Evidence map›Paper›PMID 42544038›Full record

ArticleEuropean heart journal. Cardiovascular Imaging2026

Prevalence and determinants of asymmetric septal hypertrophy (ASH) in diseases of left ventricular hypertrophy (LVH).

Hunain Shiwani, João Augusto, Constantin-Cristian Topriceanu, Adam Ioannou, Stefania Rosmini, Viviana Maestrini, Rebecca Hughes, Kristopher Knott, Anish Bhuva, Benjamin Dowsing and 14 more

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Article in European heart journal. Cardiovascular Imaging, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

What it found

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2 · The registry

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3 · Its place in the literature

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0 citing papers in PubMed.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

24 authors.

Hunain ShiwaniInstitute of Cardiovascular Science, University College London, 62 Huntley St, London WC1E 6DD, UK.ORCID 0000-0002-0046-2884
João AugustoInstitute of Cardiovascular Science, University College London, 62 Huntley St, London WC1E 6DD, UK.
Constantin-Cristian TopriceanuInstitute of Cardiovascular Science, University College London, 62 Huntley St, London WC1E 6DD, UK.ORCID 0000-0001-5826-9617
Adam IoannouInstitute of Cardiovascular Science, University College London, 62 Huntley St, London WC1E 6DD, UK.ORCID 0000-0001-5017-8657
Stefania RosminiBarts Heart Centre, The Cardiovascular Magnetic Resonance Imaging Unit and the Inherited Cardiovascular Diseases Unit, St Bartholomew's Hospital, West Smithfield, London EC1A 7BE, UK.ORCID 0000-0002-5682-7950
Viviana MaestriniDepartment of Clinical, Internal Medicine, Anesthesiological and Cardiovascular Sciences, Sapienza University of Rome, Rome, Italy.
Rebecca HughesInstitute of Cardiovascular Science, University College London, 62 Huntley St, London WC1E 6DD, UK.ORCID 0000-0003-2110-5234
Kristopher KnottInstitute of Cardiovascular Science, University College London, 62 Huntley St, London WC1E 6DD, UK.ORCID 0000-0003-1611-817X
Anish BhuvaInstitute of Cardiovascular Science, University College London, 62 Huntley St, London WC1E 6DD, UK.ORCID 0000-0001-7532-7815
Benjamin DowsingInstitute of Cardiovascular Science, University College London, 62 Huntley St, London WC1E 6DD, UK.
Jessica ArticoInstitute of Cardiovascular Science, University College London, 62 Huntley St, London WC1E 6DD, UK.
Iain PierceInstitute of Cardiovascular Science, University College London, 62 Huntley St, London WC1E 6DD, UK.ORCID 0000-0001-8546-5023
Thomas TreibelInstitute of Cardiovascular Science, University College London, 62 Huntley St, London WC1E 6DD, UK.
James HowardNational Heart and Lung Institute, Imperial College London, London SW7 2AZ, UK.
Charlotte ManistyInstitute of Cardiovascular Science, University College London, 62 Huntley St, London WC1E 6DD, UK.
Peter KellmanNational Heart, Lung, and Blood Institute, National Institutes of Health Bethesda, USA.
Rebecca KozorKolling Institute, Royal North Shore Hospital, and University of Sydney, Sydney, Australia.ORCID 0000-0002-6437-5018
Richard SteedsDepartment of Cardiology, Queen Elizabeth Hospital Birmingham, University Hospitals Birmingham NHS Foundation Trust and University of Birmingham, Birmingham, UK.
Gabriella CapturInstitute of Cardiovascular Science, University College London, 62 Huntley St, London WC1E 6DD, UK.ORCID 0000-0002-5662-0642
Saidi MohiddinBarts Heart Centre, The Cardiovascular Magnetic Resonance Imaging Unit and the Inherited Cardiovascular Diseases Unit, St Bartholomew's Hospital, West Smithfield, London EC1A 7BE, UK.
Luis LopesInstitute of Cardiovascular Science, University College London, 62 Huntley St, London WC1E 6DD, UK.
Marianna FontanaInstitute of Cardiovascular Science, University College London, 62 Huntley St, London WC1E 6DD, UK.ORCID 0000-0002-9233-9831
James MoonInstitute of Cardiovascular Science, University College London, 62 Huntley St, London WC1E 6DD, UK.ORCID 0000-0001-8071-1491
Rhodri DaviesInstitute of Cardiovascular Science, University College London, 62 Huntley St, London WC1E 6DD, UK.ORCID 0000-0001-7630-7517

Funding

Barts Health NHS trustsBritish Heart Foundation SP/20/2/34841CytokineticsGenzymeiFASTMedical Research Council UK Research and Innovation Clinical Academic Research MR/T005181/1Mycardium AIMyCardium AI LtdNational Institute for Health and Care ResearchNational Institute for Health and Care Research University College London Hospitals Biomedical Research CentreNational Institutes of Health and Care Research Biomedical Research CentresSanofiUCLH Biomedical Research CentreUniversity College London Hospitals
6 · The paper itself

Abstract

aimsTo determine the prevalence of asymmetric septal hypertrophy (ASH) across health and in diseases associated with left ventricular hypertrophy (LVH), including hypertrophic cardiomyopathy (HCM). METHODS AND

resultsWe analysed two complementary datasets. First, a large UK Biobank healthy reference cohort (n = 4020) was used to model demographic determinants of septal-to-lateral wall thickness ratio (SLR) and to provide the reference group for age-, sex-, and body surface area-adjusted comparisons. Second, a multi-cohort clinical CMR dataset included 1655 subjects comprising local healthy volunteers, athletes, patients with hypertension, aortic stenosis, Fabry disease, amyloid light chain (AL) amyloidosis, amyloid transthyretin (ATTR) amyloidosis, and HCM. LVH was defined by maximum wall thickness (MWT) ≥15 mm and asymmetry defined as SLR≥1.3. Left ventricular morphology was classified as normal, asymmetric remodelling (SLR≥1.3; MWT<15 mm), symmetric hypertrophy (SLR<1.3; MWT≥15 mm) or ASH (SLR≥1.3; MWT≥15 mm). ASH was highly prevalent in HCM (61%) but was also observed in ATTR amyloidosis (37%), AS (26%), and AL amyloidosis (23%). In the healthy reference cohort, a higher septal-to-lateral ratio was independently associated with older age, female sex, and larger body surface area (P < 0.001). After adjustment for these demographic factors, only HCM retained a clinically meaningful excess in septal asymmetry (ΔSLR = +0.27; P < 0.001). In contrast, the apparent asymmetry in non-HCM cohorts was partly explained by demographic variation. After adjustment, only HCM showed a clinically meaningful excess in SLR, whereas other disease cohorts showed either no material difference or small negative differences relative to healthy controls.

conclusionASH is a common but non-specific finding in diseases associated with LVH. Septal asymmetry increases with age and body-size and is more pronounced in women. After adjusting for age, sex, and body-size, disproportionate septal asymmetry was most characteristic of HCM.

Indexed as

Cardiomyopathy, HypertrophicHeart SeptumHypertrophy, Left VentricularMagnetic Resonance Imaging, CineAdultAgedAmyloidosisCase-Control StudiesCohort StudiesFemaleHumansMaleMiddle AgedPrevalenceReference ValuesRisk Assessmentamyloidosisaortic stenosisasymmetric septal hypertrophycardiovascular magnetic resonancehypertrophic cardiomyopathyleft ventricular hypertrophy

Identifiers

PMID42544038
PMCPMC13623422

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