A 14-year-old female with history of vasovagal syncope presented in cardiogenic shock following one week of weakness, rhinorrhea, congestion, and fatigue. She was hypotensive (90/60s), tachycardic, had dry mucous membranes and abdominal pain. A rapid COVID swab returned positive. An electrocardiogram showed diffuse ST elevation. Troponin level was elevated to 1.32 ng/mL (nl 0.000-0.013ng/mL). Other labs were reassuring without signs of end-organ dysfunction.
An echocardiogram revealed diminished function with a left ventricular ejection fraction (LVEF) of 37% and a large pericardial effusion. She developed tamponade physiology and underwent pericardiocentesis with pericardial drain placement. She developed cardiac arrest and underwent extracorporeal cardiopulmonary resuscitation (ECPR). Post-cannulation echocardiogram revealed LVEF of 20%, LV dilation, and severe mitral regurgitation requiring an apical vent to decompress the left heart. Endomyocardial biopsies were without significant myocardial inflammation. Anti-complement antibodies confirmed complement-mediated myocarditis. She received Remdesivir, IVIG, and eculizumab to target the complement pathway. At discharge, she had regained normal systolic function with LVEF of 57%.
Discussion:
Children < 16 years-old have a 37 times greater risk of developing myocarditis if infected with SARS-CoV-2 as compared to their uninfected peers1,11. MIS-C has been well-described along with its management5,11. There are fewer descriptions of isolated COVID myocarditis. The pathophysiology of COVID-19-associated myocarditis is variable with direct cellular injury and T-cell-mediated cytotoxicity as the predominant postulated factors.9,10,12 Tocilizumab has been used due to its action against interleukin-6, a key contributor to the hyper-inflammatory process.3 Preliminary data from a study comparing patients with and without COVID-19 demonstrated higher levels of complement activation in those affected by COVID-19. 8 For our patient, eculizumab was the agent of choice for its action against complement C5 and its inhibition of the formation of membrane attack complex (MAC).4 Our case suggests efficacy in a targeted therapy against the complement pathway in managing myocarditis in COVID-19.
