***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: The objective of this study was to assess the effect of coenzyme Q10 ( CoQ10 ) as supplementation to conventional antifailure drugs on quality of life and cardiac function in children with chronic heart failure due to dilated cardiomyopathy ( DCM ) . The study was an open-label prospect i ve study performed in two of the largest pediatric centers in Thail and from August 2000 to June 2003 . A total of 15 patients with idiopathic chronic DCM were included , with the median age of 4.4 years ( range , 0.6 - 16.3 ) . Presenting symptoms were congestive heart failure in 12 cases ( 80 % ) , cardiogenic shock in 2 cases ( 13.3 % ) , and cardiac arrhythmia in 1 case ( 6.7 % ) . Sixty-one percent of patients were in the New York Heart Association functional class 2 ( NYHA 2 ) , 31 % in NYHA 3 , and 8 % in NYHA 4 . Cardiothoracic ratio from chest x-ray , left ventricular ejection fraction , and left ventricular end diastolic dimension in echocardiogram were 0.62 ( range , 0.55 - 0.78 ) , 30 % ( range , 20 - 40 ) , and 5.2 cm ( range , 3.8 - 6.5 ) , respectively . CoQ10 was given at a dosage of 3.1 ? 0.6 mg/kg/day for 9 months as a supplementation to a fixed amount of conventional antifailure drugs throughout the study . At follow-up periods of 1 , 3 , 6 , and 9 months , NYHA functional class was significantly improved , as was CT ratio and QRS duration at 3 and 9 months follow-up with CoQ10 when compared to the baseline and post-discontinuation of CoQ10 at 9 months ( range , 4.8 - 10.8 ) . However , when multiple comparisons were taken into consideration , there was no statistical significant improvement . In addition to the conventional antifailure drugs , CoQ10 may improve NYHA class and CT ratio and shorten ventricular depolarization in children with chronic idiopathic DCM BACKGROUND The number of patients awaiting heart transplantation is increasing in proportion to the waiting period for a donor . Studies have shown that coenzyme Q10 ( CoQ10 ) has a beneficial effect on patients with heart failure . HYPOTHESIS The purpose of the present double-blind , placebo-controlled , r and omized study was to assess the effect of CoQ10 on patients with end-stage heart failure and to determine if CoQ10 can improve the pharmacological bridge to heart transplantation . METHODS A prospect i ve double-blind design was used . Thirty-two patients with end-stage heart failure awaiting heart transplantation were r and omly allocated to receive either 60 mg U/day of Ultrasome -- CoQ10 ( special preparation to increase intestinal absorption ) or placebo for 3 months . All patients continued their regular medication regimen . Assessment s included anamnesis with an extended question naire based partially on the Minnesota Living with Heart Failure Question naire , 6-min walk test , blood tests for atrial natriuretic factor ( ANF ) and tumor necrosis factor ( TNF ) , and echocardiography . RESULTS Twenty-seven patients completed the study . The study group showed significant improvement in the 6-min walk test and a decrease in dyspnea , New York Heart Association ( NYHA ) classification , nocturia , and fatigue . No significant changes were noted after 3 months of treatment in echocardiography parameters ( dimensions and contractility of cardiac chambers ) or ANF and TNF blood levels . CONCLUSIONS The administration of CoQ10 to heart transplant c and i date s led to a significant improvement in functional status , clinical symptoms , and quality of life . However , there were no objective changes in echo measurements or ANF and TNF blood levels .  Coenzyme Q10 may serve as an optional addition to the pharmacologic armamentarium of patients with end-stage heart failure . The apparent discrepancy between significant clinical improvement and unchanged cardiac status requires further investigation Despite major advances in treatment  congestive heart failure ( CHF )  is still one of the major causes of morbidity and mortality . Coenzyme Q10 is a naturally occurring substance that has antioxidant and membrane stabilizing properties . Administration of coenzyme Q10 in conjunction with st and ard medical therapy has been reported to augment myocardial kinetics , increase cardiac output , elevate the ischemic threshold , and enhance functional capacity in patients with congestive heart failure . The aim of this study was to investigate some of these cl aims . Seventeen patients ( mean New York Heart Association functional class 3.0 ± 0.4 ) were enrolled in an open-label study . After 4 months of coenzyme Q10 , therapy , functional class improved 20 % ( 3.0 ± 0.4 to 2.4 ± 0.6 , p < 0.001 ) and there was a 27 % improvement in mean CHF score ( 2.8 ± 0.4 to 2.2 ± 0.4 , p < 0.001 ) . Percent change in the resting variables included the following : left ventricular ejection fraction ( LVEF ) , + 34.8 % ; cardiac output , + 15.7 % ; stroke volume index , + 18.9 % ; end-diastolic volume area , −8.4 % ; systolic blood pressure ( SBP ) , −4.4 % ; and Emax , ( SBP end-systolic volume index [ ESVI ] ) + 11.7 % . MVo2 decreased by 5.3 % ( 31.9 ± 2.6 to 30.2 ± 2.4 , p = NS ) . Therapy with coenzyme Q10 was associated with a mean 25.4 % increase in exercise duration and a 14.3 % increase in workload . Percent changes after therapy include the following : exercise LVEF , + 24.6 % ; cardiac output , + 19.1 % ; stroke volume index , + 13.2 % ; heart rate , + 6.5 % ; SBP , −4.3 % ; SBP ESVI , + 18.6 % ; end-diastolic volume ( EDV ) area , −6.0 % ; MVo2 , −7.0 % ; and ventricular compliance ( % δ SV EDV ) improved < 100 % . In summary , coenzyme Q10 therapy is associated with significant functional , clinical , and hemodynamic improvements within the context of an extremely favorable benefit-to-risk ratio . Coenzyme Q10  enhances cardiac output by exerting a positive inotropic effect upon the myocardium as well as mild vasodilatation The long-term efficacy and safety of HMG-CoA reductase inhibitors ( statins ) have been established in large multicenter trials . Inhibition of this enzyme , however , results in decreased synthesis of cholesterol and other products downstream of mevalonate , such as CoQ10 or dolichol . This was a r and omized double-blind , placebo-controlled study that examined the effects of CoQ10 and placebo in hypercholesterolemic patients treated by atorvastatin . Eligible patients were given 10mg/day of atorvastatin for 16 weeks . Half of the patients ( n=24 ) were supplemented with 100mg/day of CoQ10 , while the other half ( n=25 ) were given the placebo .  Serum LDL-C levels in the CoQ10 group decreased by 43 % , while in the placebo group by 49 % . The HDL-C increment was more striking in the CoQ10 group than in the placebo group . All patients showed definite reductions of plasma CoQ10 levels in the placebo group , by 42 % . All patients supplemented with CoQ10 showed striking increases in plasma CoQ10 by 127 % . In conclusion atorvastatin definitely decreased plasma CoQ10 levels and supplementation with CoQ10 increased their levels . These changes in plasma CoQ10 levels showed no relation to the changes in serum AST , ALT and CK levels . Further studies are needed , however , for the evaluation of CoQ10 supplementation in statin therapy OBJECTIVES The aim of this study was to evaluate the relationship between plasma oxidized low-density lipoprotein ( oxLDL ) , a marker of oxidative stress , and the prognosis of patients with chronic congestive heart failure ( CHF ) . BACKGROUND Oxidative stress appears to play a role in the pathophysiology of CHF . We have recently reported the usefulness of plasma oxLDL as a marker of oxidative stress in CHF patients with dilated cardiomyopathy . METHODS We measured the plasma level of oxLDL by s and wich enzyme-linked immunosorbent assay using a specific monoclonal antibody against oxLDL in 18 age-matched normal subjects and in 84 patients with chronic CHF ( New York Heart Association functional class II to IV ) and monitored them prospect ively for a mean follow-up period of 780 days . RESULTS Plasma oxLDL level was significantly higher in severe CHF patients than in control subjects and mild CHF patients . A significant negative correlation existed between the plasma level of oxLDL and left ventricular ejection fraction ( LVEF ) and a significant positive correlation between the plasma level of oxLDL and plasma norepinephrine level .  Twenty-six patients had cardiac events ; 14 had cardiac death and 12 were hospitalized for heart failure or other cardiovascular events .  Among 10 variables including LVEF and neurohumoral factors , only high plasma levels of brain natriuretic peptide and oxLDL were shown to be independent predictors of mortality . CONCLUSIONS These results indicate that the plasma level of oxLDL is a useful predictor of mortality in patients with CHF , suggesting that oxidative stress plays an important role in the pathophysiology of CHF There are numerous reasons to believe that deficiency of coenzyme Q10 ( ubiquinone ) may exacerbate the poor contractility of myocardial cells in patients with heart failure . Not only does coenzyme Q10 play a central role in mitochondrial oxidative phosphorylation ( 1 ) , but it may also act as an antioxidant scavenger ( 2 ) . Because the myocardium of patients with congestive heart failure demonstrates oxidative stress ( 3 ) and coenzyme Q10 prevents lipid peroxidation ( 4 ) , this substance conceivably could prevent myocardial destruction . Furthermore , the concentration of coenzyme Q10 is decreased in myocardial cells of patients with advanced heart failure ( 5 ) , and the extent of myocardial coenzyme Q10 deficiency correlates with the clinical severity of heart failure ( 5 , 6 ) . It is thus not surprising that nutritional supplementation with coenzyme Q10 has been proposed as a treatment for congestive heart failure , that it is extensively advertised , and that it is commonly used by patients with this condition . Many small studies have been published , but most were uncontrolled and unblinded . Approximately 31 Japanese clinical reports describe favorable effects with intravenous or oral coenzyme Q10 ( 7 ) . The studies involved only a small number of patients with heart failure and tended to include patients with cardiac disease of various causes . Nevertheless , in 1974 the Japanese government approved marketing of coenzyme Q10 for the treatment of heart failure . The few U.S. and European studies have had conflicting results . Some controlled studies showed no effect ( 8 , 9 ) , but their limitations make the results inconclusive . Other trials noted improvement ( 10 - 13 ) , but concerns about end points , small numbers of patients , and the lack of blinding have limited the acceptance of these studies . With such conflicting data , r and omized , controlled , and blinded studies are needed to test the hypothesis that patients with advanced heart failure are deficient in coenzyme Q10 and that oral supplementation with coenzyme Q10 results in clinical improvement . We therefore evaluated the effects of coenzyme Q10 supplementation on left ventricular ejection fraction and exercise tolerance in patients with symptomatic heart failure despite st and ard medical therapy . Methods We performed a r and omized , double-blind , placebo-controlled trial to compare the effects of oral coenzyme Q10 ( 200 mg/d ) and placebo . The two primary end points were change in ejection fraction , as assessed by nuclear ventriculography , and change in peak oxygen consumption . The study protocol was approved by the human volunteers committee of the University of Maryl and School of Medicine . Inclusion and Exclusion Criteria Patients with New York Heart Association functional class III or IV disease were eligible for inclusion in this study . All patients had ejection fractions less than 40 % ( documented by radionuclide ventriculography ) and maximal oxygen consumption less than 17.0 mL/kg of body weight per minute or less than 50 % of the predicted value . These criteria were used to select symptomatic patients who would have the potential to improve . The mean peak oxygen consumption in our patients was 13.1 mL/kg per minute . In comparison , the peak oxygen consumption criterion for cardiac transplantation is generally considered to be less than 14.0 mL/kg per minute , and the mean peak oxygen consumption in nonexercising normal elderly persons ( mean age , 67 years ) has been reported to be 19.0 mL/kg per minute ( 14 ) . Patients were required to have been receiving an unchanged medical regimen for at least 1 month . Patients who had previously taken coenzyme Q10 were excluded . Baseline Testing At baseline , three procedures were performed . First , a grade d symptom-limited cardiopulmonary exercise test using the Naughton protocol was conducted to assess maximal oxygen consumption . The test was 
    Output:
    
RESULT Extracted data for Seven systematic review s for primary outcomes , net changes in cardiac output , cardiac index , New York Heart Association functional classification , improved survival , based on existing evidence , there is a case for use of CoQ10 as an adjunctive therapy in congestive heart failure , especially in those patients unable to tolerate mainstream medical therapies .
Evidence suggests that the CoQ10 supplement may be a useful tool for managing patients with heart failure