Abstract
We sought to identify the immunobiologic underpinnings of cardiac involvement as a postacute sequela of coronavirus disease 2019 (COVID-19) by comparing acute and convalescent populations. For the latter, an integrated analysis of cytokine levels, cardiac magnetic resonance imaging, and cardiopulmonary exercise capacity was performed. Unlike acute cardiac injury, which was associated with heightened tumor necrosis factor alpha (TNF-α) but not interleukin 18 (IL-18), convalescent myocardial inflammation/edema correlated with IL-18 but not TNF-α. Thus, inflammation is not a monolith in relation to cardiac involvement in the setting of COVID-19. Instead, convalescent cardiac involvement may emerge from mechanisms distinct from acute injury, and appropriately targeted therapies may prevent postacute sequalae of COVID-19.