View source for Section 8: Conclusion (from DOI: 10.1007/s11886-020-01292-3)

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<b>From publication:</b> "Cardiovascular Complications in Patients with COVID-19: Consequences of Viral Toxicities and Host Immune Response" published as Curr Cardiol Rep; 2020 04 21 ; 22 (5) 32. DOI: https://doi.org/10.1007/s11886-020-01292-3 <br><br><h3><u>Section 8: Conclusion</u></h3><p>SARS-CoV-2 has become a worldwide health threat, with the numbers of infected patients growing rapidly. An increased incidence of cardiac injury has been observed among those with severe infection. The mechanism of cardiac injury is unclear but likely involves a combination of direct viral damage and immune-mediated damage by inflammatory cytokines/chemokines and cytotoxic immune cell response in the later stages of infection. The host immune response and contributors to cytokine storm in SARS-CoV-2 infection are complex. Significant depletion and dysregulation of T lymphocytes may contribute to immune dysregulation and hyperactivity. Cardiac damage in the setting of cytokine storm may be analogous to that seen in cardiotoxicity from CAR-T. Treatments for COVID-19 are bimodal, with one group of treatments targeted toward early infection and viral replication, and another group targeted toward immune modulation in the later, systemic inflammatory phase of infection. With the advent of single cell immune phenotyping technologies, it will be important to perform comprehensive immune surveys of infected patients to better understand systemic perturbations with the infection and downstream cardiovascular effects. More data are needed to help guide us toward definitive treatment and protection of the cardiovascular system in COVID-19 infection.</p>