Predictors of functional recovery and fibrosis evolution in myocarditis
A Lobo, M C Almeida, I Neves, N Ferreira, R Teixeira, R Fontes-CarvalhoAbstract
Background
Myocarditis presents with heterogeneous inflammatory, structural, and functional patterns. The relationships between acute myocardial edema, biochemical injury markers, early ventricular dysfunction, and late gadolinium enhancement (LGE)-defined fibrosis remain incompletely understood. Clarifying these interactions may improve the characterization of disease evolution.
Methods
We studied 157 patients with CMR-confirmed myocarditis who underwent standardized cine imaging, T1/T2 mapping, and LGE. Myocardial edema was quantified as the number of T2-positive LV segments; fibrosis was defined as LGE-positive segments at baseline and follow-up. Biochemical markers (troponin T, CRP, NT-proBNP) were analysed. Associations were assessed using Spearman correlation and linear regression. Determinants of LVEF recovery and fibrosis evolution were evaluated with logistic and ordinal regression. Follow-up CMR was available in 63 patients.
Results
Median edema burden was 6 segments (IQR 3–8) and median fibrosis burden was 4 segments (IQR 2–6). Edema correlated with troponin (ρ = 0.67, p < 0.001), NT-proBNP (ρ = 0.41, p < 0.001), and CRP (ρ = 0.27, p = 0.001). Greater edema burden was associated with larger LV end-diastolic volume (p = 0.02) and lower LVEF (p = 0.04). Baseline fibrosis showed no association with edema (p = 0.10) or biochemical markers (all p > 0.10). Median LVEF was 57% (IQR 53–60); among the 21 patients (13%) with LVEF <50%, 17 (81%) recovered to ≥50% on follow-up. LVEF recovery was not associated with edema, baseline fibrosis, or biomarkers (all p > 0.20);. Among the 63 patients with serial CMR, fibrosis regressed in 32%, remained stable in 55%, and progressed in 13%. Neither edema burden nor biochemical injury indices were associated with fibrosis persistence or progression (all p ≥ 0.30).
Conclusions
Acute inflammatory burden correlates with biochemical injury and early functional impact but does not predict the extent or evolution of LGE-defined fibrosis. The persistence of fibrosis in a subset of patients, despite similar inflammatory severity at presentation, suggests that additional determinants such as intrinsic myocardial susceptibility, including potential genetic predisposition, may modulate long-term structural remodeling. Identifying these patients early and understanding the mechanisms underlying persistent fibrosis are key priorities for future research.