title: Left ventricular function in patients with toxic cardiomyopathy and with idiopathic dilated cardiomyopathy treated with Doxorubicin.
abstract: 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.
authors.affiliation: Tbilisi State Medical University, Department of Internal Medicine.
authors.forename: N A
authors.initials: NA
authors.lastname: Katamadze
authors.forename: K P
authors.initials: KP
authors.lastname: Lartsuliani
authors.forename: M P
authors.initials: MP
authors.lastname: Kiknadze
mesh_terms: D000328:Adult; D000903:Antibiotics, Antineoplastic / Q000008:administration & dosage / Q000009:adverse effects*; D002311:Cardiomyopathy, Dilated / Q000139:chemically induced* / Q000000981:diagnostic imaging / Q000503:physiopathology; D004305:Dose-Response Relationship, Drug; D004317:Doxorubicin / Q000008:administration & dosage / Q000009:adverse effects*; D004452:Echocardiography; D005260:Female; D005500:Follow-Up Studies; D006321:Heart / Q000187:drug effects* / Q000503:physiopathology; D019337:Hematologic Neoplasms / Q000175:diagnosis / Q000188:drug therapy* / Q000503:physiopathology; D006801:Humans; D008297:Male; D008875:Middle Aged; D009367:Neoplasm Staging; D011379:Prognosis; D012307:Risk Factors; D013318:Stroke Volume / Q000187:drug effects* / Q000502:physiology; D016277:Ventricular Function, Left / Q000187:drug effects / Q000502:physiology*
chemical_list: D000903:Antibiotics, Antineoplastic; D004317:Doxorubicin