COVID-19 and cardiovascular disease: from basic mechanisms to clinical perspectives.
Identifieur interne : 000752 ( Main/Exploration ); précédent : 000751; suivant : 000753COVID-19 and cardiovascular disease: from basic mechanisms to clinical perspectives.
Auteurs : Masataka Nishiga [États-Unis] ; Dao Wen Wang [République populaire de Chine] ; Yaling Han [République populaire de Chine] ; David B. Lewis [États-Unis] ; Joseph C. Wu [États-Unis]Source :
- Nature reviews. Cardiology [ 1759-5010 ] ; 2020.
Descripteurs français
- KwdFr :
- Betacoronavirus (physiologie), Comorbidité (MeSH), Facteurs de risque (MeSH), Humains (MeSH), Infections à coronavirus (métabolisme), Infections à coronavirus (physiopathologie), Infections à coronavirus (épidémiologie), Maladies cardiovasculaires (métabolisme), Maladies cardiovasculaires (physiopathologie), Maladies cardiovasculaires (épidémiologie), Pandémies (MeSH), Pneumopathie virale (métabolisme), Pneumopathie virale (physiopathologie), Pneumopathie virale (épidémiologie), Prise en charge de la maladie (MeSH).
- MESH :
- métabolisme : Infections à coronavirus, Maladies cardiovasculaires, Pneumopathie virale.
- physiologie : Betacoronavirus.
- physiopathologie : Infections à coronavirus, Maladies cardiovasculaires, Pneumopathie virale.
- épidémiologie : Infections à coronavirus, Maladies cardiovasculaires, Pneumopathie virale.
- Comorbidité, Facteurs de risque, Humains, Pandémies, Prise en charge de la maladie.
English descriptors
- KwdEn :
- Betacoronavirus (physiology), COVID-19 (MeSH), Cardiovascular Diseases (epidemiology), Cardiovascular Diseases (metabolism), Cardiovascular Diseases (physiopathology), Comorbidity (MeSH), Coronavirus Infections (epidemiology), Coronavirus Infections (metabolism), Coronavirus Infections (physiopathology), Disease Management (MeSH), Humans (MeSH), Pandemics (MeSH), Pneumonia, Viral (epidemiology), Pneumonia, Viral (metabolism), Pneumonia, Viral (physiopathology), Risk Factors (MeSH), SARS-CoV-2 (MeSH).
- MESH :
- epidemiology : Cardiovascular Diseases, Coronavirus Infections, Pneumonia, Viral.
- metabolism : Cardiovascular Diseases, Coronavirus Infections, Pneumonia, Viral.
- physiology : Betacoronavirus.
- physiopathology : Cardiovascular Diseases, Coronavirus Infections, Pneumonia, Viral.
- COVID-19, Comorbidity, Disease Management, Humans, Pandemics, Risk Factors, SARS-CoV-2.
Abstract
Coronavirus disease 2019 (COVID-19), caused by a strain of coronavirus known as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has become a global pandemic that has affected the lives of billions of individuals. Extensive studies have revealed that SARS-CoV-2 shares many biological features with SARS-CoV, the zoonotic virus that caused the 2002 outbreak of severe acute respiratory syndrome, including the system of cell entry, which is triggered by binding of the viral spike protein to angiotensin-converting enzyme 2. Clinical studies have also reported an association between COVID-19 and cardiovascular disease. Pre-existing cardiovascular disease seems to be linked with worse outcomes and increased risk of death in patients with COVID-19, whereas COVID-19 itself can also induce myocardial injury, arrhythmia, acute coronary syndrome and venous thromboembolism. Potential drug-disease interactions affecting patients with COVID-19 and comorbid cardiovascular diseases are also becoming a serious concern. In this Review, we summarize the current understanding of COVID-19 from basic mechanisms to clinical perspectives, focusing on the interaction between COVID-19 and the cardiovascular system. By combining our knowledge of the biological features of the virus with clinical findings, we can improve our understanding of the potential mechanisms underlying COVID-19, paving the way towards the development of preventative and therapeutic solutions.
DOI: 10.1038/s41569-020-0413-9
PubMed: 32690910
PubMed Central: PMC7370876
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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Cardiology</title><idno type="eISSN">1759-5010</idno><imprint><date when="2020" type="published">2020</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Betacoronavirus (physiology)</term><term>COVID-19 (MeSH)</term><term>Cardiovascular Diseases (epidemiology)</term><term>Cardiovascular Diseases (metabolism)</term><term>Cardiovascular Diseases (physiopathology)</term><term>Comorbidity (MeSH)</term><term>Coronavirus Infections (epidemiology)</term><term>Coronavirus Infections (metabolism)</term><term>Coronavirus Infections (physiopathology)</term><term>Disease Management (MeSH)</term><term>Humans (MeSH)</term><term>Pandemics (MeSH)</term><term>Pneumonia, Viral (epidemiology)</term><term>Pneumonia, Viral (metabolism)</term><term>Pneumonia, Viral (physiopathology)</term><term>Risk Factors (MeSH)</term><term>SARS-CoV-2 (MeSH)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Betacoronavirus (physiologie)</term><term>Comorbidité (MeSH)</term><term>Facteurs de risque (MeSH)</term><term>Humains (MeSH)</term><term>Infections à coronavirus (métabolisme)</term><term>Infections à coronavirus (physiopathologie)</term><term>Infections à coronavirus (épidémiologie)</term><term>Maladies cardiovasculaires (métabolisme)</term><term>Maladies cardiovasculaires (physiopathologie)</term><term>Maladies cardiovasculaires (épidémiologie)</term><term>Pandémies (MeSH)</term><term>Pneumopathie virale (métabolisme)</term><term>Pneumopathie virale (physiopathologie)</term><term>Pneumopathie virale (épidémiologie)</term><term>Prise en charge de la maladie (MeSH)</term></keywords><keywords scheme="MESH" qualifier="epidemiology" xml:lang="en"><term>Cardiovascular Diseases</term><term>Coronavirus Infections</term><term>Pneumonia, Viral</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Cardiovascular Diseases</term><term>Coronavirus Infections</term><term>Pneumonia, Viral</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Infections à coronavirus</term><term>Maladies cardiovasculaires</term><term>Pneumopathie virale</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Betacoronavirus</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Betacoronavirus</term></keywords><keywords scheme="MESH" qualifier="physiopathologie" xml:lang="fr"><term>Infections à coronavirus</term><term>Maladies cardiovasculaires</term><term>Pneumopathie virale</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Cardiovascular Diseases</term><term>Coronavirus Infections</term><term>Pneumonia, Viral</term></keywords><keywords scheme="MESH" qualifier="épidémiologie" xml:lang="fr"><term>Infections à coronavirus</term><term>Maladies cardiovasculaires</term><term>Pneumopathie virale</term></keywords><keywords scheme="MESH" xml:lang="en"><term>COVID-19</term><term>Comorbidity</term><term>Disease Management</term><term>Humans</term><term>Pandemics</term><term>Risk Factors</term><term>SARS-CoV-2</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Comorbidité</term><term>Facteurs de risque</term><term>Humains</term><term>Pandémies</term><term>Prise en charge de la maladie</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Coronavirus disease 2019 (COVID-19), caused by a strain of coronavirus known as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has become a global pandemic that has affected the lives of billions of individuals. Extensive studies have revealed that SARS-CoV-2 shares many biological features with SARS-CoV, the zoonotic virus that caused the 2002 outbreak of severe acute respiratory syndrome, including the system of cell entry, which is triggered by binding of the viral spike protein to angiotensin-converting enzyme 2. Clinical studies have also reported an association between COVID-19 and cardiovascular disease. Pre-existing cardiovascular disease seems to be linked with worse outcomes and increased risk of death in patients with COVID-19, whereas COVID-19 itself can also induce myocardial injury, arrhythmia, acute coronary syndrome and venous thromboembolism. Potential drug-disease interactions affecting patients with COVID-19 and comorbid cardiovascular diseases are also becoming a serious concern. In this Review, we summarize the current understanding of COVID-19 from basic mechanisms to clinical perspectives, focusing on the interaction between COVID-19 and the cardiovascular system. By combining our knowledge of the biological features of the virus with clinical findings, we can improve our understanding of the potential mechanisms underlying COVID-19, paving the way towards the development of preventative and therapeutic solutions.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">32690910</PMID><DateCompleted><Year>2020</Year><Month>08</Month><Day>24</Day></DateCompleted><DateRevised><Year>2020</Year><Month>12</Month><Day>18</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1759-5010</ISSN><JournalIssue CitedMedium="Internet"><Volume>17</Volume><Issue>9</Issue><PubDate><Year>2020</Year><Month>09</Month></PubDate></JournalIssue><Title>Nature reviews. Cardiology</Title><ISOAbbreviation>Nat Rev Cardiol</ISOAbbreviation></Journal><ArticleTitle>COVID-19 and cardiovascular disease: from basic mechanisms to clinical perspectives.</ArticleTitle><Pagination><MedlinePgn>543-558</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1038/s41569-020-0413-9</ELocationID><Abstract><AbstractText>Coronavirus disease 2019 (COVID-19), caused by a strain of coronavirus known as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has become a global pandemic that has affected the lives of billions of individuals. Extensive studies have revealed that SARS-CoV-2 shares many biological features with SARS-CoV, the zoonotic virus that caused the 2002 outbreak of severe acute respiratory syndrome, including the system of cell entry, which is triggered by binding of the viral spike protein to angiotensin-converting enzyme 2. Clinical studies have also reported an association between COVID-19 and cardiovascular disease. Pre-existing cardiovascular disease seems to be linked with worse outcomes and increased risk of death in patients with COVID-19, whereas COVID-19 itself can also induce myocardial injury, arrhythmia, acute coronary syndrome and venous thromboembolism. Potential drug-disease interactions affecting patients with COVID-19 and comorbid cardiovascular diseases are also becoming a serious concern. In this Review, we summarize the current understanding of COVID-19 from basic mechanisms to clinical perspectives, focusing on the interaction between COVID-19 and the cardiovascular system. By combining our knowledge of the biological features of the virus with clinical findings, we can improve our understanding of the potential mechanisms underlying COVID-19, paving the way towards the development of preventative and therapeutic solutions.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Nishiga</LastName><ForeName>Masataka</ForeName><Initials>M</Initials><Identifier Source="ORCID">http://orcid.org/0000-0001-5676-7671</Identifier><AffiliationInfo><Affiliation>Stanford Cardiovascular Institute, Stanford, CA, USA. mnishiga@stanford.edu.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Medicine, Division of Cardiovascular Medicine, Stanford University School of Medicine, Stanford, CA, USA. mnishiga@stanford.edu.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Dao Wen</ForeName><Initials>DW</Initials><AffiliationInfo><Affiliation>Division of Cardiology, Department of Internal Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science & Technology, Wuhan, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Han</LastName><ForeName>Yaling</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Cardiovascular Research Institute, Department of Cardiology, General Hospital of Northern Theater Command, Shenyang, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lewis</LastName><ForeName>David B</ForeName><Initials>DB</Initials><AffiliationInfo><Affiliation>Division of Allergy, Immunology, and Rheumatology, Department of Pediatrics, Stanford University School of Medicine, Stanford, CA, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wu</LastName><ForeName>Joseph C</ForeName><Initials>JC</Initials><Identifier Source="ORCID">http://orcid.org/0000-0002-6068-8041</Identifier><AffiliationInfo><Affiliation>Stanford Cardiovascular Institute, Stanford, CA, USA. joewu@stanford.edu.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Medicine, Division of Cardiovascular Medicine, Stanford University School of Medicine, Stanford, CA, USA. joewu@stanford.edu.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Radiology, Stanford University School of Medicine, Stanford, CA, USA. joewu@stanford.edu.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2020</Year><Month>07</Month><Day>20</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Nat Rev Cardiol</MedlineTA><NlmUniqueID>101500075</NlmUniqueID><ISSNLinking>1759-5002</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000073640" MajorTopicYN="N">Betacoronavirus</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000086382" MajorTopicYN="N">COVID-19</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002318" MajorTopicYN="Y">Cardiovascular Diseases</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015897" MajorTopicYN="N">Comorbidity</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018352" MajorTopicYN="Y">Coronavirus Infections</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D019468" MajorTopicYN="N">Disease Management</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D058873" MajorTopicYN="Y">Pandemics</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011024" MajorTopicYN="Y">Pneumonia, Viral</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012307" MajorTopicYN="N">Risk Factors</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000086402" MajorTopicYN="N">SARS-CoV-2</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate 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Lewis</name><name sortKey="Nishiga, Masataka" sort="Nishiga, Masataka" uniqKey="Nishiga M" first="Masataka" last="Nishiga">Masataka Nishiga</name><name sortKey="Wu, Joseph C" sort="Wu, Joseph C" uniqKey="Wu J" first="Joseph C" last="Wu">Joseph C. Wu</name><name sortKey="Wu, Joseph C" sort="Wu, Joseph C" uniqKey="Wu J" first="Joseph C" last="Wu">Joseph C. Wu</name><name sortKey="Wu, Joseph C" sort="Wu, Joseph C" uniqKey="Wu J" first="Joseph C" last="Wu">Joseph C. Wu</name></country><country name="République populaire de Chine"><region name="Hubei"><name sortKey="Wang, Dao Wen" sort="Wang, Dao Wen" uniqKey="Wang D" first="Dao Wen" last="Wang">Dao Wen Wang</name></region><name sortKey="Han, Yaling" sort="Han, Yaling" uniqKey="Han Y" first="Yaling" last="Han">Yaling Han</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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