Background:
Inflammatory heart diseases (IHD) comprise heterogeneous entities with distinct etiologies, resulting in variable structural and functional cardiac alterations. Cardiac magnetic resonance (CMR) imaging has evolved as the non-invasive gold standard for the detection and tissue characterization of IHD. However, differentiating acute viral myocarditis from autoimmune myocarditis secondary to connective tissue disease (CTD) remains challenging using CMR. This study aimed to characterize differences in CMR phenotypes and to identify imaging and clinical parameters associated with left ventricular (LV) systolic dysfunction.
Methods:
We retrospectively analyzed patients with inflammatory heart disease (IHD) from two established registries, including acute myocarditis from the BioCVI registry and autoimmune myocardial involvement in connective tissue disease from the MARCIE registry. Both entities were compared with respect to functional parameters (LV ejection fraction [EF], RVEF, GLS), structural parameters (EDVi, ESVi, myocardial mass), and tissue characteristics (T1-, T2-mapping, LGE mass). Subsequently, linear regression analyses were performed to identify imaging and serological parameters independently associated with LV dysfunction.
Results:
Patients with autoimmune myocardial involvement were more often female (77% vs. 39%, p<0.001), and had fewer heart failure symptoms. Despite higher inflammatory activity (T2 42.2±2.0 vs. 40.5±3.6 ms, p=0.002), CTD patients demonstrated preserved systolic function and less structural myocardial damage, with higher LVEF (58.5±9.9% vs. 47.7±14.7%, p<0.001), lower myocardial mass (51.1±13.5 vs. 58.2±17.4 g/m², p=0.012), and markedly less LGE (1.3±2.1 vs. 3.2±2.8 segments, p<0.001). In multivariable analysis, reduced LVEF was mainly determined by LGE mass (β=−0.38) and NT-proBNP (β=−0.23), followed by myocardial mass (β=−0.21), while T2 showed a weak positive association (β=0.16).
Conclusion:
Despite exhibiting more pronounced myocardial inflammation, patients with CTD demonstrated preserved systolic function and fewer structural alterations compared with those with viral myocarditis. IHD–related systolic dysfunction thus appears to result primarily from irreversible structural remodeling rather than the degree of active inflammation. These findings highlight the potential reversibility of acute inflammatory changes and underline the need for prospective studies to assess their prognostic relevance, particularly in CTD-associated cardiac involvement.
