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Myocardial Inflammation and Dysfunction in COVID-19-Associated Myocardial Injury
Ludwig T Weckbach1,2,3,4, Adrian Curta5, Stephanie Bieber1,4
1Medical Department I (L.T.W., S.B., A.K., J.B., C.S., S.K., M.O., S. Massberg, J.H., U.G.), Ludwig-Maximilians-University, Munich, Germany.
Insights
COVID-19 patients with myocardial injury show reduced heart strain and myocarditis patterns on MRI. Macrophage increase was noted, but not widespread lymphocytic myocarditis, with some recovery observed.
Area of Science:
- Cardiology
- Infectious Diseases
- Medical Imaging
Background:
- Myocardial injury in COVID-19 is linked to poor outcomes, but its frequency and causes like myocarditis are uncertain.
- Elevated troponin levels indicate myocardial injury, a significant concern in coronavirus disease 2019 (COVID-19) patients.
Purpose of the Study:
- To prospectively assess myocardial injury in hospitalized COVID-19 patients.
- To characterize cardiac changes using echocardiography, cardiac MRI, and endomyocardial biopsy.
Main Methods:
- Prospective assessment of 18 COVID-19 patients with myocardial injury.
- Utilized transthoracic echocardiography, cardiac MRI, and endomyocardial biopsy.
- Analyzed left ventricular ejection fraction, global longitudinal strain, and myocardial tissue characteristics.
Main Results:
- Reduced left ventricular global longitudinal strain (-11.2%) observed.
- Cardiac MRI revealed nonischemic myocardial injury in 83.3% and myocarditis criteria in 38.9%.
- Endomyocardial biopsies showed increased macrophages in all patients, with lymphocytic myocarditis in one; SARS-CoV-2 RNA was undetectable.
Conclusions:
- COVID-19 myocardial injury presents with reduced left ventricular strain and myocarditis patterns on MRI.
- Endomyocardial biopsies indicated macrophage activation rather than predominant lymphocytic myocarditis.
- Functional cardiac improvements were noted during follow-up.
Background:
Myocardial injury, defined by elevated troponin levels, is associated with adverse outcome in patients with coronavirus disease 2019 (COVID-19). The frequency of cardiac injury remains highly uncertain and confounded in current publications; myocarditis is one of several mechanisms that have been proposed.
Methods:
We prospectively assessed patients with myocardial injury hospitalized for COVID-19 using transthoracic echocardiography, cardiac magnetic resonance imaging, and endomyocardial biopsy.
Results:
Eighteen patients with COVID-19 and myocardial injury were included in this study. Echocardiography revealed normal to mildly reduced left ventricular ejection fraction of 52.5% (46.5%-60.5%) but moderately to severely reduced left ventricular global longitudinal strain of -11.2% (-7.6% to -15.1%). Cardiac magnetic resonance showed any myocardial tissue injury defined by elevated T1, extracellular volume, or late gadolinium enhancement with a nonischemic pattern in 16 patients (83.3%). Seven patients (38.9%) demonstrated myocardial edema in addition to tissue injury fulfilling the Lake-Louise criteria for myocarditis. Combining cardiac magnetic resonance with speckle tracking echocardiography demonstrated functional or morphological cardiac changes in 100% of investigated patients. Endomyocardial biopsy was conducted in 5 patients and revealed enhanced macrophage numbers in all 5 patients in addition to lymphocytic myocarditis in 1 patient. SARS-CoV-2 RNA was not detected in any biopsy by quantitative real-time polymerase chain reaction. Finally, follow-up measurements of left ventricular global longitudinal strain revealed significant improvement after a median of 52.0 days (-11.2% [-9.2% to -14.7%] versus -15.6% [-12.5% to -19.6%] at follow-up; P=0.041).
Conclusions:
In this small cohort of COVID-19 patients with elevated troponin levels, myocardial injury was evidenced by reduced echocardiographic left ventricular strain, myocarditis patterns on cardiac magnetic resonance, and enhanced macrophage numbers but not predominantly lymphocytic myocarditis in endomyocardial biopsies.
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