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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Cardiovascular complications in COVID-19</title><author><name sortKey="Long, Brit" sort="Long, Brit" uniqKey="Long B" first="Brit" last="Long">Brit Long</name><affiliation><nlm:aff id="af0005">Brooke Army Medical Center, Department of Emergency Medicine, 3841 Roger Brooke Dr, Fort Sam Houston, TX 78234, United States</nlm:aff></affiliation></author><author><name sortKey="Brady, William J" sort="Brady, William J" uniqKey="Brady W" first="William J." last="Brady">William J. Brady</name><affiliation><nlm:aff id="af0010">Department of Emergency Medicine, University of Virginia School of Medicine, Charlottesville, VA 22903, United States</nlm:aff></affiliation></author><author><name sortKey="Koyfman, Alex" sort="Koyfman, Alex" uniqKey="Koyfman A" first="Alex" last="Koyfman">Alex Koyfman</name><affiliation><nlm:aff id="af0015">The University of Texas Southwestern Medical Center, Department of Emergency Medicine, 5323 Harry Hines Boulevard, Dallas, TX 75390, United States</nlm:aff></affiliation></author><author><name sortKey="Gottlieb, Michael" sort="Gottlieb, Michael" uniqKey="Gottlieb M" first="Michael" last="Gottlieb">Michael Gottlieb</name><affiliation><nlm:aff id="af0020">Department of Emergency Medicine, Rush University Medical Center, Chicago, IL 60612, United States</nlm:aff></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">32317203</idno><idno type="pmc">7165109</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7165109</idno><idno type="RBID">PMC:7165109</idno><idno type="doi">10.1016/j.ajem.2020.04.048</idno><date when="2020">2020</date><idno type="wicri:Area/Pmc/Corpus">000861</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000861</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Cardiovascular complications in COVID-19</title><author><name sortKey="Long, Brit" sort="Long, Brit" uniqKey="Long B" first="Brit" last="Long">Brit Long</name><affiliation><nlm:aff id="af0005">Brooke Army Medical Center, Department of Emergency Medicine, 3841 Roger Brooke Dr, Fort Sam Houston, TX 78234, United States</nlm:aff></affiliation></author><author><name sortKey="Brady, William J" sort="Brady, William J" uniqKey="Brady W" first="William J." last="Brady">William J. Brady</name><affiliation><nlm:aff id="af0010">Department of Emergency Medicine, University of Virginia School of Medicine, Charlottesville, VA 22903, United States</nlm:aff></affiliation></author><author><name sortKey="Koyfman, Alex" sort="Koyfman, Alex" uniqKey="Koyfman A" first="Alex" last="Koyfman">Alex Koyfman</name><affiliation><nlm:aff id="af0015">The University of Texas Southwestern Medical Center, Department of Emergency Medicine, 5323 Harry Hines Boulevard, Dallas, TX 75390, United States</nlm:aff></affiliation></author><author><name sortKey="Gottlieb, Michael" sort="Gottlieb, Michael" uniqKey="Gottlieb M" first="Michael" last="Gottlieb">Michael Gottlieb</name><affiliation><nlm:aff id="af0020">Department of Emergency Medicine, Rush University Medical Center, Chicago, IL 60612, United States</nlm:aff></affiliation></author></analytic><series><title level="j">The American Journal of Emergency Medicine</title><idno type="ISSN">0735-6757</idno><idno type="eISSN">1532-8171</idno><imprint><date when="2020">2020</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><sec><title>Background</title><p>The coronavirus disease of 2019 (COVID-19) is caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). While systemic inflammation and pulmonary complications can result in significant morbidity and mortality, cardiovascular complications may also occur.</p></sec><sec><title>Objective</title><p>This brief report evaluates cardiovascular complications in the setting of COVID-19 infection.</p></sec><sec><title>Discussion</title><p>The current COVID-19 pandemic has resulted in over one million infected worldwide and thousands of death. The virus binds and enters through angiotensin-converting enzyme 2 (ACE2). COVID-19 can result in systemic inflammation, multiorgan dysfunction, and critical illness. The cardiovascular system is also affected, with complications including myocardial injury, myocarditis, acute myocardial infarction, heart failure, dysrhythmias, and venous thromboembolic events. Current therapies for COVID-19 may interact with cardiovascular medications.</p></sec><sec><title>Conclusions</title><p>Emergency clinicians should be aware of these cardiovascular complications when evaluating and managing the patient with COVID-19.</p></sec></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="World Health Organization" uniqKey="World Health Organization">World Health Organization</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Coronavirus Disease Covid" uniqKey="Coronavirus Disease Covid">Coronavirus Disease 2019 (COVID-19)</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="World Health Organization" uniqKey="World Health Organization">World Health Organization</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Driggin, E" uniqKey="Driggin E">E. 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<front><journal-meta><journal-id journal-id-type="nlm-ta">Am J Emerg Med</journal-id><journal-id journal-id-type="iso-abbrev">Am J Emerg Med</journal-id><journal-title-group><journal-title>The American Journal of Emergency Medicine</journal-title></journal-title-group><issn pub-type="ppub">0735-6757</issn><issn pub-type="epub">1532-8171</issn><publisher><publisher-name>W B Saunders</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">32317203</article-id><article-id pub-id-type="pmc">7165109</article-id><article-id pub-id-type="publisher-id">S0735-6757(20)30277-1</article-id><article-id pub-id-type="doi">10.1016/j.ajem.2020.04.048</article-id><article-categories><subj-group subj-group-type="heading"><subject>Article</subject></subj-group></article-categories><title-group><article-title>Cardiovascular complications in COVID-19</article-title></title-group><contrib-group><contrib contrib-type="author" id="au0005"><name><surname>Long</surname><given-names>Brit</given-names></name><degrees>MD</degrees><email>brit.long@yahoo.com</email><xref rid="af0005" ref-type="aff">a</xref><xref rid="cr0005" ref-type="corresp">⁎</xref></contrib><contrib contrib-type="author" id="au0010"><name><surname>Brady</surname><given-names>William J.</given-names></name><degrees>MD</degrees><email>WB4Z@hscmail.mcc.virginia.edu</email><xref rid="af0010" ref-type="aff">b</xref></contrib><contrib contrib-type="author" id="au0015"><name><surname>Koyfman</surname><given-names>Alex</given-names></name><degrees>MD</degrees><xref rid="af0015" ref-type="aff">c</xref></contrib><contrib contrib-type="author" id="au0020"><name><surname>Gottlieb</surname><given-names>Michael</given-names></name><degrees>MD</degrees><xref rid="af0020" ref-type="aff">d</xref></contrib></contrib-group><aff id="af0005"><label>a</label>Brooke Army Medical Center, Department of Emergency Medicine, 3841 Roger Brooke Dr, Fort Sam Houston, TX 78234, United States</aff><aff id="af0010"><label>b</label>Department of Emergency Medicine, University of Virginia School of Medicine, Charlottesville, VA 22903, United States</aff><aff id="af0015"><label>c</label>The University of Texas Southwestern Medical Center, Department of Emergency Medicine, 5323 Harry Hines Boulevard, Dallas, TX 75390, United States</aff><aff id="af0020"><label>d</label>Department of Emergency Medicine, Rush University Medical Center, Chicago, IL 60612, United States</aff><author-notes><corresp id="cr0005"><label>⁎</label>Corresponding author at: 3841 Roger Brooke Dr, Fort Sam Houston, TX 78234, United States. <email>brit.long@yahoo.com</email></corresp></author-notes><pub-date pub-type="pmc-release"><day>18</day><month>4</month><year>2020</year></pub-date><pmc-comment> PMC Release delay is 0 months and 0 days and was based on .</pmc-comment>
<pub-date pub-type="epub"><day>18</day><month>4</month><year>2020</year></pub-date><history><date date-type="received"><day>7</day><month>4</month><year>2020</year></date><date date-type="rev-recd"><day>11</day><month>4</month><year>2020</year></date><date date-type="accepted"><day>14</day><month>4</month><year>2020</year></date></history><permissions><license><license-p>Since January 2020 Elsevier has created a COVID-19 resource centre with free information in English and Mandarin on the novel coronavirus COVID-19. The COVID-19 resource centre is hosted on Elsevier Connect, the company's public news and information website. Elsevier hereby grants permission to make all its COVID-19-related research that is available on the COVID-19 resource centre - including this research content - immediately available in PubMed Central and other publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active.</license-p></license></permissions><abstract id="ab0005"><sec><title>Background</title><p>The coronavirus disease of 2019 (COVID-19) is caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). While systemic inflammation and pulmonary complications can result in significant morbidity and mortality, cardiovascular complications may also occur.</p></sec><sec><title>Objective</title><p>This brief report evaluates cardiovascular complications in the setting of COVID-19 infection.</p></sec><sec><title>Discussion</title><p>The current COVID-19 pandemic has resulted in over one million infected worldwide and thousands of death. The virus binds and enters through angiotensin-converting enzyme 2 (ACE2). COVID-19 can result in systemic inflammation, multiorgan dysfunction, and critical illness. The cardiovascular system is also affected, with complications including myocardial injury, myocarditis, acute myocardial infarction, heart failure, dysrhythmias, and venous thromboembolic events. Current therapies for COVID-19 may interact with cardiovascular medications.</p></sec><sec><title>Conclusions</title><p>Emergency clinicians should be aware of these cardiovascular complications when evaluating and managing the patient with COVID-19.</p></sec></abstract><kwd-group id="ks0005"><title>Keywords</title><kwd>COVID-19</kwd><kwd>Infectious disease</kwd><kwd>Cardiovascular</kwd><kwd>Dysrhythmia</kwd><kwd>Acute myocardial infarction</kwd><kwd>Heart failure</kwd><kwd>Myocarditis</kwd><kwd>Troponin</kwd></kwd-group></article-meta></front><body><sec id="s0005"><label>1</label><title>Introduction</title><p id="p0005">The coronavirus disease of 2019 (COVID-19) caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) first appeared in Wuhan, China [<xref rid="bb0005" ref-type="bibr">[1]</xref>, <xref rid="bb0010" ref-type="bibr">[2]</xref>, <xref rid="bb0015" ref-type="bibr">[3]</xref>]. It was officially declared a pandemic by the World Health Organization in March 2020 [<xref rid="bb0005" ref-type="bibr">1</xref>,<xref rid="bb0015" ref-type="bibr">3</xref>]. As of April 11, 2020, the COVID-19 pandemic has resulted in over 490,000 cases and 18,500 deaths in the United States, with all 50 states affected [<xref rid="bb0010" ref-type="bibr">2</xref>]. Over one million people are now infected worldwide [<xref rid="bb0005" ref-type="bibr">[1]</xref>, <xref rid="bb0010" ref-type="bibr">[2]</xref>, <xref rid="bb0015" ref-type="bibr">[3]</xref>, <xref rid="bb0020" ref-type="bibr">[4]</xref>]. While much of the focus has been on the pulmonary complications, it is important for emergency clinicians to be aware of the cardiovascular complications, which can be a significant contributor to the mortality associated with this disease [<xref rid="bb0020" ref-type="bibr">[4]</xref>, <xref rid="bb0025" ref-type="bibr">[5]</xref>, <xref rid="bb0030" ref-type="bibr">[6]</xref>, <xref rid="bb0035" ref-type="bibr">[7]</xref>, <xref rid="bb0040" ref-type="bibr">[8]</xref>, <xref rid="bb0045" ref-type="bibr">[9]</xref>]. This brief report will provide a focused overview of cardiovascular complications associated with COVID-19, including myocardial injury and myocarditis, acute myocardial infarction (AMI), heart failure, dysrhythmias, and venous thromboembolic events (VTE).</p></sec><sec id="s0010"><label>2</label><title>Methods</title><p id="p0010">Authors searched PubMed and Google Scholar for articles using the keywords “COVID-19”, “SARS-CoV-2”, “heart”, “cardiac”, “cardiovascular”, “myocardial injury”, “myocarditis”, “acute myocardial infarction”, “acute coronary syndrome”, “dysrhythmia”, “arrhythmia”, “heart failure”, “venous thromboembolism”, “coagulable”. Authors included case reports, retrospective studies, prospective studies, systematic reviews and meta-analyses, clinical guidelines, and narrative reviews focusing on COVID-19 and cardiovascular effects and complications. Preprinted articles were also included. The literature search was restricted to studies published in English. Emergency physicians with experience in critical appraisal of the literature reviewed all of the articles and decided which studies to include for the review by consensus, with a focus on emergency medicine-relevant articles. A total of 45 articles were selected for inclusion.</p></sec><sec id="s0015"><label>3</label><title>Discussion</title><sec id="s0020"><label>3.1</label><title>Pathophysiology and clinical features</title><p id="p0015">SARS-CoV-2 is an enveloped, non-segmented, single-stranded, positive-sense RNA virus [<xref rid="bb0010" ref-type="bibr">2</xref>,<xref rid="bb0025" ref-type="bibr">[5]</xref>, <xref rid="bb0030" ref-type="bibr">[6]</xref>, <xref rid="bb0035" ref-type="bibr">[7]</xref>, <xref rid="bb0040" ref-type="bibr">[8]</xref>, <xref rid="bb0045" ref-type="bibr">[9]</xref>]. Angiotensin-converting enzyme 2 (ACE2) is a protein found on the surface of lung alveolar epithelial cells and enterocytes of the small intestine, which has been proposed as the entry site for SARS-CoV-2 [<xref rid="bb0050" ref-type="bibr">10</xref>]. ACE2 breaks down angiotensin II, a pro-inflammatory factor in the lung. Inhibition of ACE2 may be another factor in lung injury, as well as the cause of the systemic inflammation with cytokine release that can result in acute respiratory distress syndrome (ARDS) and multiorgan dysfunction [<xref rid="bb0055" ref-type="bibr">[11]</xref>, <xref rid="bb0060" ref-type="bibr">[12]</xref>, <xref rid="bb0065" ref-type="bibr">[13]</xref>]. Disruption in immune system regulation, increased metabolic demand, and procoagulant activity likely account for some of the increased risk of adverse outcomes in those with COVID-19-related cardiovascular disease (CVD) [<xref rid="bb0040" ref-type="bibr">8</xref>,<xref rid="bb0045" ref-type="bibr">9</xref>,<xref rid="bb0070" ref-type="bibr">14</xref>]. Specifically, systemic inflammation can destabilize vascular plaques, while the viral illness increases cytokine activity, increasing cardiac demand, similar to influenza [<xref rid="bb0075" ref-type="bibr">15</xref>,<xref rid="bb0080" ref-type="bibr">16</xref>]. Recent research, however, has suggested that the virus may also cause direct damage to the heart utilizing ACE2 receptors located within cardiac tissue [<xref rid="bb0085" ref-type="bibr">17</xref>].</p><p id="p0020">The prevalence of CVD in COVID-19 patients is unclear, but preexisting CVD may be associated with a more severe COVID-19 infection [<xref rid="bb0020" ref-type="bibr">[4]</xref>, <xref rid="bb0025" ref-type="bibr">[5]</xref>, <xref rid="bb0030" ref-type="bibr">[6]</xref>,<xref rid="bb0090" ref-type="bibr">18</xref>,<xref rid="bb0095" ref-type="bibr">19</xref>]. A meta-analysis of 1527 patients with COVID-19 found that the prevalence of hypertension was 17.1% and cardiac disease was 16.4%, and that these patients were more likely to require critical care [<xref rid="bb0090" ref-type="bibr">18</xref>]. Another study of 44,672 patients with COVID-19 found that a history of CVD was associated with a nearly five-fold increase in the case fatality rate when compared with patients without CVD (10.5% vs. 2.3%) [<xref rid="bb0025" ref-type="bibr">5</xref>]. Other studies suggest similar findings with increased risk of mortality in patients with prior CVD [<xref rid="bb0025" ref-type="bibr">[5]</xref>, <xref rid="bb0030" ref-type="bibr">[6]</xref>, <xref rid="bb0035" ref-type="bibr">[7]</xref>, <xref rid="bb0040" ref-type="bibr">[8]</xref>, <xref rid="bb0045" ref-type="bibr">[9]</xref>,<xref rid="bb0095" ref-type="bibr">19</xref>].</p><p id="p0025">Severe or critical cases account for less than 20% of patients with COVID-19 [<xref rid="bb0025" ref-type="bibr">[5]</xref>, <xref rid="bb0030" ref-type="bibr">[6]</xref>, <xref rid="bb0035" ref-type="bibr">[7]</xref>, <xref rid="bb0040" ref-type="bibr">[8]</xref>, <xref rid="bb0045" ref-type="bibr">[9]</xref>,<xref rid="bb0095" ref-type="bibr">[19]</xref>, <xref rid="bb0100" ref-type="bibr">[20]</xref>, <xref rid="bb0105" ref-type="bibr">[21]</xref>, <xref rid="bb0110" ref-type="bibr">[22]</xref>, <xref rid="bb0115" ref-type="bibr">[23]</xref>]. Patients with critical illness may present with pneumonia, ARDS, multiorgan dysfunction, and hemodynamic instability, as well as several cardiovascular complications [<xref rid="bb0025" ref-type="bibr">[5]</xref>, <xref rid="bb0030" ref-type="bibr">[6]</xref>, <xref rid="bb0035" ref-type="bibr">[7]</xref>, <xref rid="bb0040" ref-type="bibr">[8]</xref>, <xref rid="bb0045" ref-type="bibr">[9]</xref>,<xref rid="bb0095" ref-type="bibr">[19]</xref>, <xref rid="bb0100" ref-type="bibr">[20]</xref>, <xref rid="bb0105" ref-type="bibr">[21]</xref>, <xref rid="bb0110" ref-type="bibr">[22]</xref>, <xref rid="bb0115" ref-type="bibr">[23]</xref>]. Cardiogenic shock is the most severe cardiac complication and may occur in those with critical illness [<xref rid="bb0025" ref-type="bibr">[5]</xref>, <xref rid="bb0030" ref-type="bibr">[6]</xref>, <xref rid="bb0035" ref-type="bibr">[7]</xref>, <xref rid="bb0040" ref-type="bibr">[8]</xref>, <xref rid="bb0045" ref-type="bibr">[9]</xref>,<xref rid="bb0095" ref-type="bibr">19</xref>]. <xref rid="f0005" ref-type="fig">Fig. 1</xref>summarizes the relationship between COVID-19 and cardiac complications.<fig id="f0005"><label>Fig. 1</label><caption><p>COVID-19 and the cardiovascular system.</p></caption><alt-text id="al0005">Fig. 1</alt-text><graphic xlink:href="gr1_lrg"></graphic></fig></p></sec><sec id="s0025"><label>3.2</label><title>Cardiovascular complications associated with COVID-19 infection</title><sec id="s0030"><label>3.2.1</label><title>Myocardial injury and myocarditis</title><p id="p0030">Prior viral illnesses, including Middle East respiratory syndrome coronavirus (MERS-CoV), have been associated with myocardial injury and myocarditis with troponin elevation, thought to be due to increased cardiac physiologic stress, hypoxia, or direct myocardial injury [<xref rid="bb0020" ref-type="bibr">4</xref>,<xref rid="bb0120" ref-type="bibr">[24]</xref>, <xref rid="bb0125" ref-type="bibr">[25]</xref>, <xref rid="bb0130" ref-type="bibr">[26]</xref>, <xref rid="bb0135" ref-type="bibr">[27]</xref>, <xref rid="bb0140" ref-type="bibr">[28]</xref>, <xref rid="bb0145" ref-type="bibr">[29]</xref>, <xref rid="bb0150" ref-type="bibr">[30]</xref>, <xref rid="bb0155" ref-type="bibr">[31]</xref>, <xref rid="bb0160" ref-type="bibr">[32]</xref>, <xref rid="bb0165" ref-type="bibr">[33]</xref>]. One of the first reports of myocardial injury associated with SARS-CoV-2 was a study of 41 patients diagnosed with COVID-19 in Wuhan, China, wherein 5 patients (12%) had a high-sensitivity troponin I above the threshold of 28 pg/mL [<xref rid="bb0035" ref-type="bibr">7</xref>]. Subsequent studies have found that myocardial injury with an elevated troponin level may occur in 7–17% of patients hospitalized with COVID-19 and 22–31% of those admitted to the intensive care unit (ICU) [<xref rid="bb0035" ref-type="bibr">[7]</xref>, <xref rid="bb0040" ref-type="bibr">[8]</xref>, <xref rid="bb0045" ref-type="bibr">[9]</xref>]. Myocarditis has also been identified with high viral loads and mononuclear infiltrates identified on autopsy of some patients with COVID-19 [<xref rid="bb0130" ref-type="bibr">[26]</xref>, <xref rid="bb0135" ref-type="bibr">[27]</xref>, <xref rid="bb0140" ref-type="bibr">[28]</xref>]. In fact, one study suggested that up to 7% of COVID-19 related deaths were due to myocarditis [<xref rid="bb0030" ref-type="bibr">6</xref>].</p><p id="p0035">Acute myocarditis presents across a variable range of clinical severity and is a significant diagnostic challenge in the COVID-19 era. Patients with COVID-19 can present with chest pain, dyspnea, dysrhythmia, and acute left ventricular dysfunction [<xref rid="bb0025" ref-type="bibr">[5]</xref>, <xref rid="bb0030" ref-type="bibr">[6]</xref>, <xref rid="bb0035" ref-type="bibr">[7]</xref>, <xref rid="bb0040" ref-type="bibr">[8]</xref>, <xref rid="bb0045" ref-type="bibr">[9]</xref>]. In patients with myocarditis and myocardial injury, serum troponin values will be abnormal. The electrocardiogram (ECG) can demonstrate a range of findings, in some cases mimicking acute coronary syndrome (ACS). The ECG abnormalities result from myocardial inflammation and include non-specific ST segment-T wave abnormalities, T wave inversion, and PR segment and ST segment deviations (depression and elevation). Echocardiography and consultation with cardiology, if either are available, is encouraged, as differentiating myocarditis and ACS is difficult. Echocardiographic evaluation is more likely to demonstrate a focal wall motion abnormality with active, significant ACS while severe forms of COVID-19-related myocarditis will show either no wall motion defects or global wall motion dysfunction [<xref rid="bb0020" ref-type="bibr">4</xref>,<xref rid="bb0160" ref-type="bibr">32</xref>]. ECG and echocardiographic abnormalities in the setting of COVID-19 are markers of illness severity and are correlated with worse outcomes [<xref rid="bb0020" ref-type="bibr">4</xref>,<xref rid="bb0145" ref-type="bibr">29</xref>,<xref rid="bb0150" ref-type="bibr">30</xref>]. Moreover, troponin elevations in patients with COVID-19 infection have been directly associated with an increased risk of adverse outcome in those patients with severe infection, including mortality [<xref rid="bb0125" ref-type="bibr">25</xref>,<xref rid="bb0145" ref-type="bibr">29</xref>,<xref rid="bb0150" ref-type="bibr">30</xref>].</p></sec><sec id="s0035"><label>3.2.2</label><title>Acute myocardial infarction</title><p id="p0040">Severe systemic inflammation increases the risk of atherosclerotic plaque disruption and AMI [<xref rid="bb0075" ref-type="bibr">15</xref>,<xref rid="bb0150" ref-type="bibr">[30]</xref>, <xref rid="bb0155" ref-type="bibr">[31]</xref>, <xref rid="bb0160" ref-type="bibr">[32]</xref>, <xref rid="bb0165" ref-type="bibr">[33]</xref>]. A 2018 study found that influenza and other select viral illnesses were associated with an increased risk of AMI within the first 7 days of disease diagnosis, with an incidence ratio of 6.1 for influenza and 2.8 for other viruses [<xref rid="bb0075" ref-type="bibr">15</xref>]. Another study of patients hospitalized for community-acquired pneumonia found an increased risk of active CVD that remained present for several years after hospitalization [<xref rid="bb0155" ref-type="bibr">31</xref>]. Due to extensive inflammation and hypercoagulability, the risk of AMI is likely present in patients with COVID-19 [<xref rid="bb0020" ref-type="bibr">4</xref>,<xref rid="bb0160" ref-type="bibr">32</xref>].</p><p id="p0045">The treatment of AMI is controversial in COVID-19 patients. In patients diagnosed with an ST elevation myocardial infarction (STEMI) and COVID-19, the American College of Cardiology (ACC) states that while fibrinolysis may be considered in those with "low risk STEMI", defined by inferior STEMI with no right ventricular involvement or lateral AMI without hemodynamic compromise, percutaneous coronary intervention (PCI) is more commonly performed at most institutions and remains the treatment of choice [<xref rid="bb0160" ref-type="bibr">32</xref>]. If PCI is pursued, staff should don appropriate personal protective equipment (PPE), and a full decontamination of the catheterization laboratory should be performed following the procedure. For suspected COVID-19 in the setting of NSTEMI, diagnostic testing prior to catheterization is recommended; the ACC note that, in properly selected patients with confirmed COVID-19, conservative therapy may be sufficient. Patients who are hemodynamically unstable in the setting of NSTEMI should be managed similarly to those with STEMI [<xref rid="bb0160" ref-type="bibr">32</xref>].</p></sec><sec id="s0040"><label>3.2.3</label><title>Acute heart failure and cardiomyopathy</title><p id="p0050">Acute heart failure can be the primary presenting manifestation of COVID-19 infection. One study found that acute heart failure may be present in 23% of patients in their initial presentation for COVID-19, with cardiomyopathy occurring in 33% of patients [<xref rid="bb0040" ref-type="bibr">8</xref>]. Another study found that heart failure was present in 24% of patients and was associated with an increased risk of mortality [<xref rid="bb0165" ref-type="bibr">33</xref>]. Among those with heart failure, nearly half did not have a known history of hypertension or CVD [<xref rid="bb0165" ref-type="bibr">33</xref>]. It is currently unknown if heart failure is due to new cardiomyopathy versus an exacerbation of previously undiagnosed heart failure [<xref rid="bb0170" ref-type="bibr">34</xref>]. It is important to be conscious of this potential cardiac dysfunction when administering intravenous fluids and avoid overaggressive fluid replacement. Importantly, right heart failure may also occur, particularly among those with ARDS and acute lung injury [<xref rid="bb0020" ref-type="bibr">4</xref>,<xref rid="bb0095" ref-type="bibr">19</xref>].</p></sec><sec id="s0045"><label>3.2.4</label><title>Dysrhythmias</title><p id="p0055">Palpitations may be a presenting symptom in over 7% of patients with COVID-19 [<xref rid="bb0130" ref-type="bibr">26</xref>]. A range of dysrhythmias have been encountered in patients with COVID-19 infection. Most frequently, sinus tachycardia is seen in such patients, resulting from multiple, simultaneous causes (hypoperfusion, fever, hypoxia, anxiety, etc) [<xref rid="bb0020" ref-type="bibr">4</xref>]. One study found that dysrhythmias were present in 17% of hospitalized and 44% of ICU patients with COVID-19 [<xref rid="bb0045" ref-type="bibr">9</xref>]. Dysrhythmias may occur in the setting of viral illness due to hypoxia, inflammatory stress, and abnormal metabolism [<xref rid="bb0020" ref-type="bibr">4</xref>]. If dysrhythmias are associated with an elevation in serum troponin, the clinician should consider myocardial injury, acute myocarditis, and ACS in the differential diagnosis [<xref rid="bb0020" ref-type="bibr">4</xref>].</p></sec><sec id="s0050"><label>3.2.5</label><title>Venous thromboembolic event</title><p id="p0060">Patients with COVID-19 are also at an increased risk of VTEs [<xref rid="bb0175" ref-type="bibr">35</xref>,<xref rid="bb0180" ref-type="bibr">36</xref>]. Systemic inflammation, abnormal coagulation status, multiorgan dysfunction, and critical illness are all potential contributing factors to the increased risk of VTE [<xref rid="bb0035" ref-type="bibr">7</xref>,<xref rid="bb0040" ref-type="bibr">8</xref>,<xref rid="bb0175" ref-type="bibr">[35]</xref>, <xref rid="bb0180" ref-type="bibr">[36]</xref>, <xref rid="bb0185" ref-type="bibr">[37]</xref>, <xref rid="bb0190" ref-type="bibr">[38]</xref>]. Studies suggest significant coagulation pathway abnormalities in patients with COVID-19, including elevated D-dimer [<xref rid="bb0035" ref-type="bibr">7</xref>,<xref rid="bb0040" ref-type="bibr">8</xref>,<xref rid="bb0175" ref-type="bibr">[35]</xref>, <xref rid="bb0180" ref-type="bibr">[36]</xref>, <xref rid="bb0185" ref-type="bibr">[37]</xref>, <xref rid="bb0190" ref-type="bibr">[38]</xref>]. One study of 25 patients with COVID-19 pneumonia found that an elevated D-dimer was present in all patients with a median of 6.06 micrograms/ml, with 10 patients having a pulmonary embolism (PE) diagnosed on computed tomography pulmonary angiography (CTPA) [<xref rid="bb0185" ref-type="bibr">37</xref>]. Patients with confirmed PE on CTPA demonstrated a median D-dimer level of 11.07 micrograms/ml [<xref rid="bb0185" ref-type="bibr">37</xref>]. D-dimer levels greater than 1 μg/mL were associated with an increased risk of death during hospitalization (odds ratio 18.4) in COVID-19-infected patients [<xref rid="bb0040" ref-type="bibr">8</xref>]. One study suggests anticoagulation, mainly with low molecular weight heparin, may be associated with reduced mortality in severe COVID-19 infections or those with D-dimer greater than six times the upper limit of normal [<xref rid="bb0195" ref-type="bibr">39</xref>].</p></sec><sec id="s0055"><label>3.2.6</label><title>Medication interactions</title><p id="p0065">Many of the newly studied medications interact extensively with other cardiovascular drugs, including antihypertensives, antiarrhythmics, anticoagulants, antiplatelets, and statins [<xref rid="bb0020" ref-type="bibr">4</xref>]. Current medications under study include antivirals (e.g., remdesivir, ribavirin, lopinavir/ritonavir, favipiravir), antimalarials (e.g., chloroquine, hydroxychloroquine), azithromycin, corticosteroids, and biologics (tocilizumab) [<xref rid="bb0020" ref-type="bibr">4</xref>,<xref rid="bb0200" ref-type="bibr">[40]</xref>, <xref rid="bb0205" ref-type="bibr">[41]</xref>, <xref rid="bb0210" ref-type="bibr">[42]</xref>]. Lopinavir/ritonavir may cause QT and PR prolongation, particularly in those with baseline QT prolongation or in those taking medications that may cause QT prolongation [<xref rid="bb0215" ref-type="bibr">43</xref>]. These medications can also affect anticoagulant medications, antiplatelet agents, and statins [<xref rid="bb0215" ref-type="bibr">43</xref>]. Chloroquine and hydroxychloroquine affect the intracellular pH, which can result in electrolyte abnormalities, cardiotoxicity, and prolonged QT intervals; they may also interact with antiarrhythmic agents [<xref rid="bb0220" ref-type="bibr">44</xref>,<xref rid="bb0225" ref-type="bibr">45</xref>]. Methylprednisolone can cause electrolyte derangements, fluid retention, and hypertension [<xref rid="bb0140" ref-type="bibr">28</xref>]. A summary of the mechanism of action and effect of these medications is located in <xref rid="t0005" ref-type="table">Table 1</xref>.<table-wrap position="float" id="t0005"><label>Table 1</label><caption><p>Medications and the cardiovascular system [<xref rid="bb0020" ref-type="bibr">4</xref>].</p></caption><alt-text id="al0010">Table 1</alt-text><table frame="hsides" rules="groups"><thead><tr><th>Medication</th><th>Mechanism</th><th>Cardiovascular effects and medication interactions</th></tr></thead><tbody><tr><td>Remdesivir</td><td>Nucleotide-analog inhibitor of RNA polymerases</td><td>- May cause hypotension, arrhythmias</td></tr><tr><td>Ribavirin</td><td>Inhibits RNA and DNA virus replication</td><td>- Interacts with anticoagulants<break></break>- May cause severe hemolytic anemia</td></tr><tr><td>Lopinavir/Ritonavir</td><td>Lopinavir inhibits protease<break></break>Ritonavir inhibits CYP3A metabolism</td><td>- Interacts with anticoagulants, antiplatelets, statins, antiarrhythmics<break></break>- May result in prolonged QTc, AV blocks, Torsades de pointes</td></tr><tr><td>Favipiravir</td><td>Inhibits RNA-dependent RNA polymerases</td><td>- Interacts with anticoagulants, statins, antiarrhythmics<break></break>- May cause severe hemolytic anemia</td></tr><tr><td>Chloroquine and Hydroxychloroquine</td><td>Changes endosomal/organelle pH</td><td>- Interacts with antiarrhythmics<break></break>- May cause direct myocardial toxicity; worsen cardiomyopathy; alter cardiac conduction; result in bundle branch block, AV block, ventricular arrhythmias, Torsades de pointes</td></tr><tr><td>Azithromycin</td><td>Interferes with protein synthesis, binds to 50s ribosome</td><td>- Interacts with anticoagulants, statins, antiarrhythmics, other QT prolonging agents<break></break>- May result in dysrhythmias, prolonged QTc, Torsades de pointes</td></tr><tr><td>Interferon</td><td>Immune system activation</td><td>- May cause direct myocardial toxicity; worsen cardiomyopathy; alter cardiac conduction; cause hypotension or cardiac ischemia</td></tr><tr><td>Methylprednisolone</td><td>Reduces inflammation</td><td>- Interacts with anticoagulants<break></break>- May cause fluid retention, hypertension, electrolyte changes</td></tr><tr><td>Tocilizumab</td><td>Inhibits IL-6</td><td>- May increase medication metabolism such as statins<break></break>- May cause hypertension</td></tr></tbody></table></table-wrap></p></sec></sec></sec><sec id="s0060"><label>4</label><title>Limitations</title><p id="p0070">The current literature evaluating cardiovascular complications and effects associated with COVID-19 suffers from several limitations, including significant heterogeneity in patient selection, outcomes, comparators, and study design, as well as low numbers of included patients and high risk of bias. With the current pandemic, a significant amount of literature is published in preprint form, prior to completion of full peer review. Further data are needed concerning the discussed cardiovascular complications and COVID-19.</p></sec><sec id="s0065"><label>5</label><title>Conclusions</title><p id="p0075">COVID-19 is associated with a number of cardiovascular complications, including myocardial injury and myocarditis, AMI, heart failure, dysrhythmias, and VTE. Some of the medications utilized to treat COVID-19 also have potential cardiac complications. It is important for the emergency clinicians to be aware of these complications when treating the COVID-19 patient.</p></sec><sec sec-type="COI-statement"><title>Declaration of competing interest</title><p id="p0085">None.</p></sec></body><back><ref-list id="bi0005"><title>References</title><ref id="bb0005"><label>1</label><element-citation publication-type="other" id="rf0005"><person-group person-group-type="author"><name><surname>World Health Organization</surname></name></person-group><article-title>WHO Director-General's opening remarks at the media briefing on COVID-19 - 11 March 2020</article-title><comment>Available online at</comment><ext-link ext-link-type="uri" xlink:href="https://www.who.int/dg/speeches/detail/whodirector-general-s-opening-remarks-at-the-media-briefing-on-covid-19---11-march-2020" id="ir0005">https://www.who.int/dg/speeches/detail/whodirector-general-s-opening-remarks-at-the-media-briefing-on-covid-19---11-march-2020</ext-link></element-citation></ref><ref 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