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Review
. 2020 Aug;20(4):311-324.
doi: 10.1007/s40256-020-00420-2.

COVID-19 Pandemic: Cardiovascular Complications and Future Implications

Dhrubajyoti Bandyopadhyay  1 , Tauseef Akhtar  2 , Adrija Hajra  3 , Manasvi Gupta  4 , Avash Das  5 , Sandipan Chakraborty  6 , Ipsita Pal  7 , Neelkumar Patel  8 , Birendra Amgai  8 , Raktim K Ghosh  9 , Gregg C Fonarow  10 , Carl J Lavie  11 , Srihari S Naidu  12
Affiliations
Review

COVID-19 Pandemic: Cardiovascular Complications and Future Implications

Dhrubajyoti Bandyopadhyay et al. Am J Cardiovasc Drugs. 2020 Aug.

Abstract

Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is now a global pandemic with the highest number of affected individuals in the modern era. Not only is the infection inflicting significant morbidity and mortality, but there has also been a significant strain to the health care system and the economy. COVID-19 typically presents as viral pneumonia, occasionally leading to acute respiratory distress syndrome (ARDS) and death. However, emerging evidence suggests that it has a significant impact on the cardiovascular (CV) system by direct myocardial damage, severe systemic inflammatory response, hypoxia, right heart strain secondary to ARDS and lung injury, and plaque rupture secondary to inflammation. Primary cardiac manifestations include acute myocarditis, myocardial infarction, arrhythmia, and abnormal clotting. Several consensus documents have been released to help manage CV disease during this pandemic. In this review, we summarize key cardiac manifestations, their management, and future implications.

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Conflict of interest statement

Dr. Gregg C. Fonarow reports research funding from the NIH and serving as a consultant for Abbott, Amgen, AstraZeneca, Bayer, CHF Solutions, Janssen, Medtronic, Merck, and Novartis. Dhrubajyoti Bandyopadhyay, Tauseef Akhtar, Adrija Hajra, Manasvi Gupta, Avash Das, Sandipan Chakraborty, Ipsita Pal, Neelkumar Patel, Birendra Amgai, Raktim K. Ghosh, Carl J. Lavie, and Srihari S. Naidu declare they have no potential conflicts of interest that might be relevant to the contents of this article.

Figures

Fig. 1
Fig. 1
Schematic representation of the COVID-19 structure and route of infection. This figure describes the structure of the SARS-CoV-2. In the respiratory system, the virus spike protein binds with the ACE2 receptor in respiratory epithelial cells and internalizes and forms a membrane fusion complex, which causes the release of the viral RNA into the host cell and results in respiratory infection. Through different pathways, the virus induces the proinflammatory response by induction of T- and B-cells and synthesis of type I IFNs, which limit the spread of the virus and cause a cytokine storm, while induction of the macrophage causes ingestion of the viral antigen [this image is generated with the help of Biorender]. SARS-CoV-2 severe acute respiratory syndrome coronavirus 2, ACE2 angiotensin converting enzyme 2, IFNs interferons, NK natural killer, TH17 T-helper 17, IL interleukin, TNF tumor necrosis factor, MCP monocyte chemoattractant protein
Fig. 2
Fig. 2
Management of STEMI in COVID-19 confirmed/suspected patients. ACEi angiotensin-converting enzyme inhibitor, BP blood pressure, CPR cardiopulmonary resuscitation, DBP diastolic blood pressure, GI gastrointestinal, GU genitourinary, H/O history of, HR heart rate, ICH intracranial hemorrhage, LA left arm, PCI percutaneous coronary intervention, RA right arm, SBP systolic blood pressure, STEMI ST-elevation myocardial infarction. *High risk individuals: 1. HR > 100/min and SBP < 100 mm of Hg, 2. pulmonary edema, 3. signs of shock, 4. CPR required. **Medical therapy: 1. antiplatelet, 2. anticoagulation, 3. high intensity statin, 4. beta blocker/ACEi
Fig. 3
Fig. 3
Workflow for hydroxychloroquine therapy in COVID-19 patients
See this image and copyright information in PMC

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