In addition to pulmonary involvement, the SARS-CoV-2 infection can impair myocardial function, triggering cases of acute myocarditis. Viral infections are common causes of this condition, which leads to focal or global myocardial inflammation, necrosis, and, in some cases, ventricular dysfunction.(7) The symptoms of myocarditis usually present as chest pain, palpitations, fatigue and syncope. Increased markers of myocardial necrosis, nonspecific ST segment and T wave changes on the electrocardiogram, global hypokinesia and pericardial effusion on the echocardiogram, as well as histological changes in the biopsy, are all used as criteria for the diagnosis of myocarditis.(8) The pathogenesis of this involvement might be associated with the infectious process triggered by SARS-CoV-2, which causes an excessive inflammatory response known as “cytokine storm”.(9) This hyperinflammatory state appears in the advanced stages of critical cases of COVID-19, causing damage to multiple organs.(10) Additionally, during pulmonary infection, fever and tachycardia increase oxygen demand by the cardiac tissue. However, gas exchange impaired by continuous blood flow to lung regions of low ventilation causes a ventilation-perfusion mismatch, resulting in blood hypoxemia and, consequently, in worsening of oxygenation of the cardiac tissue.(11)
Yokoo et al.(4) described the case of a patient diagnosed with COVID-19, who was over 80 years old and had a history of hypertension and ischemic stroke. Laboratory tests showed high levels of troponin T, electrocardiogram showed no signs of ischemia, and echocardiogram showed an ejection fraction of 35%. This patient underwent a Cardiovascular Magnetic Resonance that revealed areas of delayed enhancement with ischemia in the left ventricular base septal wall, as well as diffuse hypokinesia and impaired global systolic function. Furthermore, cases of myocarditis associated with COVID-19 have also been reported in young people(12) and individuals with no cardiovascular risk.(13)
Patients with cardiac injury related to SARS-CoV-2 infection have an acute manifestation of COVID-19 with greater severity, characterized by elevated levels of C-reactive protein and more intense pulmonary involvement,(13) similar to the patient in the case study. The mortality rate is also influenced by the myocardial injury associated with COVID-19, being higher than 50% among patients with cardiac injury compared to 5% among those without it(14)
In the present case report, in addition to myocarditis, the patient presented diffuse cerebral edema. Several mechanisms are proposed for the neurological complications caused by COVID-19. The first hypothesis is based on the hematogenous or axonal retrograde pathway with viral accumulation in endothelial and neuronal cells. Brain damage may also be related to pneumonia caused by SARS-CoV-2, seeing that when the virus passes through the lung parenchyma, it triggers an exaggerated accumulation of neutrophils, increased vascular permeability and the formation of exudates, leading to hypoxemia. In the brain, hypoxia promotes increased anaerobic metabolism, causing vasodilation and cerebral edema.(15) In this regard, the cerebral involvement of the patient in this case probably occurred due to severe hypoxia, which was also related to the occurrence of circulatory shock.