***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: Doxorubicin ( Dox ) , a mainstay of adjuvant breast cancer treatment , is associated with cardiac toxicity in the form of left ventricular dysfunction ( LVD ) , LV diastolic dysfunction , or LV systolic dysfunction . Study objectives were to evaluate the prevalence of LVD in long-term breast cancer survivors treated with Dox  and determine if brain-type natriuretic peptide ( BNP ) may help identify patients at risk for LVD . Patients who participated in prospect i ve clinical trials of adjuvant Dox-based chemotherapy for breast cancer with a baseline left ventricular ( LV ) ejection fraction evaluation from 1999 to 2006 were retrospectively identified from the St Vincent ’s University Hospital data base . Patients were invited to undergo transthoracic echocardiography , BNP analysis , and cardiovascular ( CV ) risk factor assessment . LVDD was defined as left atrial volume index > 34 mL/m2 and /or lateral wall E prime < 10 m/s , and LVSD as LVEF < 50 % . Of 212 patients identified , 154 participated , 19 patients had died ( no cardiac deaths ) , and 39 declined . Mean age was 60.7 [ 55:67 ] years . A majority of the patients ( 128 , 83 % ) had low CV risk ( 0/1 risk factors ) , 21 ( 13.6 % ) had 2 RFs , and 5 ( 3.2 % ) ≥3 RFs . BMI was 27.2 ± 4.9 kg/m2 .  Median Dox dose was 240 mg/m2 [ 225–298 ] ; 92 patients ( 59.7 % ) received ≤240 mg/m2 and 62 ( 40.3 % ) > 240 mg/m2 . Baseline LVEF was 68.2 ± 8 % . At follow-up of 10.8 ± 2.2 years , LVEF was 64.4 ± 6 % . Three ( 1.9 % ) subjects had LVEF < 50 % and one ( 0.7 % ) had LVDD  . Dox > 240 mg/m2 was associated with any LVEF drop . BNP levels at follow-up were 20.3 pg/ml [ 9.9–36.5 ] and 21.1 pg/ml [ 9.8–37.7 ] in those without LVD and 61.5 pg/ml [ 50–68.4 ] in those with LVD ( p = 0.04 ) . Long-term prospect i ve data describing the impact of Dox on cardiotoxicity are sparse . At over 10 years of follow-up , decreases in LVEF are common , and dose related , but LVD as defined is infrequent ( 2.6 % ) . Monitoring with BNP for sub clinical LVD needs further evaluation AIM To evaluate the effectiveness of L-arginine in the prevention of endothelial dysfunction , which may be a predictor of anthracycline-induced myocardial injury , in patients with acute leukemia ( AL ) on the background of anthracycline antibiotics low cumulative doses from 100 to 200 mg/m2 . MATERIAL S AND METHODS A total of 81 adult AL patients ( 38 males and 43 females with the age of 16 - 59 years ) were studied . The patients were divided into two groups : group I ( n = 34 ) , AL patients treated with chemotherapy ( CT ) and L-arginine hydrochloride ; group II ( n = 47 ) - AL patients treated with CT only .  Cardiac evaluation and endothelial function assessment were performed at baseline and after second CT .  Electrocardiography ( ECG ) parameters , lipid peroxidation activity , antioxidant protection and NO system state were evaluated . RESULTS The bioelectric activity abnormalities of the myocardium were observed in studied patients with low cardiac risk after induction CT . In case of L-arginine administration , only minimal daily ECG changes were recorded . A significant difference in the lipid peroxidation and antioxidant defense system activity in patients of groups I and II was determined . We noticed deepening of endothelial dysfunction on the background of cytostatic therapy with anthracycline antibiotics compared with baseline values in patients of group II . It was found that prophylactic L-arginine increases superoxide dismutase level and reduces the total NOS activity due to its inducible isoform . CONCLUSION The leading factor of anthracycline-induced cardiotoxicity is the imbalance between free radical generation and their inactivation that leads to endothelial dysfunction development . L-arginine eliminates the prooxidant-antioxidant imbalance and improves the endothelial function BACKGROUND Anthracycline ( ANT ) chemotherapy is associated with cardiotoxicity . Prevention with β-blockers remains controversial . OBJECTIVES This prospect i ve , r and omized , double-blind , placebo-controlled study sought to evaluate the role of carvedilol in preventing ANT cardiotoxicity . METHODS The authors r and omized 200 patients with HER2-negative breast cancer tumor status and normal left ventricular ejection fraction ( LVEF ) referred for ANT ( 240 mg/m2 ) to receive carvedilol or placebo until chemotherapy completion . The primary endpoint was prevention of a ≥10 % reduction in LVEF at 6 months . Secondary outcomes were effects of carvedilol on troponin I , B-type natriuretic peptide , and diastolic dysfunction . RESULTS Primary endpoint occurred in 14 patients ( 14.5 % ) in the carvedilol group and 13 patients ( 13.5 % ) in the placebo group ( p = 1.0 ) . No differences in changes of LVEF or B-type natriuretic peptide were noted between groups . A significant difference existed between groups in troponin I levels over time , with lower levels in the carvedilol group ( p = 0.003 ) . Additionally , a lower incidence of diastolic dysfunction was noted in the carvedilol group ( p = 0.039 ) . A nonsignificant trend toward a less-pronounced increase in LV end-diastolic diameter during the follow-up was noted in the carvedilol group ( 44.1 ± 3.64 mm to 45.2 ± 3.2 mm vs. 44.9 ± 3.6 mm to 46.4 ± 4.0 mm ; p = 0.057 ) . CONCLUSIONS In this largest clinical trial of β-blockers for prevention of cardiotoxicity under contemporary ANT dosage , the authors noted a 13.5 % to 14.5 % incidence of cardiotoxicity . In this scenario , carvedilol had no impact on the incidence of early onset of LVEF reduction . However , the use of carvedilol result ed in a significant reduction in troponin levels and diastolic dysfunction . ( Carvedilol Effect in Preventing Chemotherapy-Induced Cardiotoxicity [ CECCY ] ; NCT01724450 ) BACKGROUND Pirarubicin ( tetrahydropyranyl-adriamycin : THP ) is a derivative of doxorubicin with reportedly less cardiotoxicity in adults . However no studies of cardiotoxicity in children treated with THP have been reported . This study was performed to assess the THP-induced cardiotoxicity for children with acute lymphoblastic leukemia ( ALL ) . PATIENTS AND METHODS This study comprised 61 asymptomatic patients aged from 7.6 to 25.7 years old . Median follow-up time after completion of anthracycline  treatment was 8.1 years ( range : 1.7 - 12.5 ) . The cumulative dose of THP ranged from 120 to 740 mg/m(2 ) with a median of 180 mg/m(2 ) . Patients underwent electrocardiogram ( ECG ) , echocardiography , the 6-min walk test ( 6MWT ) , and measurements of serum brain natriuretic peptide ( BNP ) before and after exercise . RESULTS All subjects showed normal left ventricular function assessed by echocardiography . Ventricular premature contraction in Holter ECG and reduced exercise tolerance in the 6MWT were detected in 2/46 ( 3.3 % ) and 5/41(12.2 % ) , respectively . Abnormal BNP levels were detected in 6/60 ( 10 % ) both before and after exercise . The cumulative dose of THP was significantly correlated with BNP levels after exercise ( r = 0.27 , P = 0.03 ) , but not with any other cardiac measurements . Further analysis revealed that subjects with a high cumulative dose ≧300 mg/m(2 ) had significantly higher BNP levels after exercise compared with subjects with a low cumulative dose < 300 mg/m(2 ) ( P = 0.04 ) . CONCLUSIONS No significant cardiac dysfunction was detected in long-term survivors who received THP treatment . The use of post-exercise BNP level to indicate high cardiotoxicity risk should be verified by further study BACKGROUND The use of antracycline ( ANT ) in breast cancer has been associated with adverse cardiac events . Two-dimensional ( 2D ) strain imaging ( SI ) can provide a more sensitive measure of altered left ventricular ( LV ) systolic function . We aim ed to evaluate the preventive effect of carvedilol administration assessed by SI in a patient with breast cancer treated with ANT .  METHODS Patients receiving ANT  were r and omly assigned to the carvedilol- or placebo-receiving group . Each received an echocardiographic examination with conventional 2D echocardiography , pulsed tissue Doppler , and 2D SI prior to and 6 months post ANT treatment . RESULTS During the 6-month follow-up period there were no patient deaths or interrupted chemotherapy treatments due to doxorubicin-induced cardiotoxicity . Both left ventricular ejection fraction ( LVEF ) and fractional shortening ( FS ) were within normal limits for all patients before and after ANT therapy . EF , FS and LV dimensions were measured using M-mode echocardiography and found to be similar in both groups before and after ANT therapy . The mean EF , FS , and LV echocardiograph baseline and control dimensions were similar in both groups after 6 months . Though baseline SI parameters were similar between the groups , there was a significant decrease in LV basal septal and basal lateral peak systolic strain in the control group compared to the carvedilol group . CONCLUSIONS These results indicate that carvedilol has a protective effect against the cardiotoxicity induced by ANT Purpose : Anthracyclines ( ANTs ) are a class of active antineoplastic agents with topoisomerase-interacting activity that are considered the most active agents for the treatment of breast cancer . We investigated the efficacy of carvedilol in the inhibition of ANT-induced cardiotoxicity . Methods : In this r and omized , single-blind , placebo-controlled study , 91 women with recently diagnosed breast cancer undergoing ANT therapy  were r and omly assigned to groups treated with either carvedilol ( n = 46 ) or placebo ( n = 45 ) . Echocardiography was performed before and at 6 months after r and omization , and absolute changes in the mean left ventricular ejection fraction , left ventricular end diastolic volume , and left ventricular end systolic volume were determined . Furthermore , the percentage change in the left atrial ( LA ) diameter and other variables of left ventricular ( LV ) diastolic function , such as transmitral Doppler parameters , including early ( E wave ) and late ( A wave ) diastolic velocities , E/A ratio and E wave deceleration time , pulmonary venous Doppler signals , including forward systolic ( S wave ) and diastolic ( D wave ) velocities into LA , late diastolic atrial reversal velocity , and early diastolic tissue Doppler mitral annular velocity ( e ' ) were measured . In addition , tissue Doppler mitral annular systolic ( s ' ) velocity , as a marker of early stage of LV systolic dysfunction , E/e ' ratio , as a determinant of LV filling pressure , and troponin I level , as a marker of myocardial necrosis were measured . Results : At the end of follow-up period , left ventricular ejection fraction did not change in the carvedilol group . However , this parameter was significantly reduced in the control group ( P < 0.001 ) . Echocardiography showed that both left ventricular end systolic volume and LA diameter were significantly increased compared with the baseline measures in the control group . In pulse Doppler studies , pulmonary venous peak atrial reversal flow velocity was significantly increased in the control group . Moreover , a significant decrease in the mitral annuli early diastolic ( e ' ) and peak systolic ( s ' ) velocities and a significant increase in the E ( the peak early diastolic velocity)/e ' ratio in the control group were also observed . However , none of these variables were adversely changed at the end of follow-up in the carvedilol group . Furthermore , the TnI level was significantly higher in the control group than in the carvedilol group ( P = 0.036 ) at 30 days after the initiation of chemotherapy . Conclusions : Prophylactic use of carvedilol may inhibit the development of anthracycline-induced cardiotoxicity , even at low doses OBJECTIVE To investigate the effect of low-dose carvedilol combined with c and esartan 
    Output:
    
Further analysis of echocardiographic parameters and biomarkers showed weak evidence of improvement in diastolic function and troponin I level by carvedilol administration .
Conclusion Preventive use of carvedilol in patients undergoing anthracycline-based chemotherapy may be associated with a reduced incidence of LVSD , higher LVEF value , better diastolic function , and lower troponin I level .
Die weitere Analyse echokardiographischer Parameter und Biomarker zeigte eine schwache Evidenz für die Verbesserung der diastolischen Funktion und des Troponin-I-Spiegels durch Gabe von Carvedilol .