The caseA 58–year–old man presented to ED because of fever, non–productive cough and worsening dyspnea. The patient’s medical history was unremarkable. On examination there was a hypoxic respiratory failure and the clinical picture rapidly evolved towards a cardiogenic shock characterized by altered mental status and cool extremities. Vital parameters: peripheral blood pressure was of 60/30 mmHg, pulse rate of 126 bpm, respiratory rate of 30 breaths/min, temperature of 38 °C. Two episodes of ventricular fibrillation were resolved by electrical shocks. The nasopharyngeal swab tested positive for COVID–19 on real–time reverse transcriptase–polymerase chain reaction assay. Arterial blood gas analysis showed a severe metabolic acidosis with hyperlactacidaemia (pH 7.26, excess basis–22 mEq/L, lactates 10 mmol/dL) and hypoxaemia. Situation evolved towards an end–organ hypoperfusion associated with multisystem organ failure (MOF). High resolution chest CT demonstrated bilateral ground glass opacities consisting of COVID–19 related interstitial pneumonia. 12–leads ECG demonstrated sinus rhythm with diffuse concave ST–segment elevation. T–T echocardiogram showed: 1) severely thickened LV walls; 2) decreased LV systolic function; 3) segmental wall motion abnormalities consisting of akinesis of the LV distal segments with relatively preserved function at the base; 4) LVEF) of 25%; 5) pericardial effusion. Thickened LV walls meant myocardial inflammatory infiltration/edema and the final diagnosis was FULMINANT COVID–19 related MYOCARDITIS. Patient underwent oro–tracheal intubation+invasive ventilation. An intra–aortic balloon pump (IABP) was placed on top of adrenaline (0.07μg/kg/min), and noradrenaline (0.1μg/kg/min) was added for worsening hypotension (systolic blood pressure: 80/67/60 mmHg). Additional therapy consisted of intravenous high dose diuretics, methyprednisolone, tucilizumab, immunoglobulin, ceftriaxone, remdesivir. After 3 weeks, patient recovered a good respiratory and haemodinamic status, LV wall thicknesses decreased and EF increased to normal values. The final outcome was favorable. DiscussionThe prevalence of fulminant myocarditis among COVID–19 patients is unclear. This simultaneous presentation of fulminant myocarditis and COVID–19 pneumonia favors an alternative pathogenetic pathway with possible acute replication and direct dissemination of the virus through the blood or the lymphatic system from the respiratory tract to the myocardium.
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