| 原发性和继发性扩张型心肌病患者心脏结构和功能发生逆转的相关因素 |
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| 引用本文： | 蔡瀚,方周菲,翁智远,晋学庆. 原发性和继发性扩张型心肌病患者心脏结构和功能发生逆转的相关因素[J]. 南方医科大学学报, 2018, 38(1): 81 |
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| 作者姓名： | 蔡瀚 方周菲 翁智远 晋学庆 |
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| 摘 要： | 目的探讨原发性和继发性扩张型心肌病患者心脏结构和功能发生逆转的发生率及其预测因素。方法采用回顾性研究方法，入选2012年1~2016年6月心血管内科住院的扩张型心肌病（DCM）患者462例，通过动态监测超声心动图结果，定义左心室射血分数（LVEF）绝对值提高≥100%，或LVEF 绝对值≥45%，且左心室舒张末期内径（LVEDD）绝对值降低≥10 mm，或LVEDD绝对值≤55 mm（男性）和≤50 mm（女性）为左心室逆重构（LVRR）。根据是否发生LVRR分为LVRR组和未LVRR组，收集患者首次入院（基线）的临床特征并分析LVRR的预测因素。结果462例患者纳入本研究，随访时间（24.13±15.60）月，在原发性扩张型心肌病患者中，与未LVRR组比，LVRR组LVEDD显著下降（P<0.01）、LVEF显著增加（P<0.01）、随访期间平均运动耐量显著增加（P<0.01）。多变量Logistic 回归分析结果提示，基线心衰病史短（OR=0.913，P<0.01）、收缩压高（OR=1.062，P<0.01）、未合并电解质紊乱比例高（OR=0.347，P<0.01）、红细胞分布宽度低（OR=0.205，P<0.01）、LVEDD小（OR=0.799，P<0.01）及LVEF高（OR=1.142，P<0.01）与发生LVRR相关。在继发性DCM患者中，与未LVRR组比，LVRR组LVEDD显著下降（P<0.01）、LVEF显著增加（P<0.01）、随访期间平均运动耐量显著增加（P<0.01）。基线心衰病史短（OR=0.954，P<0.01）、红细胞分布宽度低（OR=1.011，P<0.01）、住院期间是否行病因干预（OR=1.073，P<0.01）与发生LVRR相关。结论部分原发性和继发性扩张型心肌病患者经标准抗心衰药物治疗和病因干预后，运动耐量改善，心脏结构和功能可以发生逆转。
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Predictive factors of left ventricular reverse remodeling in patients with idiopathic orsecondary dilated cardiomyopathy |
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| Abstract: | Objective To investigate the occurrence of left ventricular reverse remodeling (LVRR) and its predictive factors inpatients with idiopathic or secondary dilated cardiomyopathy (DCM). Methods A cross-sectional survey was conducted in aconsecutive cohort of patients with DCM admitted in our department between January, 2012 and June, 2016. Based on dynamicechocardiographic findings, LVRR was defined as an absolute increase in left ventricular ejection fraction (LVEF) by ≥100% oran absolute value of LVEF ≥45% with simultaneously an absolute decrease in end-diastolic diameter (LVEDD) ≥10 mm or anabsolute value of LVEDD ≤55 mm (in men) or ≤50 mm (in women). The patients with LVRR and those without LVRR werecompared 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 ofheart 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 wasreduced (P<0.01), LVEF was improved (P<0.01), and the mean exercise tolerance was increased significantly (P<0.01) comparedwith 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. Conclusion The exercise tolerance, cardiacstructure and function can be reversed in some of the patients with idiopathic or secondary DCM by administration ofstandard therapy for heart failure and etiological treatment. |
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