A current review of COVID-19 for the cardiovascular specialist.
Identifieur interne : 001497 ( Main/Corpus ); précédent : 001496; suivant : 001498A current review of COVID-19 for the cardiovascular specialist.
Auteurs : Joshua P. Lang ; Xiaowen Wang ; Filipe A. Moura ; Hasan K. Siddiqi ; David A. Morrow ; Erin A. BohulaSource :
- American heart journal [ 1097-6744 ] ; 2020.
English descriptors
- KwdEn :
- Adenosine Monophosphate (analogs & derivatives), Adenosine Monophosphate (therapeutic use), Alanine (analogs & derivatives), Alanine (therapeutic use), Antimalarials (therapeutic use), Antiviral Agents (therapeutic use), Betacoronavirus (immunology), Betacoronavirus (pathogenicity), Biomarkers (blood), COVID-19 (MeSH), Cardiovascular Diseases (complications), Chloroquine (therapeutic use), Coronavirus Infections (complications), Coronavirus Infections (drug therapy), Humans (MeSH), Hydroxychloroquine (therapeutic use), Hypoxia (complications), Pandemics (MeSH), Plasma (immunology), Pneumonia, Viral (complications), Pneumonia, Viral (drug therapy), Receptor, Angiotensin, Type 2 (metabolism), Risk Factors (MeSH), SARS-CoV-2 (MeSH), Takotsubo Cardiomyopathy (etiology), Virus Internalization (MeSH).
- MESH :
- chemical , analogs & derivatives : Adenosine Monophosphate, Alanine.
- chemical , blood : Biomarkers.
- chemical , metabolism : Receptor, Angiotensin, Type 2.
- chemical , therapeutic use : Adenosine Monophosphate, Alanine, Antimalarials, Antiviral Agents, Chloroquine, Hydroxychloroquine.
- complications : Cardiovascular Diseases, Coronavirus Infections, Hypoxia, Pneumonia, Viral.
- drug therapy : Coronavirus Infections, Pneumonia, Viral.
- etiology : Takotsubo Cardiomyopathy.
- immunology : Betacoronavirus, Plasma.
- pathogenicity : Betacoronavirus.
- COVID-19, Humans, Pandemics, Risk Factors, SARS-CoV-2, Virus Internalization.
Abstract
Although coronavirus disease 2019 (COVID-19) predominantly disrupts the respiratory system, there is accumulating experience that the disease, particularly in its more severe manifestations, also affects the cardiovascular system. Cardiovascular risk factors and chronic cardiovascular conditions are prevalent among patients affected by COVID-19 and associated with adverse outcomes. However, whether pre-existing cardiovascular disease is an independent determinant of higher mortality risk with COVID-19 remains uncertain. Acute cardiac injury, manifest by increased blood levels of cardiac troponin, electrocardiographic abnormalities, or myocardial dysfunction, occurs in up to ~60% of hospitalized patients with severe COVID-19. Potential contributors to acute cardiac injury in the setting of COVID-19 include (1) acute changes in myocardial demand and supply due to tachycardia, hypotension, and hypoxemia resulting in type 2 myocardial infarction; (2) acute coronary syndrome due to acute atherothrombosis in a virally induced thrombotic and inflammatory milieu; (3) microvascular dysfunction due to diffuse microthrombi or vascular injury; (4) stress-related cardiomyopathy (Takotsubo syndrome); (5) nonischemic myocardial injury due to a hyperinflammatory cytokine storm; or (6) direct viral cardiomyocyte toxicity and myocarditis. Diffuse thrombosis is emerging as an important contributor to adverse outcomes in patients with COVID-19. Practitioners should be vigilant for cardiovascular complications of COVID-19. Monitoring may include serial cardiac troponin and natriuretic peptides, along with fibrinogen, D-dimer, and inflammatory biomarkers. Management decisions should rely on the clinical assessment for the probability of ongoing myocardial ischemia, as well as alternative nonischemic causes of injury, integrating the level of suspicion for COVID-19.
DOI: 10.1016/j.ahj.2020.04.025
PubMed: 32497913
PubMed Central: PMC7252118
Links to Exploration step
pubmed:32497913Le document en format XML
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Moura</name><affiliation><nlm:affiliation>Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA.</nlm:affiliation></affiliation></author><author><name sortKey="Siddiqi, Hasan K" sort="Siddiqi, Hasan K" uniqKey="Siddiqi H" first="Hasan K" last="Siddiqi">Hasan K. Siddiqi</name><affiliation><nlm:affiliation>Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA.</nlm:affiliation></affiliation></author><author><name sortKey="Morrow, David A" sort="Morrow, David A" uniqKey="Morrow D" first="David A" last="Morrow">David A. 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Lang</name><affiliation><nlm:affiliation>Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA.</nlm:affiliation></affiliation></author><author><name sortKey="Wang, Xiaowen" sort="Wang, Xiaowen" uniqKey="Wang X" first="Xiaowen" last="Wang">Xiaowen Wang</name><affiliation><nlm:affiliation>Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA.</nlm:affiliation></affiliation></author><author><name sortKey="Moura, Filipe A" sort="Moura, Filipe A" uniqKey="Moura F" first="Filipe A" last="Moura">Filipe A. Moura</name><affiliation><nlm:affiliation>Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA.</nlm:affiliation></affiliation></author><author><name sortKey="Siddiqi, Hasan K" sort="Siddiqi, Hasan K" uniqKey="Siddiqi H" first="Hasan K" last="Siddiqi">Hasan K. Siddiqi</name><affiliation><nlm:affiliation>Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA.</nlm:affiliation></affiliation></author><author><name sortKey="Morrow, David A" sort="Morrow, David A" uniqKey="Morrow D" first="David A" last="Morrow">David A. Morrow</name><affiliation><nlm:affiliation>Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA; Critical Care Cardiology Section, Brigham and Women's Hospital, Harvard Medical School, Boston, MA.</nlm:affiliation></affiliation></author><author><name sortKey="Bohula, Erin A" sort="Bohula, Erin A" uniqKey="Bohula E" first="Erin A" last="Bohula">Erin A. Bohula</name><affiliation><nlm:affiliation>Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA; Critical Care Cardiology Section, Brigham and Women's Hospital, Harvard Medical School, Boston, MA. Electronic address: ebohula@bwh.harvard.edu.</nlm:affiliation></affiliation></author></analytic><series><title level="j">American heart journal</title><idno type="eISSN">1097-6744</idno><imprint><date when="2020" type="published">2020</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adenosine Monophosphate (analogs & derivatives)</term><term>Adenosine Monophosphate (therapeutic use)</term><term>Alanine (analogs & derivatives)</term><term>Alanine (therapeutic use)</term><term>Antimalarials (therapeutic use)</term><term>Antiviral Agents (therapeutic use)</term><term>Betacoronavirus (immunology)</term><term>Betacoronavirus (pathogenicity)</term><term>Biomarkers (blood)</term><term>COVID-19 (MeSH)</term><term>Cardiovascular Diseases (complications)</term><term>Chloroquine (therapeutic use)</term><term>Coronavirus Infections (complications)</term><term>Coronavirus Infections (drug therapy)</term><term>Humans (MeSH)</term><term>Hydroxychloroquine (therapeutic use)</term><term>Hypoxia (complications)</term><term>Pandemics (MeSH)</term><term>Plasma (immunology)</term><term>Pneumonia, Viral (complications)</term><term>Pneumonia, Viral (drug therapy)</term><term>Receptor, Angiotensin, Type 2 (metabolism)</term><term>Risk Factors (MeSH)</term><term>SARS-CoV-2 (MeSH)</term><term>Takotsubo Cardiomyopathy (etiology)</term><term>Virus Internalization (MeSH)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analogs & derivatives" xml:lang="en"><term>Adenosine Monophosphate</term><term>Alanine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="blood" xml:lang="en"><term>Biomarkers</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Receptor, Angiotensin, Type 2</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Adenosine Monophosphate</term><term>Alanine</term><term>Antimalarials</term><term>Antiviral Agents</term><term>Chloroquine</term><term>Hydroxychloroquine</term></keywords><keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Cardiovascular Diseases</term><term>Coronavirus Infections</term><term>Hypoxia</term><term>Pneumonia, Viral</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Coronavirus Infections</term><term>Pneumonia, Viral</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Takotsubo Cardiomyopathy</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Betacoronavirus</term><term>Plasma</term></keywords><keywords scheme="MESH" qualifier="pathogenicity" xml:lang="en"><term>Betacoronavirus</term></keywords><keywords scheme="MESH" xml:lang="en"><term>COVID-19</term><term>Humans</term><term>Pandemics</term><term>Risk Factors</term><term>SARS-CoV-2</term><term>Virus Internalization</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Although coronavirus disease 2019 (COVID-19) predominantly disrupts the respiratory system, there is accumulating experience that the disease, particularly in its more severe manifestations, also affects the cardiovascular system. Cardiovascular risk factors and chronic cardiovascular conditions are prevalent among patients affected by COVID-19 and associated with adverse outcomes. However, whether pre-existing cardiovascular disease is an independent determinant of higher mortality risk with COVID-19 remains uncertain. Acute cardiac injury, manifest by increased blood levels of cardiac troponin, electrocardiographic abnormalities, or myocardial dysfunction, occurs in up to ~60% of hospitalized patients with severe COVID-19. Potential contributors to acute cardiac injury in the setting of COVID-19 include (1) acute changes in myocardial demand and supply due to tachycardia, hypotension, and hypoxemia resulting in type 2 myocardial infarction; (2) acute coronary syndrome due to acute atherothrombosis in a virally induced thrombotic and inflammatory milieu; (3) microvascular dysfunction due to diffuse microthrombi or vascular injury; (4) stress-related cardiomyopathy (Takotsubo syndrome); (5) nonischemic myocardial injury due to a hyperinflammatory cytokine storm; or (6) direct viral cardiomyocyte toxicity and myocarditis. Diffuse thrombosis is emerging as an important contributor to adverse outcomes in patients with COVID-19. Practitioners should be vigilant for cardiovascular complications of COVID-19. Monitoring may include serial cardiac troponin and natriuretic peptides, along with fibrinogen, D-dimer, and inflammatory biomarkers. Management decisions should rely on the clinical assessment for the probability of ongoing myocardial ischemia, as well as alternative nonischemic causes of injury, integrating the level of suspicion for COVID-19.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">32497913</PMID><DateCompleted><Year>2020</Year><Month>08</Month><Day>26</Day></DateCompleted><DateRevised><Year>2021</Year><Month>01</Month><Day>10</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1097-6744</ISSN><JournalIssue CitedMedium="Internet"><Volume>226</Volume><PubDate><Year>2020</Year><Month>08</Month></PubDate></JournalIssue><Title>American heart journal</Title><ISOAbbreviation>Am Heart J</ISOAbbreviation></Journal><ArticleTitle>A current review of COVID-19 for the cardiovascular specialist.</ArticleTitle><Pagination><MedlinePgn>29-44</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">S0002-8703(20)30133-2</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.ahj.2020.04.025</ELocationID><Abstract><AbstractText>Although coronavirus disease 2019 (COVID-19) predominantly disrupts the respiratory system, there is accumulating experience that the disease, particularly in its more severe manifestations, also affects the cardiovascular system. Cardiovascular risk factors and chronic cardiovascular conditions are prevalent among patients affected by COVID-19 and associated with adverse outcomes. However, whether pre-existing cardiovascular disease is an independent determinant of higher mortality risk with COVID-19 remains uncertain. Acute cardiac injury, manifest by increased blood levels of cardiac troponin, electrocardiographic abnormalities, or myocardial dysfunction, occurs in up to ~60% of hospitalized patients with severe COVID-19. Potential contributors to acute cardiac injury in the setting of COVID-19 include (1) acute changes in myocardial demand and supply due to tachycardia, hypotension, and hypoxemia resulting in type 2 myocardial infarction; (2) acute coronary syndrome due to acute atherothrombosis in a virally induced thrombotic and inflammatory milieu; (3) microvascular dysfunction due to diffuse microthrombi or vascular injury; (4) stress-related cardiomyopathy (Takotsubo syndrome); (5) nonischemic myocardial injury due to a hyperinflammatory cytokine storm; or (6) direct viral cardiomyocyte toxicity and myocarditis. Diffuse thrombosis is emerging as an important contributor to adverse outcomes in patients with COVID-19. Practitioners should be vigilant for cardiovascular complications of COVID-19. Monitoring may include serial cardiac troponin and natriuretic peptides, along with fibrinogen, D-dimer, and inflammatory biomarkers. Management decisions should rely on the clinical assessment for the probability of ongoing myocardial ischemia, as well as alternative nonischemic causes of injury, integrating the level of suspicion for COVID-19.</AbstractText><CopyrightInformation>Copyright © 2020 Elsevier Inc. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Lang</LastName><ForeName>Joshua P</ForeName><Initials>JP</Initials><AffiliationInfo><Affiliation>Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Xiaowen</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Moura</LastName><ForeName>Filipe A</ForeName><Initials>FA</Initials><AffiliationInfo><Affiliation>Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Siddiqi</LastName><ForeName>Hasan K</ForeName><Initials>HK</Initials><AffiliationInfo><Affiliation>Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Morrow</LastName><ForeName>David A</ForeName><Initials>DA</Initials><AffiliationInfo><Affiliation>Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA; Critical Care Cardiology Section, Brigham and Women's Hospital, Harvard Medical School, Boston, MA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bohula</LastName><ForeName>Erin A</ForeName><Initials>EA</Initials><AffiliationInfo><Affiliation>Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA; Critical Care Cardiology Section, Brigham and Women's Hospital, Harvard Medical School, Boston, MA. Electronic address: ebohula@bwh.harvard.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>05</Month><Day>03</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Am Heart J</MedlineTA><NlmUniqueID>0370465</NlmUniqueID><ISSNLinking>0002-8703</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000962">Antimalarials</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000998">Antiviral Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D015415">Biomarkers</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance 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MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006886" MajorTopicYN="N">Hydroxychloroquine</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000860" MajorTopicYN="N">Hypoxia</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D058873" MajorTopicYN="N">Pandemics</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010949" MajorTopicYN="N">Plasma</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011024" MajorTopicYN="N">Pneumonia, Viral</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="Y">complications</QualifierName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D044139" MajorTopicYN="N">Receptor, 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