Left ventricular function in patients with toxic cardiomyopathy and with idiopathic dilated cardiomyopathy treated with Doxorubicin.

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.