Abstract

Coronavirus disease 2019 (COVID-19) in children is rarely severe. However, severe courses occur, especially in the presence of risk factors. A minority of children develop pediatric inflammatory multisystem syndrome (PIMS) with substantial morbidity. While the importance of cardiac involvement after PIMS is well established, its role after severe acute COVID-19 remains unclear. We aim to compare cardiac sequelae of children after severe acute COVID-19 using cardiac MRI and compare them with patients after PIMS. For this prospective cohort study, we recruited patients with acute COVID or PIMS in a single center. Clinical follow-up, lab work, ECG, and echocardiography were done within 2 days after disease onset and 3-6 months after discharge. At the last visit 3-6 months later, cardiac MRI (CMR) with late gadolinium enhancement (LGE) was performed to evaluate cardiac sequelae and compare both groups. Data were obtained from n = 14 patients with PIMS and n = 7 patients with severe acute COVID-19. At the start of the respective disease, left ventricular (LV) ejection fraction was reduced in seven patients with PIMS but none in the acute COVID-19 group. Transient mitral valve insufficiency was present in 38% of patients, of whom PIMS accounted for 7/8 cases. Eight patients (38%) with PIMS presented coronary artery abnormalities, with normalization in 7/8 patients. A significant decrease in LV mass index 3-6 months after disease onset was observed in both groups. MRI follow-up revealed non-ischemic myocardial pattern of LGE in 12/21 patients- in all (6/6) after severe acute COVID-19 and in less than half (6/14) after PIMS. Normal body weight-adjusted stroke volumes and end-diastolic volumes were found in 20/21 patients. We show that children suffering from severe acute COVID-19 have a similar, or worse, cardiac risk profile as patients with PIMS. Both patient groups should therefore receive close pediatric cardiac follow-up examinations. Cardiac MRI is the technique of choice, as most patients presented with delayed LGE as a sign of persistent cardiac injury despite normalization of laboratory and echocardiographic findings.

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