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Cardiac Magnetic Resonance Imaging as a Risk Stratification Tool in COVID-19 Myocarditis
Olga Nedeljkovic-Arsenovic1,2, Arsen Ristić3, Nemanja Đorđević3
1Department of Magnetic Resonance Imaging, Centre for Radiology, University Clinical Centre of Serbia, Pasterova 2, 11000 Belgrade, Serbia.
Insights
COVID-19 can cause myocardial injury, indicated by late gadolinium enhancement (LGE) in cardiac MRI. Elevated troponin, chest pain, and fatigue predict LGE, which may link to persistent symptoms.
Area of Science:
- Cardiology
- Infectious Diseases
- Medical Imaging
Background:
- Persistent symptoms after COVID-19 infection are common in previously healthy individuals.
- Myocardial injury following COVID-19 inflammation is increasingly recognized.
- The link between myocardial damage and long-term post-COVID symptoms requires further investigation.
Purpose of the Study:
- To identify myocardial injury in patients post-COVID-19 inflammation.
- To explore if myocardial damage contributes to persistent symptoms after COVID-19.
- To assess the role of cardiac magnetic resonance (CMR) in evaluating COVID-19 myocarditis outcomes.
Main Methods:
- Retrospective study of 139 patients (Jan-June 2021) without prior cardiac/pulmonary disease.
- Clinical work-up, lab analysis, cardiac ultrasound, and CMR with multi-parametric sequences.
- Analysis of late gadolinium enhancement (LGE) as a marker for myocarditis.
Main Results:
- 39% of patients showed LGE, indicating myocarditis.
- Higher fibrinogen, D-dimer, and troponin levels were observed in patients with LGE.
- Chest pain, fatigue, and elevated troponin independently predicted LGE; septal LGE predicted arrhythmias.
Conclusions:
- Myocardial injury is present in a significant portion of patients after COVID-19.
- CMR is a valuable tool for detecting COVID-19-related myocarditis and assessing risk.
- Myocardial damage may underlie persistent symptoms, warranting further research.
Abstract:
The aim of this retrospective study was to identify myocardial injury after COVID-19 inflammation and explore whether myocardial damage could be a possible cause of the persistent symptoms following COVID-19 infection in previously healthy individuals. This study included 139 patients who were enrolled between January and June 2021, with a mean age of 46.7 ± 15.2 years, of whom 68 were men and 71 were women without known cardiac or pulmonary diseases. All patients underwent clinical work-up, laboratory analysis, cardiac ultrasound, and CMR on a 1.5 T scanner using a recommended protocol for morphological and functional assessment before and after contrast media application with multi-parametric sequences. In 39% of patients, late gadolinium enhancement (LGE) was found as a sign of myocarditis. Fibrinogen was statistically significantly higher in patients with LGE than in those without LGE (4.3 ± 0.23 vs. 3.2 ± 0.14 g/L, p < 0.05, respectively), as well as D-dimer (1.8 ± 0.3 vs. 0.8 ± 0.1 mg/L FEU). Also, troponin was statistically significantly higher in patients with myocardial LGE (13.1 ± 0.4 ng/L) compared to those with normal myocardium (4.9 ± 0.3 ng/L, p < 0.001). We demonstrated chest pain, fatigue, and elevated troponin to be independent predictors for LGE. Septal LGE was shown to be a predictor for arrhythmias. The use of CMR is a potential risk stratification tool in evaluating outcomes following COVID-19 myocarditis.
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