***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 Low heart rate variability ( HRV ) is associated with a higher risk of death in patients with heart disease and in elderly subjects and with a higher incidence of coronary heart disease ( CHD ) in the general population . Methods and Results We studied the predictive value of HRV for CHD and death from several causes in a population study of 14 672 men and women without CHD , aged 45 to 65 , by using the case-cohort design . At baseline , in 1987 to 1989 , 2-minute rhythm strips were recorded . Time-domain  measures of HRV  were determined in a r and om sample of 900 subjects , for all subjects with incident CHD ( 395 subjects ) , and for all deaths ( 443 subjects ) that occurred through 1993 . Relative rates of incident CHD and cause-specific death in tertiles of HRV were computed with Poisson regression for the case-cohort design . Subjects with low HRV had an adverse cardiovascular risk profile and an elevated risk of incident CHD and death . The increased risk of death could not be attributed to a specific cause and could not be explained by other risk factors . Conclusions Low HRV was associated with increased risk of CHD and death from several causes . It is hypothesized that low HRV is a marker of less favorable health Objective : Days of high ambient carbon dioxide ( CO ) have been associated with increased hospital admissions for cardiac disease . This study was conducted to determine if daily concentrations of CO and fine particulates ( PM2.5 ) are associated with daily changes in heart rate variability . Methods : Each of 36 adults with coronary artery disease had personal exposure to PM2.5 and CO measured along with heart rate variability for one 24-hour period each week for up to 10 weeks . Results : Among those not taking beta-receptor blockers , there was a positive association between the st and ard deviation of the R-to-R intervals and CO ( P = 0.02 ) . No effect was found for PM2.5 . Conclusions : Urban exposure to CO may exert a biologic effect on the heart , which may be modified by medications Objective Exposure to air pollution is associated with increases in cardiovascular morbidity and mortality . This study was undertaken to determine the effect of diesel exhaust inhalation on heart rhythm and heart rate variability in healthy volunteers and patients with coronary heart disease . Design and setting Double-blind r and omised crossover studies in a university teaching hospital . Patients 32 healthy non-smoking volunteers and 20 patients with prior myocardial infa rct ion . Interventions All 52 subjects were exposed for 1 h to dilute diesel exhaust ( particle concentration 300 μg/m3 ) or filtered air . Main outcome measures Heart rhythm and heart rate variability were monitored during and for 24 h after the exposure using  continuous ambulatory electrocardiography  and assessed using st and ard time and frequency domain analysis . Results No significant arrhythmias occurred during or following exposures . Patients with coronary heart disease had reduced autonomic function in comparison to healthy volunteers , with reduced st and ard deviations of the NN interval ( SDNN , p<0.001 ) and triangular index ( p<0.001 ) . Diesel exhaust did not affect heart rate variability compared with filtered air ( p>0.05 for all ) in healthy volunteers ( SDNN 101±6 vs 91±6 , triangular index 20±1 vs 21±1 ) or patients with coronary heart disease ( SDNN 47±5 vs 38±4 , triangular index 8±1 vs 7±1 ) . Conclusions Brief exposure to dilute diesel exhaust does not alter heart rhythm or heart rate variability in healthy volunteers or well-treated patients with stable coronary heart disease . Autonomic dysfunction does not appear to be a dominant mechanism that can explain the observed excess in cardiovascular events following exposure to combustion-derived air pollution Objective : To measure the inflammatory and autonomic responses of healthy humans and patients with coronary artery disease to controlled concentrations of two specific components of vehicle derived air pollution , carbon particles and sulphur dioxide ( SO2 ) . Methods : Placebo controlled , double blind , r and om order human challenge study examining the effects of carbon particles ( 50 μg/m3 ) and SO2 ( 200 parts per billion ( ppb ) ) on heart rate variability ( HRV ) and circulating markers of inflammation and coagulation in healthy volunteers and patients with stable angina . Results : In healthy volunteers , markers of cardiac vagal control did not fall in response to particle exposure but , compared with the response to air , increased transiently immediately after exposure ( root mean square of successive RR interval differences ( RMSSD ) 15 ( 5 ) ms with carbon particles and 4 ( 3 ) ms ) with air , p < 0.05 ) . SO2 exposure result ed in no immediate change but a significant reduction in HRV markers of cardiac vagal control at four hours ( RMSSD −2 ( 3.6 ) ms with air , −7 ( 2.7 ) ms with SO2 , p < 0.05 ) . No such changes were seen in patients with stable angina . Neither pollutant caused any change in markers of inflammation or coagulation at zero , four , or 24 hours . Conclusion : In healthy volunteers , short term exposure to pure carbon particles does not cause adverse effects on HRV or a systemic inflammatory response . The adverse effects of vehicle derived particulates are likely to be caused by more reactive species found on the particle surface . SO2 exposure does , however , reduce cardiac vagal control , a response that would be expected to increase susceptibility to ventricular arrhythmia Evidence from animal studies suggests that beta-blockers can act within the central nervous system to increase cardiac vagal motoneuron activity . We have attempted to determine whether such an effect is evident in healthy humans , by examining the effects of lipophilic and hydrophilic agents on heart rate variability and cardiac vagal reflexes . A total of 20 healthy volunteers took part in the study . Autonomic studies were performed after 72 h of treatment with placebo , atenolol or metoprolol in a blinded cross-over design . ECG recordings were taken at rest and during mental and orthostatic stress . Heart rate variability was measured in the time and frequency domains . The effects on heart rate of two opposing cardiac vagal reflexes were examined . Trigeminal stimulation causing vagal stimulation , and isometric forearm muscle contraction ( ' muscle heart reflex ' ) causing vagal inhibition , were performed alone and simultaneously . At rest , during mental stress and during trigeminal stimulation , beta-blocker therapy was associated with significantly increased high-frequency beat-to-beat heart rate variability when compared with placebo . There were no significant differences in effects on heart rate or heart rate variability between atenolol and metoprolol . Analysis of the muscle heart reflex , alone and with simultaneous trigeminal stimulation , showed that the magnitude of the R-R interval response was significantly greater after beta-blocker therapy compared with placebo , but the effects of atenolol and metoprolol were equivalent . beta-Blocker therapy increased cardiac vagal activity , as shown by measures of high-frequency heart rate variability and reflex studies . Lipophilic and hydrophilic beta-blockers appeared to be equally efficacious in increasing the cardiac vagal modulation of heart rate Summary Background Long-term exposure to pollution can lead to an increase in the rate of decline of lung function , especially in older individuals and in those with chronic obstructive pulmonary disease ( COPD ) , whereas shorter-term exposure at higher pollution levels has been implicated in causing excess deaths from ischaemic heart disease and exacerbations of COPD . We aim ed to assess the effects on respiratory and cardiovascular responses of walking down a busy street with high levels of pollution compared with walking in a traffic-free area with lower pollution levels in older adults . Methods In this r and omised , crossover study , we recruited men and women aged 60 years and older with angiographically proven stable ischaemic heart disease or stage 2 Global initiative for Obstructive Lung Disease ( GOLD ) COPD who had been clinical ly stable for 6 months , and age-matched healthy volunteers . Individuals with ischaemic heart disease or COPD were recruited from existing data bases or outpatient respiratory and cardiology clinics at the Royal Brompton & Harefield NHS Foundation Trust and age-matched healthy volunteers using advertising and existing data bases . All participants had abstained from smoking for at least 12 months and medications were taken as recommended by participants ' doctors during the study . Participants were r and omly assigned by drawing numbered disks at r and om from a bag to do a 2 h walk either along a commercial street in London ( Oxford Street ) or in an urban park ( Hyde Park ) . Baseline measurements of participants were taken before the walk in the hospital laboratory . During each walk session , black carbon , particulate matter ( PM ) concentrations , ultrafine particles , and nitrogen dioxide ( NO2 ) concentrations were measured . Findings Between October , 2012 , and June , 2014 , we screened 135 participants , of whom 40 healthy volunteers , 40 individuals with COPD , and 39 with ischaemic heart disease were recruited . Concentrations of black carbon , NO2 , PM10 , PM2.5 , and ultrafine particles were higher on Oxford Street than in Hyde Park . Participants with COPD reported more cough ( odds ratio [ OR ] 1·95 , 95 % CI 0·96–3·95 ; p<0·1 ) , sputum ( 3·15 , 1·39–7·13 ; p<0·05 ) , shortness of breath ( 1·86 , 0·97–3·57 ; p<0·1 ) , and wheeze ( 4·00 , 1·52–10·50 ; p<0·05 ) after walking down Oxford Street compared with Hyde Park . In all participants , irrespective of their disease status , walking in Hyde Park led to an increase in lung function ( forced expiratory volume in the first second [ FEV1 ] and forced vital capacity [ FVC ] ) and a decrease in pulse wave velocity ( PWV ) and augmentation index up to 26 h after the walk . By contrast , these beneficial responses were attenuated after walking on Oxford Street . In participants with COPD , a reduction in FEV1 and FVC , and an increase in R5–20 were associated with an increase in during-walk exposure to NO2 , ultrafine particles and PM2.5 , and an increase in PWV and augmentation index with NO2 and ultrafine particles . In healthy volunteers , PWV and augmentation index were associated both with black carbon and ultrafine particles . Interpretation Short-term exposure to traffic pollution prevents the beneficial cardiopulmonary effects of walking in people with COPD , ischaemic heart disease , and those free from chronic cardiopulmonary diseases . Medication use might reduce the adverse effects of air pollution in individuals with ischaemic heart disease . Policies should aim to control ambient levels of air pollution along busy streets in view of these negative health effects . Funding British Heart Foundation Epidemiological studies have shown that air pollution is associated with increased cardiovascular mortality . Although the pathophysiological mechanisms behind this association have remained largely unknown , it has been suggested that changes in cardiac autonomic function may play a role . In this study , we investigated the association between acute carbon monoxide ( CO ) exposure and cardiac autonomic function as measured by heart rate variability ( HRV ) in subjects with stable coronary artery disease .  Twenty‐four hour ambulatory electrocardiographic recording with simultaneous continuous personal CO concentration monitoring was performed in six male patients with angiographically verified coronary artery disease three times with 1‐week intervals . Time domain measures of HRV were calculated for 5‐min segments before and during the CO exposure periods . For further analysis CO exposures were divided into low ( ≤2·7 p.p.m . ) and high ( > 2·7 p.p.m . ) CO exposure periods . The mean of maximum CO levels during 61 CO exposure periods was 4·6 p.p.m . ( SD 5·0 p.p.m . ) . High CO exposure was associated with an increase in the square root of the mean of the sum of the squares of differences between adjacent RR intervals ( r‐MSSD ) ( P = 0·034 ) . Heart rate remained unchanged during the CO exposure . In conclusion , acute CO exposure which represented most likely exposure derived from traffic seems to modify cardiac autonomic control in patients with stable coronary artery disease OBJECTIVE : To test the feasibility of creating a valid and reliable checklist with the following features : appropriate for assessing both r and omised and non-r and omised studies ; provision of both an overall score for study quality and a profile of scores not only for the quality of reporting , internal validity ( bias and confounding ) and power , but also for external validity . DESIGN : A pilot version was first developed , based on epidemiological principles , review s , and existing checklists for r and omised studies . Face and content validity were assessed by three experienced review ers and reliability was determined using two raters assessing 10 r and omised and 10 non-r and omised studies . Using different raters , the checklist was revised and tested for internal consistency ( Kuder-Richardson 20 ) , test-retest and inter-rater reliability ( Spearman correlation coefficient and sign rank test ; kappa statistics ) , criterion validity , and respondent burden . MAIN RESULTS : The performance of the checklist improved considerably after revision of a pilot version . The Quality Index had high internal consistency ( KR-20 : 0.89 ) as did the subscales apart from external validity ( KR-20 : 0.54 ) . Test-retest ( r 0.88 ) and inter-rater ( r 0.75 ) reliability of the Quality Index were good . Reliability of the subscales varied from good ( bias 
    Output:
    
In conclusion , there is strong evidence that air pollution can have adverse effects on cardiovascular function in persons living with CAD .