COVID-19 AND CARDIOVASCULAR DISEASE Syed Saad MD 1 , Murtuza Ali MD 2 , and Neeraj Jain MD 3 .
1. Cardiology Fellow, Louisiana State University School of Medicine, New Orleans. 2. Professor of Cardiology and Pharmacology, Louisiana State University School of Medicine, New Orleans. 3. Associate Professor of Cardiology, Louisiana State University School of Medicine, New Orleans.
Corresponding author: Syed Saad, MD. LSUHSC Section of Cardiology. Room 342, 533 Bolivar St.
New Orleans, LA70112. Email: ssaad@lsuhsc.edu
ABSTRACT COVID-19 is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which has overwhelmed healthcare systems, strangled economies and led to over 2.3 million deaths globally. Up to half of infected people are asymptomatic. If symptoms appear, they range from mild respiratory and gastrointestinal symptoms to cardiovascular and pulmonary complications that may prove fatal. Underlying cardiovascular diseases are associated with significantly worse patient outcomes and increased mortality. Accordingly, it is imperative that people with cardiovascular disease avoid SARS-COV-2 exposure and seek prompt medical attention if they develop symptoms. In this review, we will highlight the cardiovascular and thrombotic manifestations of COVID-19 infection.
BACKGROUND With at times several thousand newly diagnosed cases on average daily and total deaths approaching 9,000 in Louisiana (as of January 2021), the COVID-19 pandemic is far from being over 1 . The fear of COVID-19 owing to its high infectivity has markedly influenced our lifestyle, not only changing the way we interact and function but also how we eat and breathe. The main symptoms of COVID-19 include fever, cough, dyspnea, sore throat, fatigue, anosmia, dysgeusia, headache and gastrointestinal problems 2 . PATHOGENESIS SARS-CoV-2 is a single-strand RNA coronavirus. It enters human cells via endocytosis by binding the angiotensin converting enzyme 2 receptor (ACE2). ACE2 is expressed in lung alveolar cells, cardiac myocytes and vascular endothelium, amongst others (figure below) 3 . Like a few other members of the coronavirus family, it is believed to have moved from bats to an intermediate host (possibly the Malayan pangolin) and then to humans 4 . Depending on the surfaces where it resides, the virus can survive up to 3 days 5 . It can be transmitted by symptomatic and asymptomatic carriers via respiratory droplets and aerosols. It has amedian incubation period of about 5 days 6 . SARS-CoV-2 can disrupt the innate immune response inciting an out-of-proportion systemic inflammatory response with consequent tissue injury and multiorgan failure in severe cases. In particular,
the cellular immune response activates the macrophages and lymphocytes and stimulates their proliferation causing a release of proinflammatory cytokines and chemokines 7 . Cytokine storm, which may contribute to multiorgan dysfunction, results from uncontrolled T cell activation along with dysregulated release of IL-1, IL-6, interferons and TNF-α 7 . Immunometabolism alterations with immune system activation are postulated to result in endothelial disruption, plaque instability and thrombosis leading to atherosclerosis and acute coronary events 8 . There have been reports of activated T cells, macrophages and SARS- COV-2 invading the myocardium directly causing fulminant myocarditis and arrhythmias 9,10 . Thrombocytopenia and elevated D-dimer levels are commonly associated with a complicated course of the disease 11 . SARS-CoV-2 impairs the balance between coagulation system and fibrinolysis via dysregulated inflammatory cascade and endothelial damage. Viral invasion of the endothelial cells has also been reported 12,13 . Formation of neutrophil extracellular traps (NET) in COVID-19 patients contribute to occlusion of pulmonary microvessels and organ damage 14 . In a recent study, NET was detected in coronary thrombus samples of all COVID-19 patients who presentedwith STEMI 15 . Increased release of von Willebrand and tissue factor along with other cytokines promote coagulation and disseminated intravascular coagulation (DIC) 16 . Liver dysfunction and elevated antiphospholipid antibodies are also hypothesized to play a role in thrombotic complications of COVID-19 17 . 24
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