Key result
Acute viral myocarditis linked to ~11.1-fold higher odds of LGE injury versus connective tissue disease.
Why the study?
Myocardial T2 elevation is a frequent CMR finding in connective tissue diseases (CTD), yet whether it translates into structural myocardial injury in the same manner as acute suspected viral myocarditis remains uncertain.
Does the association between myocardial inflammatory activity (T2 elevation) and structural injury (LGE) on CMR differ between patients with connective tissue disease-associated myocardial involvement and those with acute suspected viral myocarditis?
Cross-Sectional (n=181)
Blinded image analysis
No
Does the association between myocardial inflammatory activity (T2 elevation) and structural injury (LGE) on CMR differ between patients with connective tissue disease-associated myocardial involvement and those with acute suspected viral myocarditis?
Myocardial T2 elevation in connective tissue disease is associated with a significantly lower prevalence of LGE-defined structural injury compared to acute suspected viral myocarditis, highlighting the need for disease-specific interpretation of CMR inflammatory markers.
CMR may reveal distinct injury patterns between viral myocarditis and CTD; leaves open differential diagnostic implications.
Background and aim 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. Methods 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. Results 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). Conclusion 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.
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Vietheer et al. (2026) conducted a cross-sectional in Active myocardial inflammation (connective tissue disease vs. acute suspected viral myocarditis) (n=181). Acute suspected viral myocarditis vs. Connective tissue disease-associated myocardial involvement was evaluated on Presence of late gadolinium enhancement (LGE)-defined myocardial injury (OR 11.14, 95% CI 4.43-27.98, p=<0.001). Acute suspected viral myocarditis had a higher likelihood of LGE injury vs connective tissue disease (88% vs 41%; adjusted OR 11.14, p<0.001) despite lower T2 values (41.0 vs 42.5 ms; p=0.002).
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