Evidence map›Paper›PMID 42330739›Full record

ArticleJACC. Advances2026

Integrating Genotyping and Left Atrial Strain Analysis Enhances Risk Stratification in Hypertrophic Cardiomyopathy.

Takashi Hiruma, Koki Nakanishi, Shunsuke Inoue, Seitaro Nomura, Yuriko Yoshida, Zhehao Dai, Ryo Abe, Takanobu Yamada, Kanna Fujita, Manami Katoh and 9 more

Abstract read
In one paragraph

Article in JACC. Advances, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

19 authors.

Takashi HirumaDepartment of Cardiovascular Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Koki NakanishiDepartment of Cardiovascular Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan. Electronic address: knakanishi82@gmail.com.
Shunsuke InoueDepartment of Cardiovascular Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan; Department of Frontier Cardiovascular Science, The University of Tokyo Graduate School of Medicine, Tokyo, Japan.
Seitaro NomuraDepartment of Cardiovascular Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan; Department of Frontier Cardiovascular Science, The University of Tokyo Graduate School of Medicine, Tokyo, Japan. Electronic address: senomura-cib@umin.ac.jp.
Yuriko YoshidaDepartment of Cardiovascular Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Zhehao DaiDepartment of Cardiovascular Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan; Department of Frontier Cardiovascular Science, The University of Tokyo Graduate School of Medicine, Tokyo, Japan.
Ryo AbeDepartment of Cardiovascular Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Takanobu YamadaDepartment of Cardiovascular Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Kanna FujitaDepartment of Cardiovascular Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Manami KatohDepartment of Cardiovascular Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan; Department of Frontier Cardiovascular Science, The University of Tokyo Graduate School of Medicine, Tokyo, Japan; Department of Pathophysiology of Heart Failure and Therapeutics, National Cerebral & Cardiovascular Center, Osaka, Japan.
Toshiyuki KoDepartment of Cardiovascular Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan; Department of Frontier Cardiovascular Science, The University of Tokyo Graduate School of Medicine, Tokyo, Japan.
Masamichi ItoDepartment of Cardiovascular Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Junichi IshidaDepartment of Cardiovascular Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Eisuke AmiyaDepartment of Cardiovascular Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Masaru HatanoDepartment of Cardiovascular Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan; Advanced Medical Center for Heart Failure, The University of Tokyo Hospital, Tokyo, Japan.
Norifumi TakedaDepartment of Cardiovascular Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan; The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Hiroyuki MoritaDepartment of Cardiovascular Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan; International University of Health and Welfare, Tokyo, Japan.
Norihiko TakedaDepartment of Cardiovascular Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Issei KomuroDepartment of Frontier Cardiovascular Science, The University of Tokyo Graduate School of Medicine, Tokyo, Japan; International University of Health and Welfare, Tokyo, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPatients with hypertrophic cardiomyopathy (HCM) who progress to left ventricular systolic dysfunction (LVSD) are at an increased risk of lethal arrhythmias and end-stage heart failure. Early identification of this high-risk subpopulation is crucial; however, current risk stratification remains insufficient.

objectivesThe objective of the study was to investigate the association of myocardial strain parameters with progression to LVSD in genotyped HCM patients.

methodsSarcomere positive was defined as harboring pathogenic or likely pathogenic variants in sarcomere-encoding genes. Speckle-tracking echocardiography was used to measure left ventricular global longitudinal strain (LVGLS) and left atrial reservoir strain (LARS). The primary endpoint was progression to LVSD (ejection fraction <50%) and the secondary endpoint was a composite of progression to LVSD, heart-failure hospitalization, and all-cause death.

resultsA total of 101 patients (23.8% sarcomere positive) were included and followed up for 5.0 (IQR: 2.4-8.7) years. No significant association was observed between genotype and strain parameters. Sarcomere positive (subdistribution HR [sHR]: 5.07; 95% CI: 1.25 to 20.6; P = 0.023) and lower LARS (sHR: 1.10 per 1% decrease; 95% CI: 1.02-1.18; P = 0.015), but not LVGLS, were significantly associated with the primary endpoint. Sarcomere-positive patients with reduced LARS faced markedly elevated incidence for the primary endpoint (sHR: 8.31; 95% CI: 2.25-30.7; P = 0.001). Consistent findings were observed in terms of the secondary endpoint (HR: 4.76; 95% CI: 1.59-14.2; P = 0.005).

conclusionsLARS was associated with progression to LVSD in HCM, potentially reflecting the preclinical stage of LVSD, whereas LVGLS was not. In this exploratory study, integrating left atrial strain analysis with genotyping may have potential value in risk stratification, with implication for early detection of vulnerable individuals.

Indexed as

geneticshypertrophic cardiomyopathyleft atriumstrain analysissystolic dysfunction

Identifiers

PMID42330739
PMCPMC13315677

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