25 Residual structural, functional and myocardial tissue abnormalities in patients with dilated cardiomyopathy in clinical remission

Introduction A subset of patients with dilated cardiomyopathy (DCM) undergo substantial left ventricular reverse remodelling with guideline-directed therapies to the point of normalisation of cardiac size and LVEF. However, it is unclear whether such patients have residual subclinical phenotypic abnormalities compared to healthy volunteers. Materials and Methods The REMIT-DCM study (Reverse remodelling and remission markers in the serial evaluation of DCM) was a prospective single-centre observational cohort study including patients with recent-onset DCM and age-/sex-matched healthy volunteers (HVOLs). Patients with DCM underwent CMR at baseline, 3-months and 12-months. Clinical remission from DCM was defined at 12-months if indexed LV end-diastolic volume (LVEDVi) had normalised, LVEF had risen by ≥10% to LVEF ≥50%, NT-proBNP had fallen below 250ng/L and symptom had resolved (NYHA class I). Results Of 70 patients with DCM (mean age 52±15 years, 79% men, baseline mean LVEF 30%), 67 completed the study and 21 (31%) were in clinical remission at 12-months (DCM-remission). Compared to HVOLs, patients with DCM-remission had lower 12-month LVEF (58±5 vs 65±4%, p<0.001), impaired LV strain (GLS/GCS/GRS: all p<0.001) and higher LVEDVi (p=0.03) and LVESVi (p<0.001). No difference in RV volumes or RVEF were observed, although those with DCM-remission had lower RV GLS than HVOLs (p=0.03). Patients with DCM-remission had higher LV mass index than HVOLs due to 30% greater extracellular matrix mass and 6% greater cellular mass. Of the patients with DCM-remission, 50% had late gadolinium enhancement, predominantly involving the mid-wall and septum. Higher native T1 (p=0.02) and a trend towards higher ECV values (p=0.06) were observed in DCM-remission patients compared to HVOLs. No difference in T2 was observed between groups. Discussion Despite apparent reversal of gross morpho-functional abnormalities, the DCM-remission phenotype remains distinguishable from HVOLs using CMR, with subclinical contractile dysfunction of both ventricles and increased LVMi driven by increased extracellular mass and, to a lesser degree, increased cellular mass. Replacement fibrosis persists in remission and is a common finding despite its association with adverse outcomes. Parametric mapping indicates residual interstitial fibrosis but not myocardial inflammation. Conclusion Patients with DCM-remission have important residual structural, functional and myocardial abnormalities despite marked clinical improvement. These may predispose to future disease relapse. Acknowledgements We thank the Royal Brompton and Harefield Cardiovascular Research Centre nurses and support staff.