Myocardial inflammatory activity and structural injury are discordant in connective tissue disease compared with acute suspected viral myocarditis: a CMR study

In connective tissue diseases (CTD), myocardial T2 elevation is a frequent CMR finding, yet whether it translates into myocardial injury remains uncertain. We compared T2 and late gadolinium enhancement (LGE) between CTD-associated myocardial involvement and acute suspected viral myocarditis, a clinical model in which inflammatory activity and structural injury commonly co-occur in the acute phase, to assess whether the association between myocardial inflammatory activity and structural injury differs between disease contexts.

Patients from two prospective institutional registries were included. Active myocardial inflammation was defined using a study-specific CMR definition based on the T2 component of the updated Lake Louise Criteria, requiring T2 elevation ≥ 40 ms, applied identically in both groups. Inflammatory activity was quantified by myocardial T2 mapping and structural injury by LGE.

A total of 181 patients were included (CTD n = 44; viral myocarditis n = 137). CTD patients were predominantly female (75% vs. 44%; p < 0.001) with comparable age (56 ± 16 vs. 52 ± 18 years; p = 0.172). Despite higher myocardial T2 in CTD (42.5 ± 2.2 vs. 41.0 ± 2.8 ms; p = 0.002; multivariable β = 1.14 ms, 95% CI 0.29-2.0; p = 0.009), structural injury was markedly less pronounced (LGE prevalence was 41% vs. 88%; p < 0.001), while native T1 and ECV did not differ significantly between groups. Acute suspected viral myocarditis was independently associated with higher LGE likelihood (adjusted OR 11.14; 95% CI 4.43-27.98; p < 0.001).

Myocardial T2 elevation in CTD may not be invariably associated with LGE-defined myocardial injury and may carry different implications than in acute suspected viral myocarditis. Disease-specific contextualization of CMR inflammatory markers is warranted.