Evidence map›Paper›PMID 23549607›Full record

ArticleCirculation. Cardiovascular imaging2013

T1 measurements identify extracellular volume expansion in hypertrophic cardiomyopathy sarcomere mutation carriers with and without left ventricular hypertrophy.

Carolyn Y Ho, Siddique A Abbasi, Tomas G Neilan, Ravi V Shah, Yucheng Chen, Bobak Heydari, Allison L Cirino, Neal K Lakdawala, E John Orav, Arantxa González and 4 more

Registry-linked trialOpen access · bronzeAbstract read
In one paragraph

Article in Circulation. Cardiovascular imaging, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT00319982 (Treatment of Preclinical Hypertrophic Cardiomyopathy With Diltiazem), which is not on this map. Cited by 112 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
112citing papers in PubMed, 2 pooled it
17.4field-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.

NCT00319982 phase2 / phase3completednot on this map

Treatment of Preclinical Hypertrophic Cardiomyopathy With Diltiazem

TypeinterventionalSponsorBrigham and Women's HospitalRan2006 to 2013Enrolled39ConditionsHypertrophic CardiomyopathyArmsDiltiazem, Placebo
3 · Its place in the literature

Who cites it

112 citing papers in PubMed, 2 syntheses or guidelines pooled it, 255 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Trial
  5. Trial
  6. Article
  7. Cardiovascular magnetic resonance for therapy monitoring in cardiomyopathies.European heart journal. Imaging methods and practice · 2026
    Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Cardiac Magnetic Resonance in Heart Failure: Diagnostic and Prognostic Assessments.Journal of cardiovascular development and disease · 2025
    Review
  13. Review
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Review
  20. Review

52 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

14 authors at 1 institution in 1 country.

Carolyn Y HoCardiovascular Division, Brigham and Women's Hospital, Boston, MA 02115, USA. cho@partners.org
Siddique A Abbasi
Tomas G Neilan
Ravi V Shah
Yucheng Chen
Bobak Heydari
Allison L Cirino
Neal K Lakdawala
E John Orav
Arantxa González
Begoña López
Javier Díez
Michael Jerosch-Herold
Raymond Y Kwong
Universidad de Navarra · ES

Funding

Using Genetics for Early Phenotyping & Prevention of Hypertrophic CardiomyopathyP20HL101408 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI HO, CAROLYN Y, SEIDMAN, CHRISTINE E · 2010 to 2011
$1.5M
NHLBI NIH HHS P20 HL101408
6 · The paper itself

Abstract

backgroundMyocardial fibrosis is a hallmark of hypertrophic cardiomyopathy (HCM) and a potential substrate for arrhythmias and heart failure. Sarcomere mutations seem to induce profibrotic changes before left ventricular hypertrophy (LVH) develops. To further evaluate these processes, we used cardiac magnetic resonance with T1 measurements on a genotyped HCM population to quantify myocardial extracellular volume (ECV). METHODS AND

resultsSarcomere mutation carriers with LVH (G+/LVH+, n=37) and without LVH (G+/LVH-, n=29), patients with HCM without mutations (sarcomere-negative HCM, n=11), and healthy controls (n=11) underwent contrast cardiac magnetic resonance, measuring T1 times pre- and postgadolinium infusion. Concurrent echocardiography and serum biomarkers of collagen synthesis, hemodynamic stress, and myocardial injury were also available in a subset. Compared with controls, ECV was increased in patients with overt HCM, as well as G+/LVH- mutation carriers (ECV=0.36±0.01, 0.33±0.01, 0.27±0.01 in G+/LVH+, G+/LVH-, controls, respectively; P≤0.001 for all comparisons). ECV correlated with N-terminal probrain natriuretic peptide levels (r=0.58; P<0.001) and global E' velocity (r=-0.48; P<0.001). Late gadolinium enhancement was present in >60% of overt patients with HCM but absent from G+/LVH- subjects. Both ECV and late gadolinium enhancement were more extensive in sarcomeric HCM than sarcomere-negative HCM.

conclusionsMyocardial ECV is increased in HCM sarcomere mutation carriers even in the absence of LVH. These data provide additional support that fibrotic remodeling is triggered early in disease pathogenesis. Quantifying ECV may help characterize the development of myocardial fibrosis in HCM and ultimately assist in developing novel disease-modifying therapy, targeting interstitial fibrosis.

Indexed as

Magnetic Resonance Imaging, CineMutationVentricular RemodelingAdolescentAdultAgedAnalysis of VarianceBiomarkersCardiomyopathy, HypertrophicCase-Control StudiesCollagenContrast MediaDisease ProgressionDNA Mutational AnalysisExtracellular MatrixFemaleBiomarkersCollagenContrast MediaGadolinium DTPAfibrosisgadoliniumgeneticshypertrophic cardiomyopathyMRI

Identifiers

PMID23549607
PMCPMC3769196
OpenAlexW1983283029

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

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.