Katamadze N A, Lartsuliani K P, Kiknadze M P
Tbilisi State Medical University, Department of Internal Medicine.
Georgian Med News. 2009 Jan(166):43-8.
Aim of the study was to investigate LV structural and functional parameters in doxorubicin chemotherapy and idiopathic dilated cardiomyopathy as well as to study dynamics of LV systolic-diastolic dysfunction in relation to the increasing doxorubicin dosage. Patients with malignant blood diseases (with non-Hodgkin's, Hodgkin's lymphoma and chronic lymphatic leukaemia) and patients with idiopathic dilated cardiomyopathy were investigated. Patients were divided into 2 groups. The first group included 49 patients (25 men and 24 women, average age was 41.2+/-2.1) with malignant blood diseases. The second group consisted of 50 patients with idiopathic dilated cardiomyopathy (39 men and 11 women, average age was 38.8+/-9.36). Patients were divided into three subgroups according to the dose of administration of doxorubicin: I subgroup--232.2+/-5.8 mg/m(2), II subgroup--388+/-15.3 mg/m(2) and III subgroup--533.1+/-13.6 mg/m(2). The LV systolic-diastolic function was evaluated twice using echo CG. Consistent dose-dependent evolution of doxorubicin cardio toxicity was observed, which eventually resulted in development of anthracycline myocardiopathy. Doxorubicin cardio toxicity is evident as early as at low total doses (232 mg/m(2)); at a "critical dose" (356-388 mg/m(2)) LV diastolic dysfunction with clinical signs of HF develops; at a total dose of 533 mg/m(2) anthracycline dilated myocardiopathy with LV systolic-diastolic dysfunction and clinical signs of HF develops in 100% of cases. In anthracycline myocardiopathy, LV undergoes the same structural and functional mass index >120 g/m(2) and idiopathic dilated myocardiopathy: LV eccentric hypertrophy (II type LV remodelling with myocardial mass index >120 g/m(2) and relative thickness of LV posterior wall <0.44); decreased LV systolic-diastolic dimensions/volumes; LV diastolic dysfunction of the restrictive type. Etiologic factor is not so important for remodelling of left ventricle, which is the basis of clinically manifested dilated cardiomyopathy.
本研究的目的是调查多柔比星化疗和特发性扩张型心肌病患者的左心室结构和功能参数，以及研究左心室收缩 - 舒张功能障碍随多柔比星剂量增加的动态变化。对患有恶性血液病（非霍奇金淋巴瘤、霍奇金淋巴瘤和慢性淋巴细胞白血病）的患者和特发性扩张型心肌病患者进行了研究。患者分为两组。第一组包括49例患有恶性血液病的患者（25名男性和24名女性，平均年龄为41.2±2.1岁）。第二组由50例特发性扩张型心肌病患者组成（39名男性和11名女性，平均年龄为38.8±9.36岁）。根据多柔比星的给药剂量，患者被分为三个亚组：I亚组——232.2±5.8mg/m²，II亚组——388±15.3mg/m²，III亚组——533.1±13.6mg/m²。使用超声心动图对左心室收缩 - 舒张功能进行了两次评估。观察到多柔比星心脏毒性呈剂量依赖性持续演变，最终导致蒽环类心肌病的发生。多柔比星心脏毒性早在低总剂量（232mg/m²）时就很明显；在“临界剂量”（356 - 388mg/m²）时，会出现伴有心力衰竭临床症状的左心室舒张功能障碍；在总剂量为533mg/m²时，100%的病例会发生伴有左心室收缩 - 舒张功能障碍和心力衰竭临床症状的蒽环类扩张型心肌病。在蒽环类心肌病中，左心室经历与特发性扩张型心肌病相同的结构和功能变化：左心室质量指数>120g/m²且为左心室偏心肥厚（II型左心室重构，心肌质量指数>120g/m²且左心室后壁相对厚度<0.44）；左心室收缩 - 舒张维度/容积减小；限制性左心室舒张功能障碍。病因因素对作为临床表现为扩张型心肌病基础的左心室重构并非十分重要。
