Evidence map›Paper›PMID 26260054›Full record

ArticleJournal of the American Heart Association2015

Impaired Myocardial Oxygenation Response to Stress in Patients With Chronic Kidney Disease.

Susie Parnham, Jonathan M Gleadle, Sripal Bangalore, Suchi Grover, Rebecca Perry, Richard J Woodman, Carmine G De Pasquale, Joseph B Selvanayagam

Open access · goldAbstract read
In one paragraph

Article in Journal of the American Heart Association, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

11 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. The impact of hematocrit on oxygenation-sensitive cardiovascular magnetic resonance.Journal of cardiovascular magnetic resonance : official journal of the Society for Cardiovascular Magnetic Resonance · 2016
    Article
  11. Article
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

8 authors at 4 institutions in 2 countries.

Susie ParnhamDepartment of Cardiovascular Medicine, Flinders Medical Centre, Bedford Park, South Australia, Australia (S.P., S.G., R.P., C.G.D.P., J.B.S.) School of Medicine, Flinders University, Bedford Park, South Australia, Australia (S.P., J.M.G., R.P., C.G.D.P., J.B.S.) South Australian Health and Medical Research Institute, Adelaide, South Australia, Australia (S.P., S.G., J.B.S.).
Jonathan M GleadleDepartment of Renal Medicine, Flinders Medical Centre, Bedford Park, South Australia, Australia (J.M.G.) School of Medicine, Flinders University, Bedford Park, South Australia, Australia (S.P., J.M.G., R.P., C.G.D.P., J.B.S.).
Sripal BangaloreCardiac Catheterization Laboratory, Cardiovascular Outcomes Group, New York University School of Medicine, New York, NY (S.B.).
Suchi GroverDepartment of Cardiovascular Medicine, Flinders Medical Centre, Bedford Park, South Australia, Australia (S.P., S.G., R.P., C.G.D.P., J.B.S.) South Australian Health and Medical Research Institute, Adelaide, South Australia, Australia (S.P., S.G., J.B.S.).
Rebecca PerryDepartment of Cardiovascular Medicine, Flinders Medical Centre, Bedford Park, South Australia, Australia (S.P., S.G., R.P., C.G.D.P., J.B.S.) School of Medicine, Flinders University, Bedford Park, South Australia, Australia (S.P., J.M.G., R.P., C.G.D.P., J.B.S.).
Richard J WoodmanFlinders Centre for Epidemiology and Biostatistics, School of Medicine, Flinders University, Bedford Park, South Australia, Australia (R.J.W.).
Carmine G De PasqualeDepartment of Cardiovascular Medicine, Flinders Medical Centre, Bedford Park, South Australia, Australia (S.P., S.G., R.P., C.G.D.P., J.B.S.) School of Medicine, Flinders University, Bedford Park, South Australia, Australia (S.P., J.M.G., R.P., C.G.D.P., J.B.S.).
Joseph B SelvanayagamDepartment of Cardiovascular Medicine, Flinders Medical Centre, Bedford Park, South Australia, Australia (S.P., S.G., R.P., C.G.D.P., J.B.S.) School of Medicine, Flinders University, Bedford Park, South Australia, Australia (S.P., J.M.G., R.P., C.G.D.P., J.B.S.) South Australian Health and Medical Research Institute, Adelaide, South Australia, Australia (S.P., S.G., J.B.S.).
Flinders Medical Centre · AUSouth Australian Health and Medical Research Institute · AUFlinders University · AUNew York University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCoronary artery disease and left ventricular hypertrophy are prevalent in the chronic kidney disease (CKD) and renal transplant (RT) population. Advances in cardiovascular magnetic resonance (CMR) with blood oxygen level-dependent (BOLD) technique provides capability to assess myocardial oxygenation as a measure of ischemia. We hypothesized that the myocardial oxygenation response to stress would be impaired in CKD and RT patients. METHODS AND

resultsFifty-three subjects (23 subjects with CKD, 10 RT recipients, 10 hypertensive (HT) controls, and 10 normal controls without known coronary artery disease) underwent CMR scanning. All groups had cine and BOLD CMR at 3 T. The RT and HT groups also had late gadolinium CMR to assess infarction/replacement fibrosis. The CKD group underwent 2-dimensional echocardiography strain to assess fibrosis. Myocardial oxygenation was measured at rest and under stress with adenosine (140 μg/kg per minute) using BOLD signal intensity. A total of 2898 myocardial segments (1200 segments in CKD patients, 552 segments in RT, 480 segments in HT, and 666 segments in normal controls) were compared using linear mixed modeling. Diabetes mellitus (P=0.47) and hypertension (P=0.57) were similar between CKD, RT, and HT groups. The mean BOLD signal intensity change was significantly lower in the CKD and RT groups compared to HT controls and normal controls (-0.89±10.63% in CKD versus 5.66±7.87% in RT versus 15.54±9.58% in HT controls versus 16.19±11.11% in normal controls, P<0.0001). BOLD signal intensity change was associated with estimated glomerular filtration rate (β=0.16, 95% CI=0.10 to 0.22, P<0.0001). Left ventricular mass index and left ventricular septal wall diameter were similar between the CKD predialysis, RT, and HT groups. None of the CKD patients had impaired global longitudinal strain and none of the RT group had late gadolinium hyperenhancement.

conclusionsMyocardial oxygenation response to stress is impaired in CKD patients and RT recipients without known coronary artery disease, and unlikely to be solely accounted for by the presence of diabetes mellitus, left ventricular hypertrophy, or myocardial scarring. The impaired myocardial oxygenation in CKD patients may be associated with declining renal function. Noncontrast BOLD CMR is a promising tool for detecting myocardial ischemia in the CKD population.

Indexed as

Oxygen ConsumptionAdenosineAdultAgedBiomarkersCase-Control StudiesContrast MediaFemaleFibrosisGlomerular Filtration RateHeart DiseasesHumansKidneyKidney TransplantationLinear ModelsMagnetic Resonance Imaging, CineAdenosineBiomarkersContrast MediagadobutrolOrganometallic CompoundsOxygenVasodilator Agentsblood oxygen level–dependentchronic kidney diseasecoronary artery diseasemyocardial ischemiamyocardial oxygenationrenal transplant

Identifiers

PMID26260054
PMCPMC4599475
OpenAlexW2131499898

What OpenQuestion holds

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LicenceCC BY-NC
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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.