BACKGROUND:Adriamycin (ADR) is a potent chemotherapeutic agent widely used in the treatment of childhood acute lymphoblastic leukemia (ALL); its clinical use is limited owing to its marked cardiotoxicity. The present study investigated the possible protective role of carvedilol on ADR-induced left ventricular dysfunction in children with ALL. METHODS AND RESULTS:Fifty children with newly diagnosed ALL were included in this study. They were divided into 2 equal groups: 1) ADR; and 2) ADR + carvedilol. Patients were evaluated with conventional 2-dimensional echocardiographic examination (2D), pulsed tissue Doppler (PTD), and 2-dimensional longitudinalstrain echocardiography (2DS) before and after therapy. Plasma lactic dehydrogenase (LDH), creatine phosphokinase (CPK), and troponin I levels were also determined before and after therapy. ADR treatment reduced left ventricular systolic dysfunction as assessed by a significant decrease in fractional shortening (FS) (2D) and global peak-systolic strain (GPSS; 2DS). In addition, ADR treatment significantly increased plasma troponin I and LDH. Pretreatment of ADR-treated patients with carvedilol resulted in a significant increase in FS (2D) and GPSS (2DS). Furthermore, carvedilol pretreatment inhibited ADR-induced increase in plasma troponin I and LDH. CONCLUSIONS: These results suggested a protective role of carvedilol against ADR-induced cardiotoxicity.
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BACKGROUND:Adriamycin (ADR) is a potent chemotherapeutic agent widely used in the treatment of childhood acute lymphoblastic leukemia (ALL); its clinical use is limited owing to its marked cardiotoxicity. The present study investigated the possible protective role of carvedilol on ADR-induced left ventricular dysfunction in children with ALL. METHODS AND RESULTS: Fifty children with newly diagnosed ALL were included in this study. They were divided into 2 equal groups: 1) ADR; and 2) ADR + carvedilol. Patients were evaluated with conventional 2-dimensional echocardiographic examination (2D), pulsed tissue Doppler (PTD), and 2-dimensional longitudinal strain echocardiography (2DS) before and after therapy. Plasma lactic dehydrogenase (LDH), creatine phosphokinase (CPK), and troponin I levels were also determined before and after therapy. ADR treatment reduced left ventricular systolic dysfunction as assessed by a significant decrease in fractional shortening (FS) (2D) and global peak-systolic strain (GPSS; 2DS). In addition, ADR treatment significantly increased plasma troponin I and LDH. Pretreatment of ADR-treated patients with carvedilol resulted in a significant increase in FS (2D) and GPSS (2DS). Furthermore, carvedilol pretreatment inhibited ADR-induced increase in plasma troponin I and LDH. CONCLUSIONS: These results suggested a protective role of carvedilol against ADR-induced cardiotoxicity.
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