<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>10(4)</volume><submitter>Krittanawong C</submitter><pubmed_abstract>In December 2019, an unprecedented outbreak of pneumonia cases associated with acute respiratory distress syndrome (ARDS) first occurred in Wuhan, Hubei Province, China. The disease, later named Coronavirus disease 2019 (COVID-19) by the World Health Organization (WHO), was caused by the Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2), and on January 30, 2020, the WHO declared the outbreak of COVID-19 to be a public health emergency. COVID-19 is now a global pandemic impacting more than 43,438,043 patients with 1,158,596 deaths globally as of August 26th, 2020. COVID-19 is highly contagious and has caused more deaths than SARS in 2002-2003 or the Middle East Respiratory Syndrome (MERS) in 2012-2013 combined and represents an unprecedented human affliction not seen since the influenza pandemic of 1918. COVID-19 has been associated with several cardiac complications, including hypercoagulability, acute myocardial injury and myocarditis, arrhythmias, and acute coronary syndromes. Patients with pre-existing cardiovascular disease (CVD) are at the highest risk for myocardial injury and mortality among infected patients. The mechanism by which COVID-infected patients develop cardiac complications remains unclear, though it may be mediated by increased ACE-2 gene expression. Despite initial concerns, there is no evidence that angiotensin-converting enzyme (ACE) inhibitor or angiotensin receptor blocker (ARB) therapy increases risk for myocardial injury among those infected with COVID-19. In the current report, we summarize the peer-reviewed and preprint literature on cardiovascular risks and complications associated with COVID-19, as well as provide insights into its pathogenesis and management.</pubmed_abstract><journal>American journal of cardiovascular disease</journal><pagination>479-489</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC7675166</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Cardiovascular risk and complications associated with COVID-19.</pubmed_title><pmcid>PMC7675166</pmcid><pubmed_authors>Virani SS</pubmed_authors><pubmed_authors>Krittanawong C</pubmed_authors><pubmed_authors>Zhang HJ</pubmed_authors><pubmed_authors>Halperin JL</pubmed_authors><pubmed_authors>Ballantyne CM</pubmed_authors><pubmed_authors>Jneid H</pubmed_authors><pubmed_authors>Bozkurt B</pubmed_authors><pubmed_authors>Sun T</pubmed_authors><pubmed_authors>Kumar A</pubmed_authors><pubmed_authors>Hahn J</pubmed_authors><pubmed_authors>Wang Z</pubmed_authors></additional><is_claimable>false</is_claimable><name>Cardiovascular risk and complications associated with COVID-19.</name><description>In December 2019, an unprecedented outbreak of pneumonia cases associated with acute respiratory distress syndrome (ARDS) first occurred in Wuhan, Hubei Province, China. The disease, later named Coronavirus disease 2019 (COVID-19) by the World Health Organization (WHO), was caused by the Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2), and on January 30, 2020, the WHO declared the outbreak of COVID-19 to be a public health emergency. COVID-19 is now a global pandemic impacting more than 43,438,043 patients with 1,158,596 deaths globally as of August 26th, 2020. COVID-19 is highly contagious and has caused more deaths than SARS in 2002-2003 or the Middle East Respiratory Syndrome (MERS) in 2012-2013 combined and represents an unprecedented human affliction not seen since the influenza pandemic of 1918. COVID-19 has been associated with several cardiac complications, including hypercoagulability, acute myocardial injury and myocarditis, arrhythmias, and acute coronary syndromes. Patients with pre-existing cardiovascular disease (CVD) are at the highest risk for myocardial injury and mortality among infected patients. The mechanism by which COVID-infected patients develop cardiac complications remains unclear, though it may be mediated by increased ACE-2 gene expression. Despite initial concerns, there is no evidence that angiotensin-converting enzyme (ACE) inhibitor or angiotensin receptor blocker (ARB) therapy increases risk for myocardial injury among those infected with COVID-19. In the current report, we summarize the peer-reviewed and preprint literature on cardiovascular risks and complications associated with COVID-19, as well as provide insights into its pathogenesis and management.</description><dates><release>2020-01-01T00:00:00Z</release><publication>2020</publication><modification>2025-04-04T22:53:21.253Z</modification><creation>2025-04-04T22:53:21.253Z</creation></dates><accession>S-EPMC7675166</accession><cross_references><pubmed>33224599</pubmed></cross_references></HashMap>