Fibrosis as detected by CMR is a frequent feature of LVH, regardless of its cause, and depends on the severity of LV remodeling. As LGE emerges as a useful tool for risk stratification also in nonischemic heart diseases, our findings have the potential to individualize treatment strategies.

A comprehensive CMR approach is a useful tool to monitor the reversible and irreversible myocardial tissue injuries over the course of myocarditis and to differentiate acute from healed myocarditis in patients with still-preserved ejection fraction.

Background— Cardiovascular magnetic resonance based on the Lake Louise Criteria is used to make the diagnosis of acute myocarditis. Novel quantitative parametric mapping techniques promise to overcome some of its limitations. We aimed to evaluate quantitative cardiovascular magnetic resonance to detect and monitor acute myocarditis. Methods and Results— Eighteen patients with clinical diagnosis of acute myocarditis (25 years [23–38 years]; 78% males) were prospectively enrolled and repeatedly underwent cardiovascular magnetic resonance at 1.5 T seven days (5–10 days) after symptom onset (FU0), after 5 weeks (FU1), and after 6 months (FU2). Eighteen age- and sex-matched healthy subjects served as controls. Cardiovascular magnetic resonance included imaging of edema, hyperemia, necrosis, and fibrosis using semiquantitative T2-weighted spin echo, T2 mapping, and T1 mapping before and 3 and 10 minutes after gadobutrol administration. Extracellular volume for diffuse and late gadolinium enhancement for focal fibrosis were assessed. Compared with controls, patients had significantly higher global T2 times at FU0 (55.1 ms [53.3–57.2 ms] versus 50.2 ms [49.2–52.0 ms]; P <0.001) and at FU1 (52.0 ms [52.0–53.2 ms]; P =0.007), which normalized at FU2 (50.9 ms [49.6–53.3 ms]; P =0.323). Global native T1 times in patients were elevated acutely (1004 ms [988–1048 ms] versus 975 ms [957–1004 ms]; P =0.002) and remained elevated throughout the follow-up (FU1: 998 ms [990–1027 ms]; P =0.014; FU2: 1000 ms [972–1027 ms]; P =0.044). Global extracellular volume fraction was statistically not different between patients and controls ( P =0.057). 77.8% (14/18) of patients had focal late gadolinium enhancement. T2 ratio was significantly elevated in patients with myocarditis at FU0 (2.2 [2.0–2.3] versus 1.6 [1.5–1.7]; P <0.001). The difference decreased during follow-up (FU1: 1.9 [1.7–1.9]; P =0.001 and FU2: 1.7 [1.7–1.8]; P =0.053). The diagnostic accuracy to discriminate between patients with acute myocarditis and healthy controls was 86% for T2>52 ms, 78% for native T1>981 ms, 74% for extracellular volume fraction >0.24, and 100% for T2 ratio >1.9. Conclusions— Although both T2 and T1 mapping reliably detected acute myocarditis, only T2 mapping discriminated between acute and healed stages, underlining the incremental value of T2 mapping.