***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: PURPOSE This study sought to estimate cardiac dysfunction ( CD ) risk for patients receiving trastuzumab ;  to characterize observed CD by severity , treatment , and clinical outcome ; to assess effects of baseline clinical risk factors on CD ; and to assess effects of cumulative doses of anthracyclines and trastuzumab on CD . PATIENTS AND METHODS A retrospective review of records for patients enrolled onto any of seven phase II and III trastuzumab clinical trials was performed . Predefined criteria were used for the diagnosis , and the New York Heart Association functional classification system was used to document CD severity . Product-limit estimates were used to summarize the cumulative anthracycline and trastuzumab doses at the time of CD onset . RESULTS Patients treated with trastuzumab  were found to be at an increased risk for CD . The incidence was greatest in patients receiving concomitant  trastuzumab and anthracycline plus cyclophosphamide ( 27 % ) . The risk was substantially lower in patients receiving paclitaxel and trastuzumab ( 13 % ) or trastuzumab alone ( 3 % to 7 % ) ; however , most of these patients had received prior anthracycline therapy . CD was noted in 8 % of patients receiving anthracycline plus cyclophosphamide and 1 % receiving paclitaxel alone . Most trastuzumab-treated patients developing CD were symptomatic ( 75 % ) , and most improved with st and ard treatment for congestive heart failure ( 79 % ) . CONCLUSION Trastuzumab is associated with an increased risk of CD , which is greatest in patients receiving concurrent anthracyclines . In most patients with metastatic breast cancer , the risk of CD can be justified given the improvement in overall survival previously reported with trastuzumab BACKGROUND The aim of this case-control study was to assess the usefulness of three-dimensional ( 3D ) speckle-tracking echocardiography in the evaluation of global left ventricular ( LV ) myocardial performance in adolescent and adult survivors of childhood cancers . METHODS Fifty-three anthracycline-treated survivors of childhood cancers ( mean age , 18.6 ± 5.1 years ) and 38 controls were studied .  Three-dimensional speckle-tracking echocardiography was performed to assess LV 3D global and segmental strain , time to peak segmental 3D strain , LV torsion , and ejection fraction . LV systolic dyssynchrony index ( SDI ) was calculated as the percentage of the st and ard deviation of times to peak strain of the 16 segments divided by the RR interval . A global performance index ( GPI ) was calculated as ( global 3D strain × torsion)/SDI . The area under the receiver operating characteristic curve was calculated to determine the capability of various echocardiographic indices to discriminate between patients and controls . RESULTS Compared with controls , patients had significantly reduced LV global 3D strain ( P < .001 ) , torsion ( P < .001 ) , and GPI ( P < .001 ) and greater SDI ( P < .001 ) . All except the basal anteroseptal segment in patients had reduced regional 3D strain compared with controls ( P < .05 for all ) . Global 3D strain ( P = .018 ) , SDI ( P = .003 ) , and GPI ( P = .02 ) were correlated with cumulative anthracycline dose . The areas under the curves for GPI , global 3D strain , 1/SDI , torsion , and ejection fraction were 0.92 , 0.79 , 0.79 , 0.79 , and 0.78 , respectively . A GPI cutoff of 10.6 ° /cm had sensitivity of 84.9 % and specificity of 81.6 % of differentiating patients from controls . CONCLUSIONS Three-dimensional speckle-tracking echocardiography enables the derivation of an index of LV global performance that incorporates LV 3D strain , dyssynchrony , and torsion for the sensitive detection of altered LV mechanics in childhood cancer survivors Background Salidroside [ 2-(4-hydroxyphenyl)ethyl-β-D-glucopyranoside ] , one of the most potent ingredients extracted from the plant Rhodiola rosea L. , has been shown to have a cardiovascular protective effect as an antioxidant , and early treatment of epirubicin-induced cardiotoxicity has been the focus of clinical chemotherapy in patients with breast cancer . However , the cardioprotective effects of salidroside on epirubicin-induced cardiotoxicity , especially early left ventricular regional systolic dysfunction , have to date been sparsely investigated . Objective The aim of this study was to investigate the protective effects of salidroside in preventing early left ventricular regional systolic dysfunction induced by epirubicin . Methods Sixty patients with histologically confirmed breast cancer were enrolled . Eligible patients were r and omized to receive  salidroside ( 600 mg/day ; n= 30 ) or placebo ( n = 30 ) starting 1 week before chemotherapy . Patients were investigated by means of echocardiography and strain rate ( SR ) imaging . We also measured plasma concentrations of reactive oxygen species ( ROS ) . All parameters were assessed at baseline and 7 days after each new epirubicin dose of 100 mg/m2 . Results A decline of the SR peak was observed at an epirubicin dose of 200 mg/m2 , with no significant differences between salidroside and placebo ( 1.35 ± 0.36 vs 1.42 ± 0.49/second ) . At growing cumulative doses of epirubicin , the SR normalized only with salidroside , showing a significant difference in comparison with placebo at epirubicin doses of 300 mg/m2 ( 1.67 ± 0.43 vs 1.32 ± 0.53/second , p < 0.05 ) and 400 mg/m2 ( 1.68±0.29 vs 1.40 ± 0.23/second , p < 0.05 ) . Moreover , a significant increase in plasma concentrations of ROS was found with placebo , but they remained unchanged with salidroside . ConclusionS alidroside can provide a protective effect on epirubicin-induced early left ventricular regional systolic dysfunction in patients with breast cancer BACKGROUND The occurrence of chronic anthracycline cardiotoxicity leading to heart failure and even death is a major concern in the treatment of childhood malignancies . Currently , most treatment protocol s use reduced anthracycline doses compared with historical exposure . The long-term effect of these reduced doses on myocardial function has not been well studied . METHODS We examined 56 asymptomatic patients . They all had been treated with anthracyclines at a cumulative dose less than 300 mg/m2 5.2 ( range : 2.0 - 15.2 ) years before the current evaluation . In all patients , st and ard two-dimensional , Doppler echocardiographic measurements , end-systolic wall stress calculation , and color Doppler myocardial imaging data were obtained . From the color Doppler myocardial imaging data , peak systolic myocardial velocities , peak systolic strain rate , and peak systolic strain [ symbol : see text ] were computed . The myocardial acceleration during isovolumetric contraction was measured at the basal left ventricular ( LV ) lateral and right ventricular free wall . Data were compared with 32 age-matched normal controls . RESULTS In asymptomatic patients previously exposed to low-dose anthracycline treatment , several changes in cardiac function were noted : 1 . LV diastolic function was abnormal with a prolonged isovolumetric relaxation time and abnormal pulmonary venous flow patterns . 2 . End-systolic wall stress was increased . 3 . LV annular motion was reduced . 4 . Systolic myocardial deformation was reduced with a significant decrease in both radial and longitudinal peak systolic strain rate and [ symbol : see text ] . CONCLUSIONS Changes in systolic and diastolic function are noted in asymptomatic patients with normal ejection fraction late after low-dose anthracycline treatment . This confirms that sub clinical LV dysfunction is present in patients after low-dose anthracycline treatment during childhood . The long-term significance of these findings warrants further follow-up BACKGROUND Oxidative stress and RAAS play an important role in the occurrence of anthracyclines-induced cardiotoxicity . Telmisartan , an angiotensin II type 1 receptor blocker , inhibits activation of superoxide sources and induces anti-inflammatory effects . METHODS The possible role of telmisartan in preventing myocardial damage induced by epirubicin ( EPI ) was investigated . Forty-nine patients free from cardiovascular diseases affected by a variety of solid cancers were examined . Eligible patients were r and omized to receive telmisartan ( 40 mg/d ; TEL , n = 25 ) or placebo ( PLA , n = 24 ) starting 1 week before chemotherapy . Patients were studied by means of echocardiography , tissue Doppler , and strain and strain rate ( SR ) imaging . We also measured plasma levels of inflammatory and oxidative stress markers . All parameters were assessed at baseline and 7 days after every new EPI dose of 100 mg/m(2 ) . RESULTS An impairment of the SR peak was observed at the EPI dose of 200 mg/m(2 ) , with no significant differences between TEL and PLA ( 1.41 + /- 0.31 vs 1.59 + /- 0.36/s ) . At growing cumulative doses of EPI , SR normalized only in TEL , showing a significant difference in comparison to PLA at EPI doses of 300 mg/m(2 ) ( 1.69 + /- 0.42 vs 1.34 + /- 0.18/s , P < .001 ) and 400 mg/m(2 ) ( 1.74 + /- 0.27 vs 1.38 + /- 0.24/s , P < .001 ) . Moreover , a significant increase in reactive oxygen species and interleukin-6 was found in PLA ; but these remained unchanged in TEL . CONCLUSIONS We confirmed that EPI-induced cardiotoxicity is primarily related to the inactivation of the cardiac antioxidant defenses . In addition , we showed that telmisartan can reduce EPI-induced radical species , antagonize the inflammation , and reverse the early myocardial impairment AIMS The benefits from anthracycline chemotherapy are undermined by potentially life-threatening cardiotoxicity . Transthoracic echocardiography is the most commonly used method for monitoring cardiotoxicity , and centres on the measurement of left ventricular systolic function . The aim of this study was to utilize two-dimensional speckle tracking echocardiography ( 2DSTE ) at baseline and immediately after anthracycline chemotherapy to investigate whether patients with significant changes in systolic function after anthracycline therapy  would also develop alterations in diastolic parameters . METHODS AND RESULTS Fifty-two women with histologically confirmed breast cancer were prospect ively recruited .  Echocardiograms were performed 1 week prior to and 1 week following chemotherapy ( always before adjuvant trastuzumab or thoracic radiotherapy ) . Conventional Doppler , tissue velocity imaging ( TVI ) , and 2DSTE were used to measure diastolic function . 2DSTE measurements included longitudinal diastolic strain , early ( E-Sr ) , and late ( A-Sr ) myocardial strain rate . 2DSTE and left ventricular ejection fraction ( LVEF ) were used to measure longitudinal systolic function . Altered LV diastolic function ( including E-Sr ) was observed in the entire cohort after chemotherapy , with a differential reduction in participants with a post therapy LVEF < 55 % . Pre-chemotherapy systolic strain was found to predict reduced E-Sr post therapy ( P = 0.04 ) . Univariate predictors of E-Sr were LVEF post therapy ( P = 0.049 ) and systolic strain post-therapy ( P = 0.01 ) . In a multivariate analysis , systolic strain after chemotherapy  was the strongest independent predictor ( P = 0.001 ) . CONCLUSION Altered LV diastolic function was observed immediately after the administration of therapeutic doses of anthracycline chemotherapy . Furthermore , our analysis indicates that the changes in diastolic function are associated with reduced systolic function The aim of this study was to describe the acute effects of anthracyclines on left ventricular systolic and diastolic function using different echocardiographic modalities . Thirteen children scheduled to receive anthracyclines were prospect ively studied . They underwent complete 2-dimensional and Doppler echocardiographic evaluations , including tissue Doppler imaging , before the first dose and < 2 hours after each of the first 3 doses of anthracyclines ( dose range 30 to 75 mg/m2 ) . After the first dose , increased end-diastolic wall thickness , decreased wall thickening , and a prolonged myocardial performance index were noted . Parameters of diastolic function changed significantly , with a lower mitral E wave , a decreased E/A ratio , and prolonged isovolumic relaxation time . Also 
    Output:
    
All studies of early myocardial changes with chemotherapy demonstrate that alterations of myocardial deformation precede significant change in left ventricular ejection fraction ( LVEF ) .
Using tissue Doppler-based strain imaging , peak systolic longitudinal strain rate has most consistently detected early myocardial changes during therapy , whereas with speckle tracking echocardiography ( STE ) , peak systolic global longitudinal strain ( GLS ) appears to be the best measure .
A 10 % to 15 % early reduction in GLS by STE during therapy appears to be the most useful parameter for the prediction of cardiotoxicity , defined as a drop in LVEF or heart failure .
In late survivors of cancer , measures of global radial and circumferential strain are consistently abnormal , even in the context of normal LVEF , but their clinical value in predicting subsequent ventricular dysfunction or heart failure has not been explored .
Thus , this systematic review confirms the value of echocardiographic myocardial deformation parameters for the early detection of myocardial changes and prediction of cardiotoxicity in patients receiving cancer therapy