***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 telomere length of replicating somatic cells is inversely correlated with age and has been reported to be associated cross-sectionally with cardiovascular disease ( CVD ) . Leukocyte telomere length , as expressed by mean terminal restriction fragment ( TRF ) length , was measured in 419 r and omly selected participants from the Cardiovascular Health Study , comprising a community-dwelling cohort recruited in four US communities . The authors investigated associations between TRF length and selected measures of sub clinical CVD/risk factors for CVD ( data were collected at the 1992/1993 clinic visit ) and incident CVD ( ascertained through June 2002 ) . In these participants ( average age = 74.2 years ( st and ard deviation , 5.2 ) ) , mean TRF length was 6.3 kilobase pairs ( st and ard deviation , 0.62 ) . Significant or borderline inverse associations were found between TRF length and diabetes , glucose , insulin , diastolic blood pressure , carotid intima-media thickness , and interleukin-6 . Associations with body size and C-reactive protein were modified by gender and age , occurring only in men and in participants aged 73 years or younger . In younger ( but not older ) participants , each shortened kilobase pair of TRF corresponded with a threefold increased risk of myocardial infa rct ion ( hazard ratio = 3.08 , 95 % confidence interval : 1.22 , 7.73 ) and stroke ( hazard ratio = 3.22 , 95 % confidence interval : 1.29 , 8.02 ) . These results support the hypotheses that telomere attrition may be related to diseases of aging through mechanisms involving oxidative stress , inflammation , and progression to CVD BACKGROUND Recent studies have shown telomere-length shortening as a risk predictor for cardiovascular disease . However , to date , no prospect i ve data are available on its potential involvement in venous thromboembolism ( VTE ) . METHODS Using leukocyte DNA sample s collected at baseline in a prospect i ve cohort of 14,916 initially healthy American men , we examined the relationship of mean telomere repeat copy number to single gene copy number ( T/S ratio ) , using a modified quantitative polymerase chain reaction protocol , amongst 108 White males who subsequently developed a first ever VTE event and amongst an equal number of age- and smoking-matched White males who remained free of vascular events during follow-up ( controls ) . RESULTS An inverse correlation between T/S ratios and age was observed in our controls ( p=0.04 ) . However , the T/S ratios were similar between cases and controls ( p=0.31 ) . Furthermore , in a multi-variable adjusted analysis , we found no evidence for an association of the observed T/S ratios with VTE risk ( odds ratio=1.20 ; 95%CI=0.58 - 2.52 ; p=0.62 ) . CONCLUSIONS The present investigation found no evidence for an association of relative telomere length with risk of incident VTE OBJECTIVES This study sought to test the hypothesis that patients with chronic heart failure ( CHF ) have shorter telomeres compared with age-balanced and gender-balanced healthy individuals . BACKGROUND Telomere length is considered to be a marker of biological aging . Chronic heart failure might be viewed as a condition associated with accelerated biological aging . METHODS The telomere length ratio of leukocytes was determined prospect ively by a quantitative polymerase chain reaction-based method in a case-control setting involving 803 participants : 183 healthy individuals and 620 CHF patients , ages 40 to 80 years , New York Heart Association functional class II to IV , and left ventricular ejection fraction of 0.40 or less . RESULTS The median telomere length ratio was 0.64 ( interquartile range [ IQR ] 0.47 to 0.88 ) in CHF patients compared with 1.05 ( IQR 0.86 to 1.29 ) in control patients ( p < 0.001 ) . The telomere length ratio in CHF patients related to severity of disease ( median value [ IQR ] of patients with New York Heart Association class II , III , or IV function was 0.67 [ 0.48 to 0.92 ] , 0.63 [ 0.46 to 0.86 ] , and 0.55 [ 0.46 to 0.75 ] , respectively ; p for trend < 0.05 ) . In addition , telomeres were shorter in patients with an ischemic compared with a nonischemic etiology of CHF . Patients with none , 1 ( coronary , cerebral , or peripheral vascular disease ) , 2 ( any combination of the previous ) , or 3 atherosclerotic manifestations had a median ( IQR ) telomere length of 0.72 ( 0.51 to 1.01 ) , 0.65 ( 0.48 to 0.87 ) , 0.48 ( 0.39 to 0.72 ) , and 0.43 ( 0.27 to 0.67 ) , respectively ( p for trend < 0.001 ) . CONCLUSIONS Telomere length is shorter in patients with CHF compared with age-balanced and gender-balanced control patients , and related to the severity of disease . In addition , telomere length was incrementally shorter according to the presence and extent of atherosclerotic disease manifestations BACKGROUND Recent data have implicated telomere length shortening as a potential risk predictor for cardiovascular disease . However , to date , prospect i ve epidemiological data are scarce . METHODS Using leukocyte DNA sample s collected at baseline in a prospect i ve cohort of 14,916 initially healthy American men , we examined the relationship of mean telomere repeat copy number to single gene copy number ( T/S ratio ) , using a re-modified quantitative polymerase chain reaction protocol , among 337 white males who subsequently developed an incident myocardial infa rct ion ( MI ) , and among an equal number of age- and smoking-matched white males who remained free of reported vascular disease during follow-up ( controls ) . RESULTS The mean follow-up time since r and omization was 3.85 y. The T/S ratio was inversely correlated with age in the controls ( R=-0.114 ; p=0.036 ) . The log(e)-transformed T/S ratios were significantly smaller in the MI cases ( 3.41+/-0.63 ) than the MI controls ( 3.52+/-0.78 ) ( p=0.01 ) . In a multi-variable adjusted analysis , decreased T/S ratio was significantly associated with risk of MI ( odds ratio=1.621 ; 95%CI=1.140 - 2.304 ; p=0.007 ) . CONCLUSIONS The present investigation has shown an association of telomere length shortening with increased risk of incident myocardial infa rct ion , further suggesting the importance of telomere biology in atherogenesis The Asklepios Study is a longitudinal population study focusing on the interplay between ageing , cardiovascular haemodynamics and inflammation in ( pre clinical ) cardiovascular disease . The 2524 participants ( 1301 women ) are a representative cohort of 35–55-year-old individuals , free from overt cardiovascular disease at study initiation , r and omly sample d from the twinned Belgian communities of Erpe – Mere and Nieuwerkerken . Baseline examinations ( all single-observer , single-device , single-site , single 2-year consecutive timeframe ) include : question naires , conventional risk factors and biochemistry . Additional phenotypes under study include : ( a ) vascular structure and function : carotid and femoral atherosclerosis ( intima – media thickness , plaque ) , arterial distension and pressure curves ( brachial , carotid , femoral ; wall-tracking and applanation tonometry ) ; ( b ) cardiac structure and function . A novel aspect of the study is ‘ integrated ’ noninvasive biomechanical assessment of cardiac , arterial and ventriculovascular function through a combination of modeling , fundamental hydraulical measurements and system identification techniques . Integrated phenotypes result from combining at least two sets of curves ( flow/pressure/distension ) . The value of this ‘ integrated ’ haemodynamic phenotype in the detection , prediction and prevention of clinical cardiovascular pathology ( atherosclerosis progression , atherothrombosis , development of heart failure ) will be tested . A second novel aspect is the systematic determination of peripheral blood leukocyte telomere length as a marker for biological ageing . During follow-up , baseline examinations will be repeated and the incidence of cardiovascular events will be monitored . Sex-specific baseline risk factor and biochemical data are provided in the current analyses . The primary aim is to build a combined data set that will act as a tool to answer a cluster of questions about ageing , haemodynamics and the emergence of cardiovascular disease , especially the incidence of atherothrombotic events and the development of adverse haemodynamic profiles ( arterial stiffening , heart failure ) . The study will reassess current risk factors and provide a long-term base for the detection of novel (epi)genetic and non-genetic risk factors and for more performant risk stratification modalities . Within these broader goals , a constant will be to strive towards more fundamental mechanistic-haemodynamic insights into cardiovascular disease processes Telomere length is linked to age‐associated diseases , with shorter telomeres in blood associated with an increased probability of mortality from infection or heart disease . Little is known about how human telomere length is regulated despite convincing data from twins that telomere length is largely heritable , uniform in various tissues during development until birth and variable between individuals . As sperm cells show increasing telomere length with age , we investigated whether age of  fathers at conception correlated with telomere length of their offspring . Telomere length in blood from 125 r and om subjects was shown to be positively associated with paternal age ( + 22 bp yr−1 , 95 % confidence interval 5.2–38.3 , P = 0.010 ) , and paternal age was calculated to affect telomere length by up to 20 % of average telomere length per generation . Males lose telomeric sequence faster than females ( 31 bp yr−1 , 17.6–43.8 , P < 0.0001 vs. 14 bp yr−1 , 3.5–24.8 , P < 0.01 ) and the rate of telomere loss slows throughout the human lifespan . These data indicate that paternal age plays a role in the vertical transmission of telomere length and may contribute significantly to the variability of telomere length seen in the human population , particularly if effects are cumulative through generations 
    Output:
    
RESULTS Considerable associations between a shorter mean telomere length and coronary heart disease have been observed .
This finding extends to vascular disease risk factors including age , sex , smoking , obesity , hypertension and diabetes .
Multiple associations between short telomere length and vascular disease characterised by atherosclerosis suggest a possible link between telomere attrition and disease mechanisms .