Why the study?
Patients with SLE are at risk of cardiac disease including antimalarial-induced cardiomyopathy, but parametric mapping findings and their relationship to antimalarial treatment duration were uncharacterized.
How do CMR T1 and T2 mapping values correlate with antimalarial treatment duration in SLE patients with and without antimalarial-induced cardiomyopathy?
How do CMR T1 and T2 mapping values correlate with antimalarial treatment duration in SLE patients with and without antimalarial-induced cardiomyopathy?
CMR T1 mapping values correlate differently with antimalarial treatment duration in SLE patients depending on the presence of antimalarial-induced cardiomyopathy, suggesting distinct underlying myocardial tissue changes.
Answers are grounded in this paper and cite their sources.
T1/T2 mapping may aid AMIC phenotyping in SLE; leaves open duration-guided monitoring or prospective validation.
PURPOSE: Patients with systemic lupus erythematosus (SLE) are at risk of cardiac disease including antimalarial-induced cardiomyopathy (AMIC). The purpose of this study is to evaluate cardiac magnetic resonance imaging parametric mapping findings in SLE patients with AMIC and investigate the relationship of T1/T2 mapping to antimalarial (AM) treatment duration. MATERIALS AND METHODS: All patients with SLE who had undergone cardiac magnetic resonance imaging with T1/T2 mapping for evaluation of suspected cardiac disease between 2018 and 2021 were evaluated and compared with healthy controls. To facilitate comparison between scanners, T1/T2 values were converted to a z -score using scanner-specific local reference values. Patients were classified into 3 groups: AMIC, myocarditis, and other (no AMIC or myocarditis). RESULTS: Forty-five SLE patients (47±17 y, 80% female; 8 [18%] with AMIC and 7 [16%] with myocarditis) and 30 healthy controls (39±15 y, 60% female) were included. Patients with AMIC had higher T1 and T2 compared with controls ( z -score 1.1±1.3 vs. 0±0.6, P =0.01 and 1.7±1.1 vs. 0±1.0, P <0.01, respectively) and lower values compared with those with myocarditis (3.7±1.6, P <0.01 and 4.0±2.0, P <0.01, respectively). T1 correlated negatively with AM treatment duration in patients without AMIC or myocarditis ( r =-0.36, P =0.048) and positively in patients with AMIC ( r =0.92, P =0.001). AM treatment duration did not correlate significantly with T1 in patients with myocarditis or with T2 in any group. CONCLUSIONS: The relationship between T1 and AM treatment duration differed between groups. Native T1 decreases with longer treatment in patients without AMIC or myocarditis, possibility due to glycosphingolipid accumulation. In patients with AMIC, increasing T1 with longer treatment could reflect fibrosis.
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Shalmon et al. (2023) studied this question.
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