***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: Using a placebo-controlled , double-blind cross-over study the potential therapeutic effect of ubiquinone ( coenzyme Q10 ) was investigated in 25 patients suffering from idiopathic dilated cardiomyopathy ( New York Heart Association functional classification I , II and III ) . Over an initial period of 4 months , 15 patients were administered verum ( 3 x 33.3 mg coenzyme Q10 x day-1 p.o . ) and subsequently given a placebo during the ensuing 4 months ( V/P ) . The sequence of treatment was reversed within the remaining 10 patients ( P/V ) . Therapeutic efficacy was assessed by means of echocardiogram , chest X-ray , radionuclide ventriculography in combination with exercise test and impedance cardiography . Control values for left ventricular function parameters were similar in both groups ; left ventricular ejection fraction : 39.5 + /- 11.5 % ( P/V ) , 37.6 + /- 17.0 % ( V/P ) ; left ventricular end-diastolic diameter : 65 + /- 9 mm ( P/V ) , 67 + /- 8 mm ( P/V ) ; and cardiac output : 5.1 + /- 1.41 x min-1 ( P/V ) , 5.1 + /- 1.11 x min-1 ( V/P ) . Chronic treatment with ubiquinone had no influence on haemodynamic parameters , electrocardiogram , incidence of ventricular arrhythmias or on exercise tolerance . It was therefore impossible to demonstrate any therapeutic effect of ubiquinone in patients suffering from idiopathic dilated cardiomyopathy In patients with chronic heart failure ( CHF ) , the addition of coenzyme Q10 to conventional therapy reduces the hospitalization rate for worsening of heart failure and the incidence of serious cardiovascular complications . The present study was planned to assess the hemodynamic mechanisms underlying this phenomenon . Cardiac hemodynamics was evaluated continuously using an ambulatory radionuclide detector ( VEST ) which allows a noninvasive monitoring of left ventricular function . Six patients wit CHF ( mean ejection fraction ( EF ) : 29 % ) clinical ly documented were studied . This study was organized as a r and omized double-blind , placebo controlled , cross-over trial . The enrolled patients , after a washout period , underwent the first hemodynamic evaluation with VEST . Subsequently they were r and omized to receive placebo or coenzyme Q10 for 4 weeks . At the end of this period they underwent the second VEST study . The third VEST study was performed after a further 4-week period with inverted treatment . Cardiac hemodynamics were evaluated during bicycle exercise . The EF in control conditions ( CC ) changed from 27 + /- 11 % , at rest , to 24 + /- 8 % , at peak exercise . During coenzyme Q10 treatment EF showed a significant increase both at rest ( 33 + /- 13 % , P < 0.05 vs CC ) and at peak exercise ( 30 + /- 12 % , P < 0.05 vs CC ) . The same trends were recorded for the stroke volume and the cardiac output . Our results demonstrate that coenzyme Q10 improves cardiac hemodynamic response to exercise in patients with CHF and suggest that noninvasive monitoring of left ventricular function allows a more reliable assessment of therapy efficacy Coenzyme Q10 ( ubiquinone ) the essential mitochondrial redox-component and endogenous antioxidant , packaged into the LDL + VLDL fractions of cholesterol , has been suggested as an important anti-risk factor for the development of atherosclerosis as explained by the oxidative theory . Forty-five hypercholesterolemic patients were r and omized in a double-blind trial in order to be treated with increasing dosages of either lovastatin ( 20 - 80 mg/day ) or pravastatin ( 10 - 40 mg/day ) over a period of 18 weeks . Serum levels of coenzyme Q10 were measured parallel to the levels of cholesterol at baseline on placebo and diet and during active treatment . A dose-related significant decline of the total serum level of coenzyme Q10 was found in the pravastatin group from 1.27 + /- 0.34 at baseline to 1.02 + /- 0.31 mmol/l at the end of the study period ( mean + /- S.D. ) , P < 0.01 . After lovastatin therapy the decrease was significant as well and more pronounced , from 1.18 + /- 0.36 to 0.84 + /- 0.17 mmol/l , P < 0.001 . Although HMG-CoA reductase inhibitors are safe and effective within a limited time horizon , continued vigilance of a possible adverse consequence from coenzyme Q10 lowering seems important during long-term therapy Abstract Background : HMG-CoA reductase inhibitors ( ‘ statins ’ ) have been associated with a decrease in ubidecarenone ( ubiquinone ) levels , a lipophilic enzyme also known as coenzyme Q10 ( CoQ10 ) , due to inhibition of mevalonate synthesis . There is speculation that a decrease in CoQ10 levels may be associated with statin-induced myopathy . The cholesterol absorption inhibitor ezetimibe increases endogenous cholesterol synthesis . The purpose of this study was to examine ( i ) the effects of ezetimibe and simvastatin on plasma CoQ10 levels and ( ii ) whether ezetimibe coadministered with simvastatin abrogates the suggested statin-induced decrease in the CoQ10 plasma levels . Methods : Seventy-two healthy male subjects were enrolled in a single-centre , r and omised , parallel-group study with three arms . Subjects received ezetimibe 10 mg/day , simvastatin 40 mg/day or the combination of ezetimibe 10 mg/day plus simvastatin 40 mg/day for 14 days . Results : Baseline CoQ10 ( 0.99 ± 0.30 mg/L ) levels for the combined groups remained unchanged in the ezetimibe group ( 0.95 ± 0.24 mg/L ) , and significantly decreased in the simvastatin and combination groups ( 0.82 ± 0.18 mg/L , p = 0.0002 and 0.7 ± 0.22 mg/L , p < 0.0001 , respectively ) . There was a correlation between the percentage change in the levels of low-density lipoprotein-cholesterol ( LDL-C ) and the percentage change in CoQ10 levels in all treatment groups ( correlation coefficient [ R ] = 0.67 , p < 0.0001 ) . The ratios of CoQ10 levels to LDL-C levels were significantly increased in all treatment groups ( p < 0.0001 ) . CoQ10 level was independent of cholesterol synthesis or absorption markers . Conclusions : Simvastatin and the combination of simvastatin and ezetimibe significantly decrease plasma CoQ10 levels whereas ezetimibe monotherapy does not . There is a significant correlation between the CoQ10 level decrease and the decrease in total and LDL-C levels in all three treatment groups , suggesting that the CoQ10 decrease may reflect the decrease in the levels of its lipoprotein carriers and might not be statin-specific . The statin-associated CoQ10 reduction is not abrogated through ezetimibe coadministration . Changes of CoQ10 levels are independent of cholesterol synthesis and absorption Inhibitors of HMG-CoA reductase are new safe and effective cholesterol-lowering agents . Elevation of alanine-amino transferase ( ALT ) and aspartate-amino transferase ( AST ) has been described in a few cases and a myopathy with elevation of creatinine kinase ( CK ) has been reported rarely . The inhibition of HMG-CoA reductase affects also the bio synthesis of ubiquinone ( CoQ10 ) . We studied two groups of five healthy volunteers treated with 20 mg/day of pravastatin ( Squibb , Italy ) or simvastatin ( MSD ) for a month . Then we treated 30 hypercholesterolemic patients in a double-blind controlled study with pravastatin , simvastatin ( 20 mg/day ) , or placebo for 3 months . At the beginning , and 3 months thereafter we measured plasma total cholesterol , CoQ10 , ALT , AST , CK , and other parameters ( urea , creatinine , uric acid , total bilirubin , gamma GT , total protein ) . Significant changes in the healthy volunteer group were detected for total cholesterol and CoQ10 levels , which underwent about a 40 % reduction after the treatment . The same extent of reduction , compared with placebo was measured in hypercholesterolemic patients treated with pravastatin or simvastatin . Our data show that the treatment with HMG-CoA reductase inhibitors lowers both total cholesterol and CoQ10 plasma levels in normal volunteers and in hypercholesterolemic patients . CoQ10 is essential for the production of energy and also has antioxidative properties . A diminution of CoQ10 availability may be the cause of membrane alteration with consequent cellular damage Reduction of serum cholesterol levels with statin therapy decreases the risk of coronary heart disease . Inhibition of HMG-CoA reductase by statin results in decreased synthesis of cholesterol and other products downstream of mevalonate , which may produce adverse effects in statin therapy . We studied the reductions of serum ubiquinol-10 and ubiquinone-10 levels in hypercholesterolemic patients treated with atorvastatin . Fourteen patients were treated with 10 mg/day of atorvastatin  , and serum lipid , ubiquinol-10 and ubiquinone-10 levels were measured before and after 8 weeks of treatment . Serum total cholesterol and LDL-cholesterol levels decreased significantly . All patients showed definite reductions of serum ubiquinol-10 and ubiquinone-10 levels , and mean levels of serum ubiquinol-10 and ubiquinone-10 levels decreased significantly from 0.81 + /- 0.21 to 0.46 + /- 0.10 microg/ml ( p < 0.0001 ) , and from 0.10 + /- 0.06 to 0.06 + /- 0.02 microg/ml ( p = 0.0008 ) , respectively . Percent reductions of ubiquinol-10 and those of total cholesterol showed a positive correlation ( r = 0.627 , p = 0.0165 ) . As atorvastatin reduces serum ubiquinol-10 as well as serum cholesterol levels in all patients , it is imperative that physicians are forewarned about the risks associated with ubiquinol-10 depletion Most systematic review s rely substantially on the assessment of the method ological quality of the individual trials . The aim of this study was to obtain consensus among experts about a set of generic core items for quality assessment of r and omized clinical trials ( RCTs ) . The invited participants were experts in the field of quality assessment of RCTs . The initial item pool contained all items from existing criteria lists . Subsequently , we reduced the number of items by using the Delphi consensus technique . Each Delphi round comprised a question naire , an analysis , and a feedback report . The feedback report included staff team decisions made on the basis of the analysis and their justification . A total of 33 international experts agreed to participate , of whom 21 completed all question naires . The initial item pool of 206 items was reduced to 9 items in three Delphi rounds . The final criteria list ( the Delphi list ) was satisfactory to all participants . It is a starting point on the way to a minimum reference st and ard for RCTs on many different research topics . This list is not intended to replace , but rather to be used alongside , existing criteria lists Several noninvasive studies have shown the effect on heart failure of treatment with coenzyme Q10 . In order to confirm this by invasive methods we studied 22 patients with mean left ventricular ( LV ) ejection fraction 26 % , mean LV internal diameter 71 mm and in NYHA class 2‐3 . The patients recieved coenzyme Q10 100 mg twice daily or placebo for 12 weeks in a r and omized double‐blinded placebo controlled investigation Seventy-nine patients with stable chronic congestive heart failure were r and omized into a double-blind , crossover placebo controlled study with 3-month treatment periods , where either 100 mg coenzyme Q10 ( CoQ10 ) or placebo was added to conventional therapy . Mean patient age was 61 + /- 10 years , ejection fraction at rest was 22 % + /- 10 % , and maximal exercise tolerance was 91 + /- 30 W. The follow-up examinations included ejection fraction ( primary objective ) , exercise test , and quality of life questions . Ejection fraction at rest , during a slight volume load , and during a submaximal supine exercise increased slightly compared with placebo : 24 % + /- 12 % versus 23 % + /- 12 % ( NS ) , 25 % + /- 13 % versus 23 % + /- 12 % ( P < .05 ) , and 23 % + /- 11 % versus 22 % + /- 11 % ( NS ) . Maximal exercise capacity increased from 94 + /- 31 W during the placebo period to 100 + /-  
    Output:
    
Pooled analyses of available r and omized controlled trials suggest that CoQ₁₀ may improve the EF in patients with CHF .