Evidence map›Paper›PMID 35169044›Full record

ArticleOpen heart2022

Copper chelation in patients with hypertrophic cardiomyopathy.

Anna Reid, Christopher Miller, John Peter Farrant, Rahul Polturi, David Clark, Simon Ray, Garth Cooper, Matthias Schmitt

Open access · goldAbstract read
In one paragraph

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 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
3.9field-weighted citation impact, top 5% 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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.

  1. Pooled it
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  4. The Yin and Yang of copper in cardiovascular health and disease.Molecular and cellular biochemistry · 2026
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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 3 institutions in 1 country.

Anna ReidCardiovascular Division, Northwest Heart Centre, Manchester University NHS Foundation Trust, Manchester, UK.
Christopher MillerCardiovascular Division, Northwest Heart Centre, Manchester University NHS Foundation Trust, Manchester, UK.
John Peter FarrantCardiovascular Division, Northwest Heart Centre, Manchester University NHS Foundation Trust, Manchester, UK john.farrant@mft.nhs.uk.ORCID 0000-0002-9241-2410
Rahul PolturiACALM Study Unit, Aston University, Birmingham, UK.
David ClarkCardiovascular Division, Northwest Heart Centre, Manchester University NHS Foundation Trust, Manchester, UK.
Simon RayCardiovascular Division, Northwest Heart Centre, Manchester University NHS Foundation Trust, Manchester, UK.
Garth CooperDivision of Cardiovascular Sciences, The University of Manchester, Manchester, UK.
Matthias SchmittCardiovascular Division, Northwest Heart Centre, Manchester University NHS Foundation Trust, Manchester, UK.
University of Manchester · GBManchester University NHS Foundation Trust · GBAston University · GB

Funding

Academy of Medical Sciences AMS-SGCL12-MILLERBritish Heart Foundation FS/17/47/32805
6 · The paper itself

Abstract

backgroundDisturbances of copper (Cu) homeostasis can lead to hypertrophic cardiac phenotypes (eg, Wilson's disease). We previously identified abnormal Cu homeostasis in patients with hypertrophic cardiomyopathy (HCM) and, therefore, hypothesised that Cu

methodsIn this medicines and healthcare products regulatory agency (MHRA) registered open-label pilot study, we treated 20 HCM patients with trientine for 6 months. Patients underwent a comprehensive assessment schedule including separate cardiac magnetic resonance imaging (CMR) and CMR

resultsTrientine treatment was safe and tolerated. Trientine caused a substantial increase in urinary copper excretion (0.42±0.2 vs 2.02±1.0, p=0.001) without affecting serum copper concentrations. Treatment was associated with significant improvements in total atrial strain and global longitudinal LV strain using both Echo and CMR. LVM decreased significantly in the treatment arm compared with the control group (-4.2 g v 1.8 g, p=0.03). A strong trend towards an absolute decrease in LVM was observed in the treatment group (p=0.06). These changes were associated with a significant change in total myocardial volume driven by a significant reduction in extracellular matrix (ECM) volume (43.83±18.42 mL vs 41.49±16.89 mL, p=0.04) as opposed to pure cellular mass reduction and occurred against a background of significant ECM volume increase in the control group (44.59±16.50 mL vs 47.48±19.30 mL, p=0.02). A non-significant 10% increase in myocardial phosphocreatine/adenosine triphosphate (PCr/ATP) ratio with trientine therapy (1.27±0.44 vs 1.4±0.39) was noted.

conclusionsCu

Indexed as

Cardiomyopathy, HypertrophicCopperTrientineBiological AvailabilityChelating AgentsDrug MonitoringExtracellular MatrixFemaleFibrosisHeart VentriclesHumansMagnetic Resonance Imaging, CineMagnetic Resonance SpectroscopyMaleMiddle AgedOrgan SizeChelating AgentsCopperTrientinecardiomyopathiescardiomyopathyhypertrophicmagnetic resonance imaging

Identifiers

PMID35169044
PMCPMC8852723
OpenAlexW4213239711

What OpenQuestion holds

Textmetadata
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.