Evidence map›Paper›PMID 29467150›Full record

ArticleJournal of the American Heart Association2018

High-Sensitivity Troponin I Levels and Coronary Artery Disease Severity, Progression, and Long-Term Outcomes.

Ayman Samman Tahhan, Pratik Sandesara, Salim S Hayek, Muhammad Hammadah, Ayman Alkhoder, Heval M Kelli, Matthew Topel, Wesley T O'Neal, Nima Ghasemzadeh, Yi-An Ko and 13 more

Open access · goldAbstract read
In one paragraph

Article in Journal of the American Heart Association, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
5.8field-weighted citation impact, top 3% 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

47 citing papers in PubMed, 97 citations in OpenAlex.

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  5. High-sensitivity cardiac troponin I and frailty: associations with the frailty index and Fried phenotype in older women.The journals of gerontology. Series A, Biological sciences and medical sciences · 2026
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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

23 authors at 4 institutions in 1 country.

Ayman Samman TahhanDivision of Cardiology, Emory Clinical Cardiovascular Research Institute, Emory University School of Medicine, Atlanta, GA.
Pratik SandesaraDivision of Cardiology, Emory Clinical Cardiovascular Research Institute, Emory University School of Medicine, Atlanta, GA.
Salim S HayekDivision of Cardiology, Emory Clinical Cardiovascular Research Institute, Emory University School of Medicine, Atlanta, GA.
Muhammad HammadahDivision of Cardiology, Emory Clinical Cardiovascular Research Institute, Emory University School of Medicine, Atlanta, GA.
Ayman AlkhoderDivision of Cardiology, Emory Clinical Cardiovascular Research Institute, Emory University School of Medicine, Atlanta, GA.
Heval M KelliDivision of Cardiology, Emory Clinical Cardiovascular Research Institute, Emory University School of Medicine, Atlanta, GA.
Matthew TopelDivision of Cardiology, Emory Clinical Cardiovascular Research Institute, Emory University School of Medicine, Atlanta, GA.
Wesley T O'NealDivision of Cardiology, Emory Clinical Cardiovascular Research Institute, Emory University School of Medicine, Atlanta, GA.
Nima GhasemzadehDivision of Cardiology, Emory Clinical Cardiovascular Research Institute, Emory University School of Medicine, Atlanta, GA.
Yi-An KoDepartment of Biostatistics and Bioinformatics, Emory University, Atlanta, GA.
Mohamad Mazen GafeerDivision of Cardiology, Emory Clinical Cardiovascular Research Institute, Emory University School of Medicine, Atlanta, GA.
Naser AbdelhadiDivision of Cardiology, Emory Clinical Cardiovascular Research Institute, Emory University School of Medicine, Atlanta, GA.
Fahad ChoudharyDivision of Cardiology, Emory Clinical Cardiovascular Research Institute, Emory University School of Medicine, Atlanta, GA.
Keyur PatelDivision of Cardiology, Emory Clinical Cardiovascular Research Institute, Emory University School of Medicine, Atlanta, GA.
Agim BeshiriDiagnostics Division, Abbott Laboratories, North Chicago, IL.
Gillian MurtaghDiagnostics Division, Abbott Laboratories, North Chicago, IL.
Jonathan KimDivision of Cardiology, Emory Clinical Cardiovascular Research Institute, Emory University School of Medicine, Atlanta, GA.
Peter WilsonDivision of Cardiology, Emory Clinical Cardiovascular Research Institute, Emory University School of Medicine, Atlanta, GA.
Leslee ShawDivision of Cardiology, Emory Clinical Cardiovascular Research Institute, Emory University School of Medicine, Atlanta, GA.
Viola VaccarinoDivision of Cardiology, Emory Clinical Cardiovascular Research Institute, Emory University School of Medicine, Atlanta, GA.
Stephen E EpsteinMedStar Heart and Vascular Institute, MedStar Washington Hospital Center, Washington, DC.
Laurence SperlingDivision of Cardiology, Emory Clinical Cardiovascular Research Institute, Emory University School of Medicine, Atlanta, GA.
Arshed A QuyyumiDivision of Cardiology, Emory Clinical Cardiovascular Research Institute, Emory University School of Medicine, Atlanta, GA aquyyum@emory.edu.
Emory University · USEmory Clinic · USAbbott (United States) · USMedStar Heart & Vascular Institute · US

Funding

Vascular Responses During Mental StressP01HL101398 · NHLBI · EMORY UNIVERSITY · PI SHEPS, DAVID SAMUEL · 2010 to 2015
$11.0M
Cell therapy for diabetic peripheral neurovascular complicationsDP3DK094346 · NIDDK · EMORY UNIVERSITY · PI CHENG, XIAODONG, YOON, YOUNG-SUP · 2011 to 2011
$6.1M
The role of the renin-angiotensin-endothelial pathway in ADRF1AG051633 · NIA · EMORY UNIVERSITY · PI HAJJAR, IHAB M, QUYYUMI, ARSHED A · 2015 to 2017
$6.0M
Metabolomics of subclinical and clinical cardiovascular diseaseP20HL113451 · NHLBI · EMORY UNIVERSITY · PI JONES, DEAN PAUL · 2012 to 2016
$4.3M
Heart Failure Clinical Trials NetworkU10HL110302 · NHLBI · EMORY UNIVERSITY · PI SMITH, ANDREW · 2012 to 2018
$2.5M
Genome-wide association study of MI in CaucasiansR01HL089650 · NHLBI · DECODE GENETICS, INC. · PI GULCHER, JEFFREY R · 2007 to 2010
$2.3M
BIOMARKERS OF ISCHEMIC OUTCOMES IN SYMPTOMATIC INTRACRANIAL STENOSIS (BIOSIS)R01NS064162 · NINDS · EMORY UNIVERSITY · PI FRANKEL, MICHAEL ROSS · 2010 to 2013
$1.0M
Injury and Repair Factors Promoting Atherosclerosis in HIVR56HL126558 · NHLBI · EMORY UNIVERSITY · PI OFOTOKUN, IGHOVWERHA, QUYYUMI, ARSHED A · 2014 to 2014
$758k
The Association between Acute Mental Stress and Electrocardiographic Left Atrial AbnormalitiesF32HL134290 · NHLBI · EMORY UNIVERSITY · PI O'NEAL, WESLEY T · 2016 to 2017
$122k
NHLBI NIH HHS F32 HL134290NHLBI NIH HHS P01 HL101398NHLBI NIH HHS P20 HL113451NHLBI NIH HHS R01 HL089650NHLBI NIH HHS R56 HL126558NHLBI NIH HHS U10 HL110302NIA NIH HHS RF1 AG051633NIDDK NIH HHS DP3 DK094346NINDS NIH HHS R01 NS064162
6 · The paper itself

Abstract

backgroundThe associations between high-sensitivity troponin I (hsTnI) levels and coronary artery disease (CAD) severity and progression remain unclear. We investigated whether there is an association between hsTnI and angiographic severity and progression of CAD and whether the predictive value of hsTnI level for incident cardiovascular outcomes is independent of CAD severity. METHODS AND

resultsIn 3087 patients (aged 63±12 years, 64% men) undergoing cardiac catheterization without evidence of acute myocardial infarction, the severity of CAD was calculated by the number of major coronary arteries with ≥50% stenosis and the Gensini score. CAD progression was assessed in a subset of 717 patients who had undergone ≥2 coronary angiograms >3 months before enrollment. Patients were followed up for incident all-cause mortality and incident cardiovascular events. Of the total population, 11% had normal angiograms, 23% had nonobstructive CAD, 20% had 1-vessel CAD, 20% had 2-vessel CAD, and 26% had 3-vessel CAD. After adjusting for age, sex, race, body mass index, smoking, hypertension, diabetes mellitus history, and renal function, hsTnI levels were independently associated with the severity of CAD measured by the Gensini score (log 2 ß=0.31; 95% confidence interval, 0.18-0.44;

conclusionsHigher hsTnI levels are associated with the underlying burden of coronary atherosclerosis, more rapid progression of CAD, and higher risk of all-cause mortality and incident cardiovascular events. Whether more aggressive treatment aimed at reducing hsTnI levels can modulate disease progression requires further investigation.

Indexed as

AgedBiomarkersCause of DeathCoronary AngiographyCoronary Artery DiseaseCoronary StenosisDisease ProgressionFemaleGeorgiaHumansIncidenceMaleMiddle AgedPredictive Value of TestsPrognosisRetrospective StudiesBiomarkersTroponin Iatherosclerosiscoronary angiographycoronary artery diseasetroponin

Identifiers

PMID29467150
PMCPMC5866331
OpenAlexW2793292495

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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.