Abstract
OBJECTIVE: To investigate the occurrence of left ventricular reverse remodeling (LVRR) and its predictive factors in patients with idiopathic or secondary dilated cardiomyopathy (DCM). METHODS: A cross-sectional survey was conducted in a consecutive cohort of patients with DCM admitted in our department between January, 2012 and June, 2016. Based on dynamic echocardiographic findings, LVRR was defined as an absolute increase in left ventricular ejection fraction (LVEF) by ≥100% or an absolute value of LVEF ≥45% with simultaneously an absolute decrease in end-diastolic diameter (LVEDD) ≥10 mm or an absolute value of LVEDD ≤55 mm (in men) or ≤50 mm (in women). The patients with LVRR and those without LVRR were compared for clinical data at admission to identify the potential factors for predicting LVRR. RESULTS: A total of 462 patients, who were followed up for 24.13±15.60 months, were included in this survey. In patients with idiopathic DCM who had LVRR, LVEDD was reduced (P < 0.01), LVEF was improved (P < 0.01) and the mean exercise tolerance was increased significantly (P < 0.01) compared with those in patients without LVRR. Multiple logistic regression analysis showed that a shorter course of heart failure (OR=0.913, P < 0.01), a high systolic blood pressure (OR=1.062, P < 0.01), absence of electrolyte imbalance (OR=0.347, P < 0.01), a low red cell distribution width (OR=0.205, P < 0.01), a smaller LVEDD (OR=0.799, P < 0.01) and a greater LVEF (OR= 1.142, P < 0.01) were independent predictors of LVRR in the idiopathic patients. In patients with secondary DCM, LVEDD was reduced (P < 0.01), LVEF was improved (P < 0.01), and the mean exercise tolerance was increased significantly (P < 0.01) compared with those in patients without LVRR. Multiple logistic regression analysis showed that a shorter course of heart failure (OR= 0.954, P < 0.01), a low red cell distribution width (OR=1.011, P < 0.01), and implementation of etiological treatment (OR=1.073, P < 0.01) were independent predictors of LVRR in patients with secondary DCM. CONCLUSIONS: The exercise tolerance, cardiac structure and function can be reversed in some of the patients with idiopathic or secondary DCM by administration of standard therapy for heart failure and etiological treatment.