***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: BACKGROUND The aim of this study was to examine whether angiotensin-converting enzyme ( ACE ) inhibition improves coronary endothelial dysfunction in patients with atherosclerosis and its risk factors and whether this was related to the ACE insertion-deletion ( I/D ) polymorphism . METHODS AND RESULTS In 56 patients with atherosclerosis or its risk factors , we studied endothelium-dependent responses with acetylcholine and endothelium-independent function with sodium nitroprusside , before and after ACE inhibition with enalaprilat . Enalaprilat did not alter either resting coronary tone or vasodilation with sodium nitroprusside . However , it potentiated the coronary microvascular and epicardial responses with acetylcholine ;  coronary blood flow increased from 82+/-7 to 90+/-8 mL/min ( P=0.05 ) after enalaprilat . Patients with depressed endothelial function ( P<0.001 ) and those with ACE DD or ID genotypes ( P=0.002 ) but not those homozygous for the I allele had the greatest improvement by multivariate analysis . Similarly , acetylcholine-mediated epicardial vasomotion improved in segments that initially constricted ( endothelial dysfunction ) : from -10.1+/-1 % to -1.4+/-2 % ( P<0.001 ) after enalaprilat .  No augmentation was observed in segments that dilated ( normal endothelial dysfunction ) with acetylcholine . Patients with the D allele , hypercholesterolemia , and smokers ( all P<0.05 ) had greater improvement . CONCLUSIONS Acute ACE inhibition improves coronary epicardial and microvascular endothelium-dependent vasomotion in patients with atherosclerosis or its risk factors who have endothelial dysfunction and presence of the D allele CONTEXT Observational studies have shown that psychosocial factors are associated with increased risk for cardiovascular morbidity and mortality , but the effects of behavioral interventions on psychosocial and medical end points remain uncertain . OBJECTIVE To determine the effect of 2 behavioral programs , aerobic exercise training and stress management training , with routine medical care on psychosocial functioning and markers of cardiovascular risk . DESIGN , SETTING , AND PATIENTS R and omized controlled trial of 134 patients ( 92 male and 42 female ; aged 40 - 84 years ) with stable ischemic heart disease ( IHD ) and exercise-induced myocardial ischemia . Conducted from January 1999 to February 2003 . INTERVENTIONS Routine medical care ( usual care ) ; usual care plus supervised aerobic exercise training for 35 minutes 3 times per week for 16 weeks ; usual care plus weekly 1.5-hour stress management training for 16 weeks . MAIN OUTCOME MEASURES Self-reported measures of general distress ( General Health Question naire [ GHQ ] ) and depression ( Beck Depression Inventory [ BDI ] ) ; left ventricular ejection fraction ( LVEF ) and wall motion abnormalities ( WMA ) ; flow-mediated dilation ; and cardiac autonomic control ( heart rate variability during deep breathing and baroreflex sensitivity ) . RESULTS Patients in the exercise and stress management groups had lower mean ( SE ) BDI scores ( exercise : 8.2 [ 0.6 ] ; stress management : 8.2 [ 0.6 ] ) vs usual care ( 10.1 [ 0.6 ] ; P = .02 ) ; reduced distress by GHQ scores ( exercise : 56.3 [ 0.9 ] ; stress management : 56.8 [ 0.9 ] ) vs usual care ( 53.6 [ 0.9 ] ; P = .02 ) ; and smaller reductions in LVEF during mental stress testing ( exercise : -0.54 % [ 0.44 % ] ; stress management : -0.34 % [ 0.45 % ] ) vs usual care ( -1.69 % [ 0.46 % ] ; P = .03 ) . Exercise and stress management were associated with lower mean ( SE ) WMA rating scores ( exercise : 0.20 [ 0.07 ] ; stress management : 0.10 [ 0.07 ] ) in a subset of patients with significant stress-induced WMA at baseline vs usual care ( 0.36 [ 0.07 ] ; P = .02 ) . Patients in the exercise and stress management groups had greater mean ( SE ) improvements in flow-mediated dilation ( exercise : mean [ SD ] , 5.6 % [ 0.45 % ] ; stress management : 5.2 % [ 0.47 % ] ) vs usual care patients ( 4.1 % [ 0.48 % ] ; P = .03 ) . In a subgroup , those receiving stress management showed improved mean ( SE ) baroreflex sensitivity ( 8.2 [ 0.8 ] ms/mm Hg ) vs usual care ( 5.1 [ 0.9 ] ms/mm Hg ; P = .02 ) and significant increases in heart rate variability ( 193.7 [ 19.6 ] ms ) vs usual care ( 132.1 [ 21.5 ] ms ; P = .04 ) . CONCLUSION For patients with stable IHD , exercise and stress management training reduced emotional distress and improved markers of cardiovascular risk more than usual medical care alone BACKGROUND The renin-angiotensin system may contribute to atherogenesis through the promotion of endothelial dysfunction . The present study was performed to determine whether angiotensin-1 ( AT(1 ) ) receptor inhibition improves endothelial dysfunction . METHODS AND RESULTS In the femoral circulation of 19 patients with atherosclerosis and of 9 control subjects , we studied microvascular responses to reactive hyperemia , angiotensin II , acetylcholine , and sodium nitroprusside before and after the administration of intra-arterial losartan ( 10 mg ) . Femoral artery flow velocity was measured with a Doppler flow wire , and the femoral vascular resistance index ( FVRI ) was calculated as mean arterial pressure divided by flow velocity . Losartan induced a minor ( 5.9+/-2 % , P=0 . 02 ) reduction in FVRI and inhibited angiotensin II-mediated vasoconstriction in both patient groups ( P<0.01 ) . After the administration of losartan , acetylcholine-mediated vasodilation was augmented in patients ( 44+/-5 % to 58+/-4 % reduction in FVRI with infusion at a rate of 150 microgram/min , P<0.001 ) but not control subjects . Vasodilation during reactive hyperemia was also greater after AT(1 ) receptor inhibition ( P=0.03 ) in patients , but the response to sodium nitroprusside remained unchanged . In a separate group of 31 patients with atherosclerosis , we investigated the effect of 8 weeks of oral losartan therapy on brachial artery flow-mediated vasodilation with the use of high-resolution ultrasound . Oral losartan therapy improved flow-mediated brachial artery dilation ( 1.4+/-0.9 % to 3.2+/-0.8 % , P=0.03 ) but had no effect on the nitroglycerin response . Serum nitrogen oxide levels increased from 21.6+/-1.7 to 26.7+/-2.4 micromol/L ( P=0.008 ) . CONCLUSIONS The results of the present study indicate that inhibition of the AT(1 ) receptor in patients with atherosclerosis reverses endothelial dysfunction by improving NO availability and therefore may have long-term therapeutic benefits 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 Objective : To determine if depression contributes to incident heart disease after accounting for genetic , behavioral , and medical factors associated with both conditions . Methods : We used a prospect i ve twin study  with a 12-year follow-up . In 1992 , lifetime diagnosis of depression was assessed in 1159 male-male twins and merged with longitudinal health data from the Vietnam Era Twin Registry Study of Aging . Incident heart disease was defined as having myocardial infa rct ion , heart surgery , or angina at 12-year follow-up when twins were 55.4 years ( st and ard deviation , 2.5 years ) of age . Risks for heart disease were computed in a logistic regression model that included comparing twins at different levels of phenotypic expression of depression and varying levels of genetic vulnerability at the same time adjusting for pertinent covariates . Results : After adjusting for sociodemographics , co-occurring psychopathology , smoking , obesity , diabetes , hypertension , and social isolation , twins at high genetic risk and exposed to depression remained at greater risk of developing ischemic heart disease ( IHD ) ( odds ratio , 2.55 ; 95 % confidence interval , 1.44 - 4.49 ) compared with those at low genetic risk and without phenotypic expression of depression . Odds ratios suggest that twins at genetic liability but without phenotypic expression were at risk of IHD , but the effect was not statistically significant . Conclusions : A history of depression is a risk factor for incident heart disease after adjusting for numerous covariates . Twins with both high genetic vulnerability and phenotypic expression of depression were at greatest risk of IHD . Trends suggest the genetic contribution to IHD that overlaps with depression may partly explain this association , but studies in larger sample s are warranted . IHD = ischemic heart disease ; VET Registry = Vietnam Era Twin Registry ; DSM-III-R = Diagnostic and Statistical Manual , Third Edition , Revised ; VETSA = Vietnam Era Twin Study of Aging ; MZ = monozygotic ; DZ = dizygotic ; MI = myocardial infa rct ion & NA ; Mental stress induces endothelial dysfunction , that is a reduction of the post‐occlusion brachial artery flow‐mediated vasodilation ( FMD ) . This does not occur in subjects highly susceptible to hypnosis ( Highs ) in either the waking or hypnotic state . The aim of the present experiment was to assess whether endothelial dysfunction is also induced by acute nociceptive stimulation and whether high hypnotisability and /or the specific instruction of analgesia prevent its occurrence in awake highly hypnotizable individuals . Thus , nine Highs and nine subjects with low susceptibility to hypnosis ( Lows ) underwent an experimental session including the administration of pressor pain and of pressor pain associated with the instruction of analgesia .  Heart rate , basal artery diameters and brachial artery flow‐mediated vasodilation were measured during stimulation and rest conditions . Heart rate exhibited slight changes not modulated by hypnotisability . During painful stimulation both Highs and Lows showed a decrease of FMD , but it was significantly less pronounced in Highs . During the administration of painful stimulation together with the instruction of analgesia , only Highs reported analgesia and their FMD no longer decreased . This study provides the first evidence of pain‐related endothelial dysfunction and extends previous findings concerning a sort of natural protection of Highs against the vascular effects of mental stress to acute pain OBJECTIVES This study was design ed to investigate the role of cortisol in stress-induced endothelial dysfunction and impaired baroreflex sensitivity ( BRS ) by blocking cortisol production with metyrapone before subjecting healthy volunteers to mental stress . BACKGROUND Mental stress raises cortisol levels and is associated with increased coronary heart disease ( CHD ) morbidity and mortality , especially from sudden cardiac death . It also causes endothelial dysfunction and impaired BRS . METHODS We measured brachial artery flow-mediated dilation ( FMD ) , a measure of endothelial function , and BRS in 36 subjects without CHD risk factors who were then r and omized in a double-blind fashion to oral metyrapone 750 mg x 2 or placebo .  Five hours later we subjected subjects to mental stress and then remeasured endothelial function and BRS . RESULTS Prestress cortisol levels were significantly higher in the placebo group at 270.5 ( 30.9 ) nmol/l versus 89.1 ( 11.8 ) nmol/l ( p = 0.01 ) , and the increase with stress was higher at 57.9 ( 17.9 ) nmol/l versus 11.2 ( 2.2 ) nmol/l ( p < 0.001 ) . In the placebo group , compared to baseline , FMD and BRS fell significantly from 4.5 % ( 0.7 % ) to 1.4 % ( 1. 
    Output:
    
Circumstantial evidence indicates that mind body therapies may have a therapeutic benefit on endothelial dysfunction , however , the aggregate data from the three small r and omized trials to date do not support this hypothesis .