Abstract
Objective: To investigate, interpret and review the findings on the development of the viral myocarditis phenotype after SARS-CoV-2 infection, as well as the pathophysiological mechanisms involved, so that it is possible to formulate therapeutic strategies to prevent and mitigate the evolution of the condition clinical. Bibliographic review: It is observed that the patients with the worst prognosis are the elderly or those who have systemic arterial hypertension, diabetes mellitus, coronary artery disease and heart failure. Studies show that around 10% of patients infected with COVID-19 developed myocarditis and that 59% of patients with cardiovascular involvement progressed to in-hospital death. This is because COVID-19 causes a myocardial injury that manifests itself by an increase in troponin levels, which is related to an increase in mortality. Other inflammation markers can be found, such as DHL, D-dimer, IL-6 and ferritin. The interaction between SARS-CoV and ACE-2 receptors can contribute to inflammation by increasing myocardial damage. Final considerations: The management of patients with myocarditis is performed through the use of immunosuppressants and antiviral drugs in order to suppress inflammatory and autoimmune responses.