Cardiac Dysfunction and Myocardial Injury Assessed by Cardiovascular Magnetic Resonance in Symptomatic Patients Recovering from COVID-19 Infection

Background: Previous investigations have highlighted myocardial damage linked to SARS-CoV-2 infection, arising from direct viral effects on cardiac tissue or indirect mechanisms driven by exaggerated immune responses. Cardiovascular magnetic resonance (CMR) imaging represents benchmark modality for identifying cardiac pathology. We aimed to determine prevalence of myocardial damage in a patients who had recently recovered from COVID-19 using CMR and exploring associated risk factors for cardiac impairment. Methods: We prospectively enrolled thirty patients post-COVID-19 recovery (Ten of them were intensive care unit (ICU) admitted) and other thirty (healthy controls) for CMR evaluation, incorporating cine sequences, T1 and T2 mapping, and late gadolinium enhancement (LGE). Quantitative assessments encompassed global ventricular function and regional T1/T2 relaxation time. Results: Relative to controls, post-COVID-19 patients exhibited reduced left ventricular ejection fraction (LVEF), enlarged left ventricular volumes, and elevated native T1 and T2 values. Abnormal CMR features were observed in 24 patients (80%), including increased myocardial T2 (n=22), myocardial LGE (n=17), and pericardial enhancement (n=10). Hospitalization was unnecessary for 66.7% of patients whereas 33.3% of patients required ICU admission. Significant disparities emerged between non-hospitalized and ICU-admitted patients in native T1 mapping (median [IQR]: 1000 [959-1080] ms vs. 1084 [1000-1108] ms; P=0.033), as well as in troponin, D-dimer, and C-reactive protein levels, though native T2 values showed no difference. Conclusion: CMR detected cardiac abnormalities in 80% (24/30) of post-COVID-19 patients, correlating with functional decline and elevated cardiac biomarkers, particularly in severe illness. These observations underscore the importance of continued surveillance for long-term cardiovascular effects of COVID infection.