***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: Objective —We tested the hypothesis that short telomere length is associated with increased risk of myocardial infa rct ion , ischemic heart disease , and early death .  Methods and Results —We measured  leukocyte telomere length  in 2 prospect i ve studies of 19 838 Danish general population participants from the Copenhagen City Heart Study and the Copenhagen General Population Study . Participants were followed for up to 19 years for incident myocardial infa rct ion ( n=929 ) , ischemic heart disease ( n=2038 ) , and death ( n=4342 ) . Follow-up was 100 % complete . Telomere length decreased linearly with increasing age in women and men in both studies ( P=7 × 10−74 to P=3 × 10−125 ) . Multifactorially adjusted hazard ratios were 1.10 ( 95 % CI 1.01–1.19 ) for myocardial infa rct ion , 1.06 ( 1.00–1.11 ) for ischemic heart disease , and 1.09 ( 1.05–1.13 ) for early death per 1000–base pair decrease in telomere length . The multifactorially adjusted hazard ratios for the shortest versus the longest decile of telomere length were 1.49 ( 1.07–2.07 ) for myocardial infa rct ion , 1.24 ( 1.01–1.53 ) for ischemic heart disease , and 1.25 ( 1.07–1.46 ) for early death . Conclusion —Short telomere length is associated with only modestly increased risk of myocardial infa rct ion , ischemic heart disease , and early death Background and Purpose — Accumulating evidence suggests that telomere length is a maker for biological aging of the cardiovascular system . Whether stroke is associated with accelerated biological aging as measured by telomere length has not been conclusively demonstrated . Our aim was to determine whether mean leukocyte telomere length is a predictor for the development of stroke . Methods — The  relative telomere length  of leukocytes was determined by quantitative polymerase chain reaction in 1309 stroke patients and 1309 age- and sex-matched control subjects as well as 858 stroke patients followed prospect ively for 5 years . For each measure , the study sample was divided into quartiles . The associations between the telomere length and risk of stroke as well as poststroke adverse outcomes were determined . Results — Mean telomere length was significantly shorter in stroke patients than in control subjects . Shorter telomere length levels were directly associated with a higher risk of stroke in the case/control sample . As compared with the fourth ( longest ) quartile , the odd ratios [ OR ] ( and 95 % confidence intervals [ CI ] ) for ischemic stroke risk were as follows : third quartile , 1.37 ( 1.04–1.82 ) ; second quartile , 1.53 ( 1.17–2.02 ) ; and first quartile , 2.12 ( 1.62–2.77 ) . Follow-up of the patients from the prospect i ve cohort also showed that shorter telomere length levels were associated with mortality from all causes but not with recurrence of stroke . Conclusions — Shorter telomere length was associated with ischemic stroke and was a strong predictor of poststroke death Background —Telomere shortening has been proposed as a marker of biological aging . Whether leukocyte telomere length is associated with mortality among patients with stable coronary artery disease ( CAD ) is unknown . Methods and Results —We measured leukocyte telomere length in 780 patients with stable CAD in a prospect i ve cohort study . Participants were categorized by quartiles of telomere length . Hazard Ratios ( HRs ) and 95 % confidence intervals were calculated for all-cause mortality , heart failure ( HF ) hospitalization , and cardiovascular ( CV ) events . After 4.4 years of follow-up there were 166 deaths . Compared with participants in the highest telomere length quartile , those in the lowest quartile were at increased risk of death ( age-adjusted HR 1.8 ; 95 % CI 1.2 to 2.9 ) . After multivariate adjustment for clinical ( HR 2.1 ; CI 1.3 to 3.3 ) , inflammatory ( HR 2.0 ; CI 1.2 to 3.2 ) , and echocardiographic ( HR 1.9 ; CI 1.0 to 3.5 ) risk factors , patients in the lowest quartile of telomere length remained at significantly increased risk of death compared to those in the highest quartile . Patients in the lowest quartile of telomere length were also at significantly increased risk of HF hospitalization ( HR 2.6 ; CI 1.1 to 6.0 ) but not CV events ( HR 1.7 ; CI 0.9 to 3.5 ) . Conclusions —Reduced leukocyte telomere length is associated with all-cause mortality in patients with stable CAD . The prognostic value of short telomeres in predicting death is not completely captured by existing clinical , inflammatory , and echocardiographic markers of risk Telomere length ( TL ) has been proposed as a marker of mitotic cell age and as a general index of human organismic aging . Short absolute leukocyte telomere length has been linked to cardiovascular-related morbidity and mortality . Our aim was to test whether the rate of change in leukocyte TL is related to mortality in a healthy elderly cohort . We examined a sub sample of 236 r and omly selected Caucasian participants from the MacArthur Health Aging Study ( aged 70 to 79 years ) .  DNA sample s from baseline and 2.5 years later were assayed for mean TL of leukocytes . Percent change in TL was calculated as a measure of TL change ( TLC ) . Associations between TL and TLC with 12-year overall and cardiovascular mortality were assessed . Over the 2.5 year period , 46 % of the study participants showed maintenance of mean bulk TL , whereas 30 % showed telomere shortening , and , unexpectedly , 24 % showed telomere lengthening . For women , short baseline TL was related to greater mortality from cardiovascular disease ( OR = 2.3 ; 95 % CI : 1.0 - 5.3 ) . For men , TLC ( specifically shortening ) , but not baseline TL , was related to greater cardiovascular mortality , OR = 3.0 ( 95 % CI : 1.1 - 8.2 ) . This is the first demonstration that rate of telomere length change ( TLC ) predicts mortality and thus may be a useful prognostic factor for longevity Objective —To determine the association between  leukocyte telomere length ( TL ) and atherosclerosis and its clinical sequelae stroke and myocardial infa rct ion . Methods and Results —Within the scope of the prospect i ve population -based Bruneck Study ,  leukocyte TL  was measured by quantitative polymerase chain reaction in 800 women and men aged 45 to 84 years ( in 1995 ) . The manifestation of cardiovascular disease ( CVD ) ( 1995–2005 ) and the progression of atherosclerosis ( 1995–2000 ) were carefully assessed . The TL was shorter in men than in women ( age-adjusted mean [ 95 % CI ] , 1.41 [ 1.33 to 1.49 ] versus 1.55 [ 1.47 to 1.62 ] ; P=0.02 ) and inversely correlated to age ( r=−0.22 , P<0.001 ) and family history of CVD ( P=0.03 ) . Participants with CVD events during follow-up ( n=88 ) had significantly shorter telomeres ( age- and sex-adjusted mean [ 95 % CI ] , 1.25 [ 1.08 to 1.42 ] versus 1.51 [ 1.45 to 1.57 ] ; P<0.001 ) . In multivariable Cox models , baseline TL emerged as a significant and independent risk predictor for the composite CVD end point and its individual components ( myocardial infa rct ion and stroke ) ; however , this was not the case for de novo stable angina and intermittent claudication . Subjects in the top and bottom TL tertile group differed in their CVD risk by a factor of 2.72 ( 95 % CI , 1.41 to 5.28 ) , which is the risk ratio attributable to a 13.9-year difference in chronological age . Remarkably , in our atherosclerosis progression model , TL was strongly associated with advanced , but not early , atherogenesis . All findings were consistent in women and men . Conclusion —Our findings indicate a differential role of telomere shortening in the various stages of atherosclerosis , with preferential involvement in advanced vessel pathology and acute vascular syndromes Telomere length ( TL ) has been implicated in the pathogenesis of age-related disorders . However , there are no prospect i ve studies directly investigating the role of TL and relevant genes in diabetes development . In the multiethnic Women ’s Health Initiative , we identified 1,675 incident diabetes case participants in 6 years of follow-up and 2,382 control participants matched by age , ethnicity , clinical center , time of blood draw , and follow-up duration .  Leukocyte TL at baseline was measured using quantitative PCR , and Mendelian r and omization analysis was conducted to test whether TL is causally associated with diabetes risk . After adjustment for matching and known diabetes risk factors , odds ratios per 1-kilobase increment were 1.00 ( 95 % CI 0.90–1.11 ) in whites , 0.95 ( 0.85–1.06 ) in blacks , 0.96 ( 0.79–1.17 ) in Hispanics , and 0.88 ( 0.70–1.10 ) in Asians . Of the 80 single nucleotide polymorphisms ( SNPs ) in nine genes involved in telomere regulation , 14 SNPs were predictive of TL , but none were significantly associated with diabetes risk . Using ethnicity-specific SNPs as r and omization instruments , we observed no statistically significant association between TL and diabetes risk ( P = 0.52 ) . Although leukocyte TL was weakly associated with diabetes risk , this association was not independent of known risk factors . These prospect i ve findings indicate limited clinical utility of TL in diabetes risk stratification among postmenopausal women Inter-individual differences in biological aging could affect susceptibility to stroke . To date , the relationship between stroke and telomere shortening remain inconclusive ; and sparse data are available for haemorrhagic stroke . A Chinese case-control study was conducted , comprising 1756 cases ( 767 atherothrombosis , 503 lacunar infa rct ion and 486 haemorrhagic strokes ) and 1801 controls . Stroke patients were prospect ively followed up for a median of 4.5 ( range , 0.1 - 6.0 ) years . Individuals with shorter telomere length had a higher presence of atherothrombotic stroke { multivariate OR ( odds ratio ) 1.37 [ 95 % CI ( confidence interval ) , 1.06 - 1.77 ] ; P=0.015 } or haemorrhagic stroke [ multivariate OR 1.48 ( 95 % CI , 1.08 - 2.02 ) ; P=0.016 ] in comparison of the lowest to highest tertile of telomere length . Particularly , in subjects with a family history of stroke , there was a significant 2.55-fold increased presence of atherothrombotic stroke ( 95 % CI , 1.87 - 3.48 ; Ptrend<0.0001 ) and a 2.33-fold increased presence of haemorrhagic stroke ( 95 % CI , 1.62 - 3.36 ; Ptrend<0.0001 ) . During the follow-up , 338 recurrent strokes and 312 deaths ( 181 from stroke or coronary heart disease and 131 from other causes ) were documented . Associations with stroke recurrence were not observed in the follow-up patients , whereas atherothrombotic stroke cases with shorter telomeres had 69 % increased risk of post-stroke death [ relative risk , 1.69 ( 95 % CI , 1.07 - 2.67 ) ; P=0.02 ] . Finally , we compared telomere lengths in 12 paired sample s of circulating leucocytes and carotid atherosclerotic plaques from patients undergoing carotid endarterectomy ; there was a positive correlation between vessel wall tissue and leucocyte telomere length . In conclusion , shorter telomere length may serve as a potential marker for the presence of atherothrombotic and haemorrhagic stroke and for the risk of post-stroke death Telomere shortening has been implicated in cardiovascular disease ( CVD ) . However , prospect i ve data on the association between relative telomere length ( RTL ) and ischaemic stroke are scarce and inconclusive Although shortened telomeres were shown associated with several risk factors of diabetes , there is lack of data on their relationship with mitochondrial dysfunction . Therefore , we compared the relationship between telomere length and mitochondrial DNA ( mtDNA ) content in patients with type 2 diabetes mellitus ( T2DM ; n = 145 ) and in subjects with normal gluc 
    Output:
    
Shortened leukocyte telomere length demonstrates a significant association with stroke , myocardial infa rct ion , and type 2 diabetes mellitus .