Evidence map›Paper›PMID 30358845›Full record

ArticleEuropean heart journal. Cardiovascular Imaging2019

Progression of myocardial fibrosis in hypertrophic cardiomyopathy: mechanisms and clinical implications.

Betty Raman, Rina Ariga, Marco Spartera, Sanjay Sivalokanathan, Kenneth Chan, Sairia Dass, Steffen E Petersen, Matthew J Daniels, Jane Francis, Robert Smillie and 7 more

Abstract read
In one paragraph

Article in European heart journal. Cardiovascular Imaging, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
73citing papers in PubMed, 1 pooled it
–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.

3 · Its place in the literature

Who cites it

73 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  18. Cardiac Magnetic Resonance in Heart Failure: Diagnostic and Prognostic Assessments.Journal of cardiovascular development and disease · 2025
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13 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

17 authors.

Betty RamanDivision of Cardiovascular Medicine, Radcliffe Department of Medicine, University of Oxford, Headley Way, Oxford, UK.
Rina ArigaDivision of Cardiovascular Medicine, Radcliffe Department of Medicine, University of Oxford, Headley Way, Oxford, UK.
Marco SparteraDivision of Cardiovascular Medicine, Radcliffe Department of Medicine, University of Oxford, Headley Way, Oxford, UK.
Sanjay SivalokanathanDivision of Cardiovascular Medicine, Radcliffe Department of Medicine, University of Oxford, Headley Way, Oxford, UK.
Kenneth ChanDivision of Cardiovascular Medicine, Radcliffe Department of Medicine, University of Oxford, Headley Way, Oxford, UK.
Sairia DassDivision of Cardiovascular Medicine, Radcliffe Department of Medicine, University of Oxford, Headley Way, Oxford, UK.
Steffen E PetersenWilliam Harvey Research Institute, NIHR Barts Biomedical Research Centre, Queen Mary University of London, London, UK.
Matthew J DanielsDivision of Cardiovascular Medicine, Radcliffe Department of Medicine, University of Oxford, Headley Way, Oxford, UK.
Jane FrancisDivision of Cardiovascular Medicine, Radcliffe Department of Medicine, University of Oxford, Headley Way, Oxford, UK.
Robert SmillieDivision of Cardiovascular Medicine, Radcliffe Department of Medicine, University of Oxford, Headley Way, Oxford, UK.
Adam J LewandowskiDivision of Cardiovascular Medicine, Radcliffe Department of Medicine, University of Oxford, Headley Way, Oxford, UK.
Eric O OhumaNuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences, Centre for Statistics in Medicine, University of Oxford, Old Road Campus, Oxford, UK.
Christopher RodgersDivision of Cardiovascular Medicine, Radcliffe Department of Medicine, University of Oxford, Headley Way, Oxford, UK.
Christopher M KramerCardiology and Radiology, University of Virginia Health System, Charlottesville, VA, USA.
Masliza MahmodDivision of Cardiovascular Medicine, Radcliffe Department of Medicine, University of Oxford, Headley Way, Oxford, UK.
Hugh WatkinsDivision of Cardiovascular Medicine, Radcliffe Department of Medicine, University of Oxford, Headley Way, Oxford, UK.
Stefan NeubauerDivision of Cardiovascular Medicine, Radcliffe Department of Medicine, University of Oxford, Headley Way, Oxford, UK.

Funding

HCMR Novel Markers of Prognosis in Hypertrophic CardiomyopathyU01HL117006 · NHLBI · UNIVERSITY OF VIRGINIA · PI KRAMER, CHRISTOPHER M., NEUBAUER, STEFAN · 2013 to 2017
$14.5M
British Heart Foundation FS/12/32/29559British Heart Foundation FS/18/3/33292British Heart Foundation RG/12/16/29939NHLBI NIH HHS U01 HL117006Wellcome Trust
6 · The paper itself

Abstract

Aims: Myocardial fibrosis as detected by late gadolinium enhancement (LGE) on cardiac magnetic resonance (CMR) is a powerful prognostic marker in hypertrophic cardiomyopathy (HCM) and may be progressive. The precise mechanisms underlying fibrosis progression are unclear. We sought to assess the extent of LGE progression in HCM and explore potential causal mechanisms and clinical implications. Methods and results: Seventy-two HCM patients had two CMR (CMR1-CMR2) at an interval of 5.7 ± 2.8 years with annual clinical follow-up for 6.3 ± 3.6 years from CMR1. A combined endpoint of heart failure progression, cardiac hospitalization, and new onset ventricular tachycardia was assessed. Cine and LGE imaging were performed to assess left ventricular (LV) mass, function, and fibrosis on serial CMR. Stress perfusion imaging and cardiac energetics were undertaken in 38 patients on baseline CMR (CMR1). LGE mass increased from median 4.98 g [interquartile range (IQR) 0.97-13.48 g] to 6.30 g (IQR 1.38-17.51 g) from CMR1 to CMR2. Substantial LGE progression (ΔLGE ≥ 4.75 g) occurred in 26% of patients. LGE increment was significantly higher in those with impaired myocardial perfusion reserve (<MPRI 1.40) and energetics (phosphocreatine/adenosine triphosphate <1.44) on baseline CMR (P ≤ 0.01 for both). Substantial LGE progression was associated with LV thinning, increased cavity size and reduced systolic function, and conferred a five-fold increased risk of subsequent clinical events (hazard ratio 5.04, 95% confidence interval 1.85-13.79; P = 0.002). Conclusion: Myocardial fibrosis is progressive in some HCM patients. Impaired energetics and perfusion abnormalities are possible mechanistic drivers of the fibrotic process. Fibrosis progression is associated with adverse cardiac remodelling and predicts an increased risk of subsequent clinical events in HCM.

Indexed as

Cardiomyopathy, HypertrophicContrast MediaDisease ProgressionFemaleFibrosisGadolinium DTPAHumansMagnetic Resonance Imaging, CineMaleMeglumineMiddle AgedMyocardiumOrganometallic CompoundsPrognosisRetrospective StudiesRisk FactorsContrast MediagadobutrolgadodiamideGadolinium DTPAgadoterate meglumineMeglumineOrganometallic Compounds

Identifiers

PMID30358845
PMCPMC6343081

What OpenQuestion holds

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LicenceCC BY
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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.