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Назва: Targeting endothelial dysfunction for protection from anthracycline-induced cardiotoxicity in patients with acute leukemia and co-morbid ischemic heart disease
Автори: Lymanets, T.
Skrypnyk, I.
Maslova, G.
Скрипник, Ігор Миколайович
Лиманець, Тетяна Володимирівна
Маслова, Ганна Сергіївна
Дата публікації: 2017
Видавець: Hematologica. Journal of the European Hematology Association
Бібліографічний опис: Lymanets T. Targeting endothelial dysfunction for protection from anthracycline-induced cardiotoxicity in patients with acute leukemia and co-morbid ischemic heart disease / T. Lymanets, I. Skrypnyk, G. Maslova // Hematologica : Abstract Book of the 22nd EHA Congress, 22-25 June 2017. – Madrid, 2017. – Vol. 102, Suppl. 1. – P. 678–679.
Короткий огляд (реферат): Cardiotoxicity of chemotherapeutic drugs, in particular anthracycline antibiotics (AA), is one of the biggest problems in treatment of patients with acute leukemia (AL). Chemotherapy with AA is accompanied by systemic endothelial dysfunction, increasing the cardiovascular toxicity risk and promoting vascular complications. Patients with co-morbid ischemic heart disease (IHD) are at extremely high risk of myocardial injury and in need of anthracycline cardiotoxicity (AC) prevention. Aim: To assess the effectiveness of L-arginine in the prevention of endothelial dysfunction as a predictor of acute AC in patients with AL and co-morbid ischemic heart disease. Materials and methods. A total of 66 patients with newly diagnosed acute leukemia (acute lymphoid leukemia – 7 patients, acute myeloid leukemia – 59 patients) and co-morbid ischemic heart disease were included in the study. The cohort consisted of 34 (51.5%) males and 32 (48.5%) females, age of 54–72 years, ECOG I-II. The duration of IHD ranged from 3 to 15 years. Chemotherapy (CT) schemes included AA (doxorubicin). The evaluation of endothelial dysfunction was performed by determining the stable metabolites of nitric oxide – nitrite anions [NO2]- and activity of total NO-synthase in serum of patients before the CT and upon reaching a cumulative dose of AA from 100 to 200 mg/m2 by doxorubicin. The mean total cumulative dose of AA reached 162,04±24,65 mg/m2 and 166,49±27,34 mg/m2 in groups I and II respectively. The study was approved by the local ethical committee and all patients gave a written consent before they were included in the study. Patients were divided into two groups: (n=36) – AL patients treated with CT; II (n=30) – AL patients, whom during the CT in order for prevention of acute AC were given L-arginine hydrochloride 4.2% 100 ml IV the day before and during administration of AA, followed by oral L-arginine aspartate for a month. Results. In the debut of AL prior to the CT in all 66 (100%) patients the increased activity of total NOS in 3.8 times compared with the norm (p˂0,001) was noted, with simultaneously reduced concentration of [NO2]- in 1.5 times relatively normal values (p˂0,05) (Table 1). As a result of two CT courses of remission induction in patients of group I the tendency to reduce the total NOS activity compared with its level before treatment was observed. At the same time the significant decrease of [NO2]- in 1.8 times relatively normal values (p <0.01) and a trend to lower their content in 1.2 times compared with the data before treatment (p>0.05) was noted. These changes constitute the violation of NO-dependent vasodilation mechanism and endothelial dysfunction intensification. Provided achieving low cumulative dose of AA in patients of group II on the background of AC prevention with L-arginine showed a significant decrease in 1.9 times the total NOS activity (p <0.001) with a simultaneous tendency to increase concentration of [NO2]- in 1.3 times (p>0.05) compared to that before treatment. Thus, during the CT with the inclusion of AA without L-arginine in patients with AL and co-morbid IHD we observed the depletion of NO substrate production, accompanied by endothelial dysfunction impairment. The additional appointment of L-arginine on the background of CT can restore synthesis of NO and, respectively, the mechanism of NO-dependent vasodilation, thus reducing the risk of early anthracycline cardiotoxicity development.
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