Coronaviruses are single-stranded RNA viruses that are widely distributed in humans and other mammals. Although most coronavirus infections in humans are mild, they have recently caused 2 major pandemics: severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome (MERS), with mortality rates of 10% and 37%, respectively. 1 SARS coronavirus 2 (SARS-CoV-2) is a type of coronavirus first discovered and isolated in December 2019 in Wuhan, central China, that is the cause of the current pandemic known as COVID-19. Common symptoms of the disease are fever, cough, myalgia, and shortness of breath. The most serious complications include acute respiratory distress syndrome (ARDS), cardiac injury, and secondary superinfection.

The pathophysiology of this virus is still unknown. Various studies indicate that patients infected with COVID-19 have high concentrations of interleukin (IL)-1 beta, interferon (IFN) gamma, IFN-inducible protein (IP)-10, and monocyte chemoattractant protein (MCP)-1. It has been shown that patients with severe illness have higher concentrations of granulocyte colony-stimulating factor (GCSF), IP-10, MCP-1, macrophage inflammatory protein (MIP)-1A, and tumor necrosis factor (TNF) alpha, indicating that the severity of the illness could be determined by cytokine storm. 2 Patients infected by COVID-19 with cardiac injury have noticeably higher plasma concentrations of IL-6, 3, 4 N-terminal fraction of pro–brain natriuretic peptide (NT-proBNP), and cardiac troponins (cTnI/T). Because cytokine storm is also the main pathophysiologic mechanism in fulminant myocarditis, it is reasonable to consider heart damage due to COVID-19. The etiology of myocarditis is highly varied and includes a wide range of infectious agents, systemic diseases, medications, and toxins. The literature on myocarditis due to coronaviruses is scant, but cardiac injury seems to be more common in patients infected by COVID-19 than in patients infected by other coronaviruses. 5 We describe the case of a 59-year-old woman with a history of hypertension, cervical degenerative arthropathy, chronic lumbar radiculopathy, lymph node tuberculosis diagnosed due to erythema nodosum, and migraine. Most notably, the patient’s regular therapy included candesartan 32 mg/d. In March 2020 the patient presented to the Emergency Department due to a feverish feeling that had lasted 5 days, accompanied by squeezing anginal chest pain in the absence of respiratory symptoms. On arrival, O2 saturation was 96% with nasal cannula at 2 L/min, and blood pressure was 75/53 mmHg. Physical examination revealed signs of peripheral hypoperfusion with normal pulmonary auscultation. Despite fluid overloading and norepinephrine, the patient remained hypotensive with signs of hypoperfusion (cool skin and elevated lactic acid at 3.9 mmol/L). Electrocardiography showed