Evidence map›Paper›PMID 12860897›Full record

Trial reportCirculation2003

Tissue Doppler imaging predicts the development of hypertrophic cardiomyopathy in subjects with subclinical disease.

Sherif F Nagueh, Judy McFalls, Denise Meyer, Rita Hill, William A Zoghbi, James W Tam, Miguel A Quiñones, Robert Roberts, A J Marian

Open access · greenAbstract readClinical TrialControlled Clinical Trial
In one paragraph

Trial report in Circulation, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed
10.2field-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

70 citing papers in PubMed, 280 citations in OpenAlex.

  1. Article
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  4. Review
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  8. Review
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  13. Article
  14. Article
  15. Clinical Interpretation and Management of Genetic Variants.JACC. Basic to translational science · 2020
    Review
  16. Review
  17. Article
  18. Article
  19. Hypertrophic cardiomyopathy: genetics and clinical perspectives.Cardiovascular diagnosis and therapy · 2019
    Review
  20. Article

10 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

9 authors at 1 institution in 1 country.

Sherif F NaguehDepartment of Medicine, Section of Cardiology, Baylor College of Medicine, Houston, Tex, USA. sherifn@bcm.tmc.edu
Judy McFalls
Denise Meyer
Rita Hill
William A Zoghbi
James W Tam
Miguel A Quiñones
Robert Roberts
A J Marian
Baylor College of Medicine · US

Funding

TUMOR NECROSIS FACTOR-ALPHA IN CONGESTIVE HEART FAILURE--MECHANISMS/RELEVANCEP50HL054313 · NHLBI · BAYLOR COLLEGE OF MEDICINE · PI MANN, DOUGLAS LOWELL · 1995 to 2004
$8.2M
SCOR IN HEART FAILUREP50HL042267 · NHLBI · BAYLOR COLLEGE OF MEDICINE · PI ROBERTS, ROBERT · 1990 to 1994
–
NHLBI NIH HHS P50 HL054313NHLBI NIH HHS P50-HL42267-01
6 · The paper itself

Abstract

backgroundSystolic (Sa) and diastolic (Ea) myocardial velocities measured by tissue Doppler (TD) imaging (TDI) recently were shown to be decreased in subjects who have mutations causing hypertrophic cardiomyopathy (HCM) but who do not have left ventricular (LV) hypertrophy. By studying these subjects at a later date, we sought to determine whether TDI predicts the subsequent evolution of the HCM phenotype. METHODS AND

resultsSerial 2D and Doppler echocardiography were performed in 12 subjects (age range, 17 to 51 years) with HCM-causing mutations on 2 occasions: before development of hypertrophy and 2 years later. Twelve age- and gender-matched family members without mutations were included as control subjects. In those with mutations, mean septal thickness and LV mass were 1.07+/-0.14 cm and 103.0+/-11 g at baseline, respectively, and increased to 1.30+/-0.36 cm and 193.0+/-78 g at follow-up (P<0.01), with 6 subjects satisfying HCM diagnostic criteria. Sa and Ea velocities in those with mutations were lower compared with control subjects at baseline and follow-up (lateral Sa, 15+/-1.2 versus 8.2+/-2.1 cm/s; lateral Ea, 16.5+/-2.8 versus 8.1+/-2.3 cm/s; P<0.01). At 2 years, left atrial volume and pulmonary venous flow indices of LV filling pressures increased, whereas TD early and late diastolic velocities decreased (all P<0.05) in those with the mutations. Control subjects had no significant interval changes of the above parameters.

conclusionsSubsequent development of HCM in subjects with initially reduced TD velocities establishes TDI as a reliable method for early identification of HCM mutation carriers.

Indexed as

Echocardiography, DopplerAdolescentAdultBlood Flow VelocityCardiomyopathy, Hypertrophic, FamilialCarrier ProteinsDisease ProgressionFemaleFollow-Up StudiesGenetic Carrier ScreeningHumansHypertrophy, Left VentricularMaleMiddle AgedMutationMyosin Binding Protein CCarrier ProteinsMyosin Binding Protein CVentricular Myosins

Identifiers

PMID12860897
PMCPMC2908312
OpenAlexW2025818746

What OpenQuestion holds

Textmetadata
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.