Evidence map›Paper›PMID 41214182›Full record

ArticleScientific reports2025

Genetic determinants of the phenotype in a Swedish cohort of patients with hypertrophic cardiomyopathy.

Kissopoulou Antheia, Fernlund Eva, Karlsson Jan-Erik, Green Henrik, Ellegård Rada, Gunnarsson Cecilia

Abstract read
In one paragraph

Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–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

2 citing papers in PubMed.

  1. Article
  2. Hypertrophic Cardiomyopathy is a Disease of Sarcomere Proteins.Methodist DeBakey cardiovascular journal · 2026
    Review
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

6 authors.

Kissopoulou AntheiaDepartment of Internal Medicine, Department of Health, Medicine and Caring Sciences, County Council of Jönköping, Linköping University, Linköping, Sweden. antheiakissopoulou@yahoo.com.
Fernlund EvaDepartment of Biomedical and Clinical Sciences, Division of Pediatrics, Linköping University, Crown Princess Victoria Children´S Hospital, Linköping University Hospital, Linköping, and Pediatric Clinic Vrinnevi Hospital, Norrköping, Sweden.
Karlsson Jan-ErikDepartment of Internal Medicine, Department of Health, Medicine and Caring Sciences, County Council of Jönköping, Linköping University, Linköping, Sweden.
Green HenrikDivision of Clinical Chemistry and Pharmacology, Department of Biomedical and Clinical Sciences, Linköping University, Linköping, Sweden.
Ellegård RadaDepartment of Clinical Genetics, and Department of Biomedical and Clinical Sciences, Linköping University, Linköping, Sweden.
Gunnarsson CeciliaDepartment of Clinical Genetics, and Department of Biomedical and Clinical Sciences, Linköping University, Linköping, Sweden.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hypertrophic cardiomyopathy (HCM), the most common inherited cardiomyopathy, is characterized by phenotypic and genetic heterogeneity. The present study describes the genotype data of a Swedish cohort of patients with HCM, the largest genetics study on Swedish HCM patients to date. The primary aims of this study were to unravel the main genetic findings and explore genotype-phenotype associations in this HCM cohort. Longitudinal data on 225 unrelated HCM index patients from the Southeast health care region in Sweden from 2010 until 2021 were assessed retrospectively. Patients were 46 ± 15.5 years-old, 67.6% males. In the cohort, 172/225 (76.4%) had genetic testing, of whom, 65/172 (38%) were considered genotype positive (G +) for a pathogenic/ likely pathogenic variant, mainly in the two most common sarcomeric genes: MYBPC3 (57%) and MYH7 (34%). In 43% (74/172) of patients, no reportable variants were detected, classified as genotype negative (G-). In the remaining 33 patients (19%), variants of uncertain significance (VUS) were identified; this group was not included in the comparative analyses. Genotype positive patients (G +) were characterized by younger age (p = 0.010), higher prevalence of family history of HCM (p < 0.001), greater maximum left ventricle wall thickness (p = 0.03) and an increased incidence of sudden cardiac death (SCD) (p = 0.045). At first clinical screening, HCM was diagnosed in 28/65(43%) in the G + families and in 2/74 (2.7%) G-families (p < 0.001). Genotype-positive HCM patients differ with respect to age at presentation, family history of the disease, morphology, incidence of SCD and presence of HCM in their family members at first clinical assessment from genotype-negative patients. Genotype negative status in this HCM cohort, though, did not confer immunity from adverse complications.

Indexed as

Cardiomyopathy, HypertrophicAdultAgedCardiac MyosinsCarrier ProteinsCohort StudiesFemaleGenetic Association StudiesGenetic Predisposition to DiseaseGenetic TestingGenotypeHumansMaleMiddle AgedMyosin Binding Protein CMyosin Heavy ChainsCardiac MyosinsCarrier ProteinsMYH7 protein, humanMyosin Binding Protein CMyosin Heavy Chains

Identifiers

PMID41214182
PMCPMC12602694

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.