LAUSR

In nonischemic dilated cardiomyopathy (DCM), diagnosis and prognosis is based on left ventricular function. Although concomitant right ventricular (RV) dysfunction is frequently observed, the underlying mechanism is currently not fully understood. We aimed to describe the characteristics of right ventricular function in DCM patients with cardiac magnetic resonance (CMR) imaging using cine and late-gadolinium enhancement (LGE) imaging. Patients with DCM and left ventricular (LV) dysfunction (ejection fraction (EF) <50%) on LGE-CMR were included prospectively. LV and RV volumes and function were quantified and RV systolic dysfunction was defined as RV ejection fraction (RVEF)<45%. The presence and pattern of LGE were assessed visually and the extent was quantified using the full-width half maximum method. Septal midmyocardial LGE pattern was defined as midwall striae or hinge-point myocardial hyperenhancement. Moreover, left atrial (LA) volumes were calculated using the bi-plane area-length method. The study included 214 DCM patients (42% female, age 58±14 years) with a mean LVEF of 34±12% and RVEF of 46±12%. RV systolic dysfunction was present in 39% and was associated with the presence of septal midwall LGE (OR 1.96 (95% CI 1.09–3.54) p=0.026). In patients with RV dysfunction, LV dilation was more severe (LV end diastolic volume (EDV) 242±97mL vs. 212±58mL, p=0.011) and LVEF was lowere (26±12% vs. 39±8%, p<0.001) (figure A). There was a weak correlation between septal LGE amount and LVEDV and RVEDV (respectively r=0.36, p=0.003 and r=0.35, p=0.005) In patients with RV dysfunction, left atrial volumes were enlarged (56±23mL/m2 vs. 46±14mL/m2, p<0.001) and LA emptying fraction was moderately correlated to RVEF (figure B), also after exclusion of patients with a history of atrial fibrillation. RVEF in DCM patients In DCM, reduced RVEF predominantly occurred in patients with a) LVEF lower than 30%, b) septal midwall enhancement, indicating progressive LV remodeling, c) LA dilation and d) LA dysfunction. This suggests that RV dysfunction in advanced DCM is drive by LV diastolic dysfunction resulting in increased afterload of the RV.