Evidence map›Paper›PMID 31014085›Full record

ArticleCirculation2019

Cardiac Troponin T and Troponin I in the General Population.

Paul Welsh, David Preiss, Caroline Hayward, Anoop S V Shah, David McAllister, Andrew Briggs, Charles Boachie, Alex McConnachie, Sandosh Padmanabhan, Claire Welsh and 5 more

Open access · greenAbstract readComparative Study
In one paragraph

Article in Circulation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 159 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
159citing papers in PubMed, 4 pooled it
23.2field-weighted citation impact, top 1% 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

159 citing papers in PubMed, 4 syntheses or guidelines pooled it, 321 citations in OpenAlex.

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  14. Cardiac Biomarkers in Chronic Kidney Disease: Signal or Noise?Clinical journal of the American Society of Nephrology : CJASN · 2026
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99 more citing papers are in PubMed but not listed here.

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

15 authors at 2 institutions in 2 countries.

Paul WelshInstitute of Cardiovascular and Medical Sciences (P.W., S.P., C.W., N.S.), University of Glasgow, United Kingdom.
David PreissMRC Population Health Research Unit, Clinical Trial Service Unit and Epidemiological Studies Unit (D. Preiss), University of Oxford, United Kingdom.
Caroline HaywardMRC Human Genetics Unit, MRC Institute of Genetics and Molecular Medicine (C.H.), University of Edinburgh, United Kingdom.
Anoop S V ShahBHF Centre for Cardiovascular Science (A.S.V.S., N.L.M.), University of Edinburgh, United Kingdom.
David McAllisterInstitute of Cardiovascular and Medical Sciences (P.W., S.P., C.W., N.S.), University of Glasgow, United Kingdom.
Andrew BriggsInstitute of Health and Wellbeing (A.B.), University of Glasgow, United Kingdom.
Charles BoachieRobertson Centre for Biostatistics (C.B., A.M.), University of Glasgow, United Kingdom.
Alex McConnachieRobertson Centre for Biostatistics (C.B., A.M.), University of Glasgow, United Kingdom.
Sandosh PadmanabhanInstitute of Cardiovascular and Medical Sciences (P.W., S.P., C.W., N.S.), University of Glasgow, United Kingdom.
Claire WelshInstitute of Cardiovascular and Medical Sciences (P.W., S.P., C.W., N.S.), University of Glasgow, United Kingdom.
Mark WoodwardThe George Institute for Global Health (M.W.), University of Oxford, United Kingdom.
Archie CampbellCentre for Genomic and Experimental Medicine, MRC Institute of Genetics and Molecular Medicine (A.C., D. Porteous), University of Edinburgh, United Kingdom.
David PorteousCentre for Genomic and Experimental Medicine, MRC Institute of Genetics and Molecular Medicine (A.C., D. Porteous), University of Edinburgh, United Kingdom.
Nicholas L MillsBHF Centre for Cardiovascular Science (A.S.V.S., N.L.M.), University of Edinburgh, United Kingdom.
Naveed SattarInstitute of Cardiovascular and Medical Sciences (P.W., S.P., C.W., N.S.), University of Glasgow, United Kingdom.
University of Edinburgh · GBJohns Hopkins University · US

Funding

British Heart Foundation FS/16/14/32023British Heart Foundation RE/13/1/30181Chief Scientist Office ASM/14/01Chief Scientist Office ASM/14/1Chief Scientist Office CZD/16/6Medical Research Council G0700704Medical Research Council MC_PC_U127592696Medical Research Council MC_UU_00007/10Medical Research Council MR/K026992/1
6 · The paper itself

Abstract

backgroundThere is great interest in widening the use of high-sensitivity cardiac troponins for population cardiovascular disease (CVD) and heart failure screening. However, it is not clear whether cardiac troponin T (cTnT) and troponin I (cTnI) are equivalent measures of risk in this setting. We aimed to compare and contrast (1) the association of cTnT and cTnI with CVD and non-CVD outcomes, and (2) their determinants in a genome-wide association study.

methodsHigh-sensitivity cTnT and cTnI were measured in serum from 19 501 individuals in Generation Scotland Scottish Family Health Study. Median follow-up was 7.8 years (quartile 1 to quartile 3, 7.1-9.2). Associations of each troponin with a composite CVD outcome (1177 events), CVD death (n=266), non-CVD death (n=374), and heart failure (n=216) were determined by using Cox models. A genome-wide association study was conducted using a standard approach developed for the cohort.

resultsBoth cTnI and cTnT were strongly associated with CVD risk in unadjusted models. After adjusting for classical risk factors, the hazard ratio for a 1 SD increase in log transformed troponin was 1.24 (95% CI, 1.17-1.32) and 1.11 (1.04-1.19) for cTnI and cTnT, respectively; ratio of hazard ratios 1.12 (1.04-1.21). cTnI, but not cTnT, was associated with myocardial infarction and coronary heart disease. Both cTnI and cTnT had strong associations with CVD death and heart failure. By contrast, cTnT, but not cTnI, was associated with non-CVD death; ratio of hazard ratios 0.77 (0.67-0.88). We identified 5 loci (53 individual single-nucleotide polymorphisms) that had genome-wide significant associations with cTnI, and a different set of 4 loci (4 single-nucleotide polymorphisms) for cTnT.

conclusionsThe upstream genetic causes of low-grade elevations in cTnI and cTnT appear distinct, and their associations with outcomes also differ. Elevations in cTnI are more strongly associated with some CVD outcomes, whereas cTnT is more strongly associated with the risk of non-CVD death. These findings help inform the selection of an optimal troponin assay for future clinical care and research in this setting.

Indexed as

Polymorphism, Single NucleotideAdultAgedCardiovascular DiseasesFemaleGenetic Predisposition to DiseaseGenome-Wide Association StudyHumansMaleMiddle AgedPredictive Value of TestsPrognosisRisk AssessmentRisk FactorsScotlandTime FactorsTroponin ITroponin Tcardiovascular diseasesgeneticsrisk factorstroponintroponin T

Identifiers

PMID31014085
PMCPMC6571179
OpenAlexW2941253250

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.