à l’admission supérieure au 99e percentile constitue un marqueur statistiquement significatif de risque de décès. En conclusion, après un an de cette pandémie mondiale, il est aujourd’hui admis que l’atteinte myocardique de la Covid-19 est fréquente et contribue à la gravité de la maladie. Les lésions cardiaques qu’elles soient directes ou indirectes, s’accompagnent d’une élévation des biomarqueurs cardiaques dont les dosages sanguins s’avèrent indispensables dans la prise en charge.
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Summary, etc. Covid-19 is responsible for myocardial injury in many infected patients, which is associated with severe disease and critical illness. The mechanisms by which SARS-CoV-2 may cause myocardial damage involve direct effect of the virus in cardiac cells and indirect effect due to the clinical consequences of Covid-19. Cardiomyocytes are well known to express Angiotensin-Converting Enzyme-2 receptors (ACE-2) to facilitate the virus cell entry, which could explain the occurrence of myocarditis, functional alterations in the myocardium, and more rarely, myocardial infarction. Myocardial injury may also be secondary to systemic inflammation or coagulopathy due to complicated Covid-19. The existence of a cardio-intestinal axis with alteration of tryptophan metabolism in the small bowel leading first to colitis and then to systemic inflammation has also been evoked to explain the myocardial injury. Morphological and metabolic disturbances of the heart during the Covid-19 are associated with elevated concentrations of cardiac blood biomarkers, mainly troponins and natriuretic peptides. The determination of these biomarkers has proven to be very useful for diagnosis, prognosis, and risk stratification. Indeed, recent data demonstrated that about 20% of infected patients admitted to the hospital have elevated troponin or BNP levels, and Covid-19 patients with elevated troponin concentrations beyond the diagnostic threshold (99th percentile) were associated with a higher risk of in-hospital mortality. In conclusion, after more than a year of a unique global pandemic, it is now clearly established that myocardial injury during Covid-19 is frequent and strongly contributes to the severity of the disease. Cardiac alterations secondary to direct infection of cardiac cells by SARS-CoV-2 or to the clinical consequences of Covid-19 are associated with elevated levels of cardiac biomarkers in blood, whose measurement is crucial in clinical decision making.
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Topical term or geographic name as entry element troponine
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Topical term or geographic name as entry element peptides natriurétiques
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Topical term or geographic name as entry element myocarde
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Topical term or geographic name as entry element SARS-CoV-2
690 ## - LOCAL SUBJECT ADDED ENTRY--TOPICAL TERM (OCLC, RLIN)
Topical term or geographic name as entry element Covid-19
690 ## - LOCAL SUBJECT ADDED ENTRY--TOPICAL TERM (OCLC, RLIN)
Topical term or geographic name as entry element myocardite
690 ## - LOCAL SUBJECT ADDED ENTRY--TOPICAL TERM (OCLC, RLIN)
Topical term or geographic name as entry element natriuretic peptides
690 ## - LOCAL SUBJECT ADDED ENTRY--TOPICAL TERM (OCLC, RLIN)
Topical term or geographic name as entry element troponin
690 ## - LOCAL SUBJECT ADDED ENTRY--TOPICAL TERM (OCLC, RLIN)
Topical term or geographic name as entry element SARS-CoV-2
690 ## - LOCAL SUBJECT ADDED ENTRY--TOPICAL TERM (OCLC, RLIN)
Topical term or geographic name as entry element Covid-19
690 ## - LOCAL SUBJECT ADDED ENTRY--TOPICAL TERM (OCLC, RLIN)
Topical term or geographic name as entry element myocarditis
690 ## - LOCAL SUBJECT ADDED ENTRY--TOPICAL TERM (OCLC, RLIN)
Topical term or geographic name as entry element myocardium
700 10 - ADDED ENTRY--PERSONAL NAME
Personal name Raynor, Alexandre
Relator term author
700 10 - ADDED ENTRY--PERSONAL NAME
Personal name Zozor, Samuel
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700 10 - ADDED ENTRY--PERSONAL NAME
Personal name Lacape, Geneviève
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700 10 - ADDED ENTRY--PERSONAL NAME
Personal name Brunel, Valery
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700 10 - ADDED ENTRY--PERSONAL NAME
Personal name Nivet-Antoine, Valérie
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Personal name Collin-Chavagnac, Delphine
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Personal name Peoc’h, Katell
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Personal name Cohen, Ariel
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Personal name Lassoued, Amin Ben
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700 10 - ADDED ENTRY--PERSONAL NAME
Personal name Chevrier, Marc
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700 10 - ADDED ENTRY--PERSONAL NAME
Personal name Alemann, Mathieu
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700 10 - ADDED ENTRY--PERSONAL NAME
Personal name Lessinger, Jean-Marc
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700 10 - ADDED ENTRY--PERSONAL NAME
Personal name Bérard, Annie M.
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Personal name Sapin, Vincent
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700 10 - ADDED ENTRY--PERSONAL NAME
Personal name Beauvieux, Marie-Christine
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700 10 - ADDED ENTRY--PERSONAL NAME
Personal name Levy, Pacifique
Relator term author
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Note Annales de Biologie Clinique | 79 | 3 | 2021-05-01 | p. 219-231 | 0003-3898
856 41 - ELECTRONIC LOCATION AND ACCESS
Uniform Resource Identifier <a href="https://shs.cairn.info/revue-annales-de-biologie-clinique-2021-3-page-219?lang=fr&redirect-ssocas=7080">https://shs.cairn.info/revue-annales-de-biologie-clinique-2021-3-page-219?lang=fr&redirect-ssocas=7080</a>

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