The impact of 2019 novel coronavirus on heart injury: A Systematic review and Meta-analysis

Evidence about COVID-19 on cardiac injury is inconsistent. We aimed to summarize available data on severity differences in acute cardiac injury and acute cardiac injury with mortality during the COVID-19 outbreak. We performed a systematic literature search across Pubmed, Embase and pre-print from D...

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Vydáno v:Progress in cardiovascular diseases Ročník 63; číslo 4; s. 518 - 524
Hlavní autoři: Li, Jing-Wei, Han, Tian-Wen, Woodward, Mark, Anderson, Craig S., Zhou, Hao, Chen, Yun-Dai, Neal, Bruce
Médium: Journal Article
Jazyk:angličtina
Vydáno: United States Elsevier Inc 01.07.2020
Published by Elsevier Inc
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ISSN:0033-0620, 1873-1740, 1532-8643, 1873-1740
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Abstract Evidence about COVID-19 on cardiac injury is inconsistent. We aimed to summarize available data on severity differences in acute cardiac injury and acute cardiac injury with mortality during the COVID-19 outbreak. We performed a systematic literature search across Pubmed, Embase and pre-print from December 1, 2019 to March 27, 2020, to identify all observational studies that reported cardiac specific biomarkers (troponin, creatine kinase–MB fraction, myoglobin, or NT-proBNP) during COVID-19 infection. We extracted data on patient demographics, infection severity, comorbidity history, and biomarkers during COVID-19 infection. Where possible, data were pooled for meta-analysis with standard (SMD) or weighted (WMD) mean difference and corresponding 95% confidence intervals (CI). We included 4189 confirmed COVID-19 infected patients from 28 studies. More severe COVID-19 infection is associated with higher mean troponin (SMD 0.53, 95% CI 0.30 to 0.75, p < 0.001), with a similar trend for creatine kinase–MB, myoglobin, and NT-proBNP. Acute cardiac injury was more frequent in those with severe, compared to milder, disease (risk ratio 5.99, 3.04 to 11.80; p < 0.001). Meta regression suggested that cardiac injury biomarker differences of severity are related to history of hypertension (p = 0.030). Also COVID19-related cardiac injury is associated with higher mortality (summary risk ratio 3.85, 2.13 to 6.96; p < 0.001). hsTnI and NT-proBNP levels increased during the course of hospitalization only in non-survivors. The severity of COVID-19 is associated with acute cardiac injury, and acute cardiac injury is associated with death. Cardiac injury biomarkers mainly increase in non-survivors. This highlights the need to effectively monitor heart health to prevent myocarditis in patients infected with COVID-19. [Display omitted]
AbstractList Evidence about COVID-19 on cardiac injury is inconsistent. We aimed to summarize available data on severity differences in acute cardiac injury and acute cardiac injury with mortality during the COVID-19 outbreak. We performed a systematic literature search across Pubmed, Embase and pre-print from December 1, 2019 to March 27, 2020, to identify all observational studies that reported cardiac specific biomarkers (troponin, creatine kinase-MB fraction, myoglobin, or NT-proBNP) during COVID-19 infection. We extracted data on patient demographics, infection severity, comorbidity history, and biomarkers during COVID-19 infection. Where possible, data were pooled for meta-analysis with standard (SMD) or weighted (WMD) mean difference and corresponding 95% confidence intervals (CI). We included 4189 confirmed COVID-19 infected patients from 28 studies. More severe COVID-19 infection is associated with higher mean troponin (SMD 0.53, 95% CI 0.30 to 0.75, p < 0.001), with a similar trend for creatine kinase-MB, myoglobin, and NT-proBNP. Acute cardiac injury was more frequent in those with severe, compared to milder, disease (risk ratio 5.99, 3.04 to 11.80; p < 0.001). Meta regression suggested that cardiac injury biomarker differences of severity are related to history of hypertension (p = 0.030). Also COVID19-related cardiac injury is associated with higher mortality (summary risk ratio 3.85, 2.13 to 6.96; p < 0.001). hsTnI and NT-proBNP levels increased during the course of hospitalization only in non-survivors. The severity of COVID-19 is associated with acute cardiac injury, and acute cardiac injury is associated with death. Cardiac injury biomarkers mainly increase in non-survivors. This highlights the need to effectively monitor heart health to prevent myocarditis in patients infected with COVID-19.
Evidence about COVID-19 on cardiac injury is inconsistent. We aimed to summarize available data on severity differences in acute cardiac injury and acute cardiac injury with mortality during the COVID-19 outbreak. We performed a systematic literature search across Pubmed, Embase and pre-print from December 1, 2019 to March 27, 2020, to identify all observational studies that reported cardiac specific biomarkers (troponin, creatine kinase–MB fraction, myoglobin, or NT-proBNP) during COVID-19 infection. We extracted data on patient demographics, infection severity, comorbidity history, and biomarkers during COVID-19 infection. Where possible, data were pooled for meta-analysis with standard (SMD) or weighted (WMD) mean difference and corresponding 95% confidence intervals (CI). We included 4189 confirmed COVID-19 infected patients from 28 studies. More severe COVID-19 infection is associated with higher mean troponin (SMD 0.53, 95% CI 0.30 to 0.75, p < 0.001), with a similar trend for creatine kinase–MB, myoglobin, and NT-proBNP. Acute cardiac injury was more frequent in those with severe, compared to milder, disease (risk ratio 5.99, 3.04 to 11.80; p < 0.001). Meta regression suggested that cardiac injury biomarker differences of severity are related to history of hypertension (p = 0.030). Also COVID19-related cardiac injury is associated with higher mortality (summary risk ratio 3.85, 2.13 to 6.96; p < 0.001). hsTnI and NT-proBNP levels increased during the course of hospitalization only in non-survivors. The severity of COVID-19 is associated with acute cardiac injury, and acute cardiac injury is associated with death. Cardiac injury biomarkers mainly increase in non-survivors. This highlights the need to effectively monitor heart health to prevent myocarditis in patients infected with COVID-19. [Display omitted]
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Evidence about COVID-19 on cardiac injury is inconsistent.BACKGROUNDEvidence about COVID-19 on cardiac injury is inconsistent.We aimed to summarize available data on severity differences in acute cardiac injury and acute cardiac injury with mortality during the COVID-19 outbreak.OBJECTIVESWe aimed to summarize available data on severity differences in acute cardiac injury and acute cardiac injury with mortality during the COVID-19 outbreak.We performed a systematic literature search across Pubmed, Embase and pre-print from December 1, 2019 to March 27, 2020, to identify all observational studies that reported cardiac specific biomarkers (troponin, creatine kinase-MB fraction, myoglobin, or NT-proBNP) during COVID-19 infection. We extracted data on patient demographics, infection severity, comorbidity history, and biomarkers during COVID-19 infection. Where possible, data were pooled for meta-analysis with standard (SMD) or weighted (WMD) mean difference and corresponding 95% confidence intervals (CI).METHODSWe performed a systematic literature search across Pubmed, Embase and pre-print from December 1, 2019 to March 27, 2020, to identify all observational studies that reported cardiac specific biomarkers (troponin, creatine kinase-MB fraction, myoglobin, or NT-proBNP) during COVID-19 infection. We extracted data on patient demographics, infection severity, comorbidity history, and biomarkers during COVID-19 infection. Where possible, data were pooled for meta-analysis with standard (SMD) or weighted (WMD) mean difference and corresponding 95% confidence intervals (CI).We included 4189 confirmed COVID-19 infected patients from 28 studies. More severe COVID-19 infection is associated with higher mean troponin (SMD 0.53, 95% CI 0.30 to 0.75, p < 0.001), with a similar trend for creatine kinase-MB, myoglobin, and NT-proBNP. Acute cardiac injury was more frequent in those with severe, compared to milder, disease (risk ratio 5.99, 3.04 to 11.80; p < 0.001). Meta regression suggested that cardiac injury biomarker differences of severity are related to history of hypertension (p = 0.030). Also COVID19-related cardiac injury is associated with higher mortality (summary risk ratio 3.85, 2.13 to 6.96; p < 0.001). hsTnI and NT-proBNP levels increased during the course of hospitalization only in non-survivors.RESULTSWe included 4189 confirmed COVID-19 infected patients from 28 studies. More severe COVID-19 infection is associated with higher mean troponin (SMD 0.53, 95% CI 0.30 to 0.75, p < 0.001), with a similar trend for creatine kinase-MB, myoglobin, and NT-proBNP. Acute cardiac injury was more frequent in those with severe, compared to milder, disease (risk ratio 5.99, 3.04 to 11.80; p < 0.001). Meta regression suggested that cardiac injury biomarker differences of severity are related to history of hypertension (p = 0.030). Also COVID19-related cardiac injury is associated with higher mortality (summary risk ratio 3.85, 2.13 to 6.96; p < 0.001). hsTnI and NT-proBNP levels increased during the course of hospitalization only in non-survivors.The severity of COVID-19 is associated with acute cardiac injury, and acute cardiac injury is associated with death. Cardiac injury biomarkers mainly increase in non-survivors. This highlights the need to effectively monitor heart health to prevent myocarditis in patients infected with COVID-19.CONCLUSIONThe severity of COVID-19 is associated with acute cardiac injury, and acute cardiac injury is associated with death. Cardiac injury biomarkers mainly increase in non-survivors. This highlights the need to effectively monitor heart health to prevent myocarditis in patients infected with COVID-19.
Author Zhou, Hao
Anderson, Craig S.
Chen, Yun-Dai
Li, Jing-Wei
Woodward, Mark
Han, Tian-Wen
Neal, Bruce
Author_xml – sequence: 1
  givenname: Jing-Wei
  surname: Li
  fullname: Li, Jing-Wei
  organization: Department of Cardiology, People's Liberation Army General Hospital, Beijing, China
– sequence: 2
  givenname: Tian-Wen
  surname: Han
  fullname: Han, Tian-Wen
  organization: Department of Cardiology, People's Liberation Army General Hospital, Beijing, China
– sequence: 3
  givenname: Mark
  surname: Woodward
  fullname: Woodward, Mark
  organization: The George Institute for Global Health, Faculty of Medicine, University of New South Wales, NSW, Australia
– sequence: 4
  givenname: Craig S.
  surname: Anderson
  fullname: Anderson, Craig S.
  organization: The George Institute for Global Health, Faculty of Medicine, University of New South Wales, NSW, Australia
– sequence: 5
  givenname: Hao
  surname: Zhou
  fullname: Zhou, Hao
  organization: Department of Cardiology, People's Liberation Army General Hospital, Beijing, China
– sequence: 6
  givenname: Yun-Dai
  surname: Chen
  fullname: Chen, Yun-Dai
  email: cyundai@vip.163.com
  organization: Department of Cardiology, People's Liberation Army General Hospital, Beijing, China
– sequence: 7
  givenname: Bruce
  surname: Neal
  fullname: Neal, Bruce
  organization: The George Institute for Global Health, Faculty of Medicine, University of New South Wales, NSW, Australia
BackLink https://www.ncbi.nlm.nih.gov/pubmed/32305557$$D View this record in MEDLINE/PubMed
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Issue 4
Keywords RR
Cardiac injury
CI
Mortality
SARS-CoV
CK-MB
hsTnI
SMD
WMD
COVID-19
ACE2
NT-proBNP
Coronavirus
Language English
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Snippet Evidence about COVID-19 on cardiac injury is inconsistent. We aimed to summarize available data on severity differences in acute cardiac injury and acute...
Evidence about COVID-19 on cardiac injury is inconsistent.BACKGROUNDEvidence about COVID-19 on cardiac injury is inconsistent.We aimed to summarize available...
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SubjectTerms Betacoronavirus
Cardiac injury
Coronavirus
Coronavirus Infections - complications
COVID-19
Heart Diseases - epidemiology
Heart Diseases - virology
Humans
Mortality
Pandemics
Pneumonia, Viral - complications
Review
SARS-CoV-2
Title The impact of 2019 novel coronavirus on heart injury: A Systematic review and Meta-analysis
URI https://www.clinicalkey.com/#!/content/1-s2.0-S0033062020300803
https://dx.doi.org/10.1016/j.pcad.2020.04.008
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