Myocardial Tissue Characterization in Cardiac Magnetic Resonance Studies of Patients Recovering From COVID-19: A Meta-Analysis.

Background Meta-analysis can identify biological factors that moderate cardiac magnetic resonance myocardial tissue markers such as native T 1 (longitudinal magnetization relaxation time constant) and T 2 (transverse magnetization relaxation time constant) in cohorts recovering from COVID-19 infection. Methods and Results Cardiac magnetic resonance studies of patients with COVID-19 using myocardial T 1 , T 2 mapping, extracellular volume, and late gadolinium enhancement were identified by database searches. Pooled effect sizes and interstudy heterogeneity (I 2 ) were estimated with random effects models. Moderators of interstudy heterogeneity were analyzed by meta-regression of the percent difference of native T 1 and T 2 between COVID-19 and control groups (%ΔT 1 [percent difference of the study-level means of myocardial T 1 in patients with COVID-19 and controls] and %ΔT 2 [percent difference of the study-level means of myocardial T 2 in patients with COVID-19 and controls]), extracellular volume, and the proportion of late gadolinium enhancement. Interstudy heterogeneities of %ΔT 1 (I 2 =76%) and %ΔT 2 (I 2 =88%) were significantly lower than for native T 1 and T 2 , respectively, independent of field strength, with pooled effect sizes of %ΔT 1 =1.24% (95% CI, 0.54%-1.9%) and %ΔT 2 =3.77% (95% CI, 1.79%-5.79%). %ΔT 1 was lower for studies in children (median age: 12.7 years) and athletes (median age: 21 years), compared with older adults (median age: 48 years). Duration of recovery from COVID-19, cardiac troponins, C-reactive protein, and age were significant moderators for %ΔT 1 and/or %ΔT 2 . Extracellular volume, adjusted by age, was moderated by recovery duration. Age, diabetes, and hypertension were significant moderators of the proportion of late gadolinium enhancement in adults. Conclusions T 1 and T 2 are dynamic markers of cardiac involvement in COVID-19 that reflect the regression of cardiomyocyte injury and myocardial inflammation during recovery. Late gadolinium enhancement and to a lesser extent extracellular volume, are more static biomarkers moderated by preexisting risk factors linked to adverse myocardial tissue remodeling.