Evidence map›Paper›PMID 24837587›Full record

ArticleJournal of the American Heart Association2014

Haptoglobin 2-2 genotype is not associated with cardiovascular risk in subjects with elevated glycohemoglobin-results from the Bruneck Study.

Raimund Pechlaner, Stefan Kiechl, Peter Willeit, Egon Demetz, Margot Haun, Siegfried Weger, Friedrich Oberhollenzer, Florian Kronenberg, Enzo Bonora, Günter Weiss and 1 more

Open access · goldAbstract read
In one paragraph

Article in Journal of the American Heart Association, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
2.0field-weighted citation impact, top 15% of its field
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

14 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.

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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

11 authors at 3 institutions in 3 countries.

Raimund PechlanerDepartment of Neurology, Medical University Innsbruck, Innsbruck, Austria (R.P., S.K., P.W., J.W.).
Stefan KiechlDepartment of Neurology, Medical University Innsbruck, Innsbruck, Austria (R.P., S.K., P.W., J.W.).
Peter WilleitDepartment of Neurology, Medical University Innsbruck, Innsbruck, Austria (R.P., S.K., P.W., J.W.) Department of Public Health and Primary Care, University of Cambridge, Cambridge, United Kingdom (P.W.).
Egon DemetzDepartment of Internal Medicine VI, Medical University Innsbruck, Innsbruck, Austria (E.D., W.).
Margot HaunDivision of Genetic Epidemiology, Medical University Innsbruck, Innsbruck, Austria (M.H., F.K.).
Siegfried WegerDepartment of Internal Medicine, Hospital of Bruneck, Bruneck, Italy (S.W., F.O.).
Friedrich OberhollenzerDepartment of Internal Medicine, Hospital of Bruneck, Bruneck, Italy (S.W., F.O.).
Florian KronenbergDivision of Genetic Epidemiology, Medical University Innsbruck, Innsbruck, Austria (M.H., F.K.).
Enzo BonoraDivision of Endocrinology, Diabetes and Metabolic Diseases, University and Hospital Trust of Verona, Verona, Italy (E.B.).
Günter WeissDepartment of Internal Medicine VI, Medical University Innsbruck, Innsbruck, Austria (E.D., W.).
Johann WilleitDepartment of Neurology, Medical University Innsbruck, Innsbruck, Austria (R.P., S.K., P.W., J.W.).
Innsbruck Medical University · ATKrankenhaus Bruneck · ITUniversity of Verona · IT

Funding

Austrian Science Fund FWF TRP 188
6 · The paper itself

Abstract

backgroundHaptoglobin (Hp) is an abundant plasma protein with antioxidant properties. The Hp 2-2 genotype has previously been linked to coronary heart disease risk in individuals with elevated glycosylated hemoglobin (HbA1c). We investigated the association of Hp and HbA1c with cardiovascular disease (CVD) in the longitudinal, population-based Bruneck Study. METHODS AND

resultsHp genotype was determined by polymerase chain reaction according to standard procedures and HbA1c concentration by a Diabetes Control and Complications Trial-aligned assay. HbA1c was measured in 1995, 2000, and 2005. Occurrence of the combined CVD endpoint of myocardial infarction or stroke was recorded between 1995 and 2010. Outcome analyses employed the Cox proportional hazards model with HbA1c category as time-varying covariate. At baseline in 1995, 806 subjects (male sex, 49.3%; age, mean ± standard deviation, 62.70 ± 11.08 years) were included. During follow-up, 123 subjects experienced at least 1 CVD event (48 suffered myocardial infarction, 68 stroke, and 7 both). Among subjects with HbA1c ≥ 6.5% (≥ 48 mmol/mol), those with the Hp 2-2 genotype did not show an elevated risk of incident CVD compared with those with other genotypes (age- and sex-adjusted hazard ratio [95% CI], 0.47 [0.19, 1.13], P=0.092) and a null association was also observed in subjects with HbA1c<6.5% (1.10 [0.75, 1.62], P=0.629) (P for interaction=0.082).

conclusionsSubjects with the Hp 2-2 genotype and elevated HbA1c compared with subjects with other Hp genotypes and elevated HbA1c did not show increased CVD risk.

Indexed as

AgedCardiovascular DiseasesFemaleGenetic Predisposition to DiseaseGenotypeGlycated HemoglobinHaptoglobinsHumansLongitudinal StudiesMaleMiddle AgedMyocardial InfarctionPolymorphism, Single NucleotideProportional Hazards ModelsProspective StudiesRisk FactorsGlycated HemoglobinHaptoglobinshemoglobin A1c protein, humancardiovascular diseasesdiabetes mellitusgenetics

Identifiers

PMID24837587
PMCPMC4309057
OpenAlexW2154194383

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

Registered trials

None linked

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.