Article in Open heart, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–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.
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
10 authors.
Oluseye Ogunmoroti *Ciccarone Center for the Prevention of Cardiovascular Disease, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA seyeogunmoroti@gmail.com.ORCID 0000-0001-5216-2544
Olatokunbo Osibogun *Department of Epidemiology, Robert Stempel College of Public Health and Social Work, Florida International University, Miami, Florida, USA.ORCID 0000-0001-8902-4356
Richard A FerraroCiccarone Center for the Prevention of Cardiovascular Disease, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Paul M NdundaDivision of Cardiology, Louisiana State University Health, Shreveport, Louisiana, USA.
Nicholas B LarsonDivision of Clinical Trials and Biostatistics, Mayo Clinic College of Medicine and Science, Rochester, Minnesota, USA.
Paul A DeckerDivision of Clinical Trials and Biostatistics, Mayo Clinic College of Medicine and Science, Rochester, Minnesota, USA.
Suzette J BielinskiDivision of Epidemiology, Mayo Clinic College of Medicine and Science, Rochester, Minnesota, USA.
Roger S BlumenthalCiccarone Center for the Prevention of Cardiovascular Disease, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Matthew J BudoffDepartment of Medicine, Lundquist Institute at Harbor-UCLA, Torrance, California, USA.
Erin D MichosCiccarone Center for the Prevention of Cardiovascular Disease, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.ORCID 0000-0002-5547-5084
Funding
Institute for Clinical and Translational ResearchUL1TR001079 · NCATS · JOHNS HOPKINS UNIVERSITY · PI FORD, DANIEL ERNEST · 2013 to 2017
$60.1M
Wake Forest Clinical and Translational Science AwardUL1TR001420 · NCATS · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI ARD, JAMY D, FOLEY, KRISTIE L · 2015 to 2023
$32.3M
Clinical and Translational Science AwardUL1TR000040 · NCATS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI GINSBERG, HENRY N · 2012 to 2015
$26.2M
SUBCLINICAL CARDIOVASCULAR DISEASE COORDINATING CENTERN01HC95159 · NHLBI · UNIVERSITY OF WASHINGTON · PI KRONMAL, RICHARD A · 2007 to 2014
$19.6M
SUBCLINICAL CARDIOVASCULAR DISEASE STUDY--FIELD CENTERN01HC95160 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI WATSON, KAROL · 2007 to 2015
$7.7M
SUBCLINICAL CARDIOVASCULAR DISEASE STUDY-FIELD CENTERN01HC95164 · NHLBI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI LIU, KIANG · 2007 to 2015
$7.0M
SUBCLINICAL CARDIOVASCULAR DISEASE STUDY--FIELD CENTERN01HC95161 · NHLBI · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI SHEA, STEVEN · 2007 to 2014
$6.4M
SUBCLINICAL CARDIOVASCULAR DISEASE STUDY--FIELD CENTERN01HC95165 · NHLBI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI BURKE, GREGORY L · 2007 to 2014
$6.3M
SUBCLINICAL CARDIOVASCULAR DISEASE STUDY--FIELD CENTERN01HC95163 · NHLBI · UNIVERSITY OF MINNESOTA · PI FOLSOM, AARON R · 2007 to 2014
$6.1M
TITLE: MULTI-ETHNIC STUDY OF ATHEROSCLEROSIS (MESA)N01HC95162 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI POST, WENDY · 2007 to 2015
$6.0M
SUBCLINICAL CARDIOVASCULAR DISEASE STUDYN01HC95166 · NHLBI · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI TRACY, RUSSELL P · 2007 to 2014
$4.0M
Multi-Scale Biology of Atherosclerosis in the Cellular Adhesion PathwayR01HL098077 · NHLBI · MAYO CLINIC ROCHESTER · PI BIELINSKI, SUZETTE JANINE · 2010 to 2014
backgroundHepatocyte growth factor (HGF) is a biomarker with potential for use in the diagnosis, treatment and prognostication of cardiovascular disease (CVD). Elevated HGF is associated with calcification in the coronary arteries. However, knowledge is limited on the role HGF may play in extracoronary calcification (ECC). This study examined whether HGF is associated with ECC in the aortic valve (AVC), mitral annulus (MAC), ascending thoracic aorta and descending thoracic aortic (DTAC).
methodsAt baseline, adults aged 45-84 years, free of CVD, in the Multi-Ethnic Study of Atherosclerosis had HGF and ECC measured by ELISA and cardiac CT scan, respectively. ECC measurements were repeated after an average of 2.4 years of follow-up. Prevalent ECC was defined as Agatston score >0 at baseline. Incident ECC was defined as Agatston score >0 at follow-up among participants with Agatston score=0 at baseline. We used Poisson and linear mixed-effects regression models to estimate the association between HGF and ECC, adjusted for sociodemographic and CVD risk factors.
resultsOf 6648 participants, 53% were women. Mean (SD) age was 62 (10) years. Median (IQR) of HGF was 905 (757-1087) pg/mL. After adjustment for CVD risk factors, the highest HGF levels (tertile 3) were associated with greater prevalence and extent of AVC, MAC and DTAC at baseline compared with the lowest tertile (tertile 1). Additionally, the risk of incident AVC and MAC increased by 62% and 45%, respectively, in demographic-adjusted models. However, the associations were not statistically significant in fully adjusted models. The highest HGF levels were also associated with 10% and 13% increase in MAC and DTAC progression, respectively, even after adjustment for CVD risk factors.
conclusionHigher HGF levels were significantly associated with a greater risk of calcification at some extracoronary sites, suggesting an alternate biological pathway that could be targeted to reduce CVD risk.
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.
Hepatocyte growth factor is associated with greater risk of extracoronary calcification: results from the multiethnic study of atherosclerosis. · full record | OpenQuestion