Evidence map›Paper›PMID 29920523›Full record

ArticlePloS one2018

Telomere length and mortality in the Ludwigshafen Risk and Cardiovascular Health study.

Irene Pusceddu, Marcus Kleber, Graciela Delgado, Wolfgang Herrmann, Winfried März, Markus Herrmann

Abstract read
In one paragraph

Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 2 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

28 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Article
  5. Inflammation, Lp(a) and cardiovascular mortality: results from the LURIC study.Clinical research in cardiology : official journal of the German Cardiac Society · 2025
    Article
  6. Article
  7. Review
  8. Paternal contributions to telomere reprogramming in fetal development.International journal of biochemistry and molecular biology · 2025
    Article
  9. Article
  10. Article
  11. Telomere Length: A Cardiovascular Biomarker and a Novel Therapeutic Target.International journal of molecular sciences · 2022
    Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors.

Irene PuscedduLaboratory of Clinical Pathology, Hospital of Bolzano, Bolzano, Italy.
Marcus KleberMedical Clinic V (Nephrology, Hypertensiology, Rheumatology, Endocrinology, Diabetology), Medical Faculty of Mannheim, University of Heidelberg, Mannheim, Germany.
Graciela DelgadoMedical Clinic V (Nephrology, Hypertensiology, Rheumatology, Endocrinology, Diabetology), Medical Faculty of Mannheim, University of Heidelberg, Mannheim, Germany.
Wolfgang HerrmannDepartement of Clinical Chemistry, University of Saarland, Homburg, Germany.
Winfried MärzMedical Clinic V (Nephrology, Hypertensiology, Rheumatology, Endocrinology, Diabetology), Medical Faculty of Mannheim, University of Heidelberg, Mannheim, Germany.
Markus HerrmannLaboratory of Clinical Pathology, Hospital of Bolzano, Bolzano, Italy.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionShort telomeres have been associated with adverse lifestyle factors, cardiovascular risk factors and age-related diseases, including cardiovascular disease (CVD), myocardial infarction, atherosclerosis, hypertension, diabetes, and also with mortality. However, previous studies report conflicting results.

objectivesThe aim of the present study has been to investigate the involvement of telomere length in all-cause and CVD mortality in subjects hospitalized for diagnostic coronary angiography of the Ludwigshafen Risk and Cardiovascular Health (LURIC) study.

methodsRelative telomere length (RTL) was measured with a Q-PCR based method in 3,316 participants of the LURIC study. Age-corrected RTL was calculated as the ratio between RTL and age. Median follow-up was 9.9 years. Cox regression and Kaplan-Maier analyses were performed to evaluate the role of RTL for all-cause and cardiovascular mortality.

resultsRTL correlated negatively with age (r = -0.09; p<0.001). In surviving patients the correlation between age and RTL was statistically significant (r = -0.088; p<0.001), but not in patients who died during follow-up (r = -0.043; p = 0.20). Patients in quartiles 2-4 of RTL had a lower hazard ratio for all-cause mortality (HR:0.822; 95%CI 0.712-0.915; p = 0.008) and CVD-mortality (HR:0.836; 95%CI 0.722-0.969; p = 0.017) when compared to those in the 1st quartile. Adjustment for major cardiovascular risk factors did not change this result, however additional adjustment for age attenuated this effect. Patients in the 4th quartile of age-corrected RTL compared to those in the 1st quartile had a lower hazard ratio for all-cause mortality, even with adjustment for major cardiovascular risk factors.

conclusionsThe present study supports the hypothesis that short telomere length increases the risk of all-cause and CVD mortality. Age appears to be an important co-variate that explains a substantial fraction of this effect. It remains unclear whether short telomeres contribute directly to the increase in mortality or if they are simply a surrogate marker for other adverse processes of aging.

Indexed as

Telomere ShorteningAgedAge FactorsCardiovascular DiseasesCase-Control StudiesCause of DeathCoronary AngiographyFemaleGermanyHospitalizationHumansKaplan-Meier EstimateMaleMiddle AgedProportional Hazards Models

Identifiers

PMID29920523
PMCPMC6007915

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.