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Distinct Cytokine Patterns Identify Acute and Convalescent Myocardial Involvement After Coronavirus Disease 2019: A
David A Zidar1,2,3, Grace A McComsey1,2, Donald D Anthony1,3
1Departments of Pathology and Medicine, Case Western Reserve University School of Medicine.
Insights
Post-COVID-19 heart issues may stem from different inflammation than acute COVID-19 heart injury. Understanding these distinct mechanisms, involving interleukin-18 (IL-18), could guide targeted therapies for long COVID cardiac sequelae.
Area of Science:
- Immunology
- Cardiology
- Infectious Diseases
Background:
- Coronavirus disease 2019 (COVID-19) can lead to cardiac involvement, a significant post-acute sequela.
- The specific immunobiologic mechanisms driving cardiac issues in acute versus convalescent COVID-19 are not fully understood.
Purpose of the Study:
- To investigate the distinct immunobiologic underpinnings of cardiac involvement in acute and convalescent phases of COVID-19.
- To compare inflammatory profiles and cardiac status between acute and post-COVID-19 populations.
Main Methods:
- Integrated analysis of cytokine levels (Tumor Necrosis Factor alpha [TNF-α] and Interleukin-18 [IL-18]).
- Cardiac magnetic resonance imaging (CMR) to assess myocardial inflammation and edema.
- Cardiopulmonary exercise capacity testing.
Main Results:
- Acute cardiac injury was associated with elevated TNF-α but not IL-18.
- Convalescent myocardial inflammation/edema correlated with IL-18 levels, independent of TNF-α.
- Distinct inflammatory profiles were observed between acute and convalescent cardiac involvement.
Conclusions:
- Inflammation is not a uniform process in COVID-19-related cardiac involvement.
- Post-acute cardiac sequelae may arise from mechanisms differing from acute cardiac injury.
- Targeted therapies addressing specific inflammatory pathways (e.g., IL-18) may be crucial for preventing long COVID cardiac complications.
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.
