Evidence map›Paper›PMID 35351822›Full record

ArticleHeart (British Cardiac Society)2022

Proteomics profiling reveals a distinct high-risk molecular subtype of hypertrophic cardiomyopathy.

Lusha W Liang, Yoshihiko Raita, Kohei Hasegawa, Michael A Fifer, Mathew S Maurer, Muredach P Reilly, Yuichi J Shimada

Open access · greenAbstract read
In one paragraph

Article in Heart (British Cardiac Society), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

16 citing papers in PubMed, 15 citations in OpenAlex.

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  12. Adopting artificial intelligence in cardiovascular medicine: a scoping review.Hypertension research : official journal of the Japanese Society of Hypertension · 2024
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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

7 authors at 2 institutions in 1 country.

Lusha W Liang *Division of Cardiology, Department of Medicine, Columbia University Irving Medical Center, New York City, New York, USA.ORCID 0000-0003-3931-4085
Yoshihiko Raita *Department of Emergency Medicine, Massachusetts General Hospital, Boston, Massachusetts, USA.
Kohei HasegawaDepartment of Emergency Medicine, Massachusetts General Hospital, Boston, Massachusetts, USA.
Michael A FiferCardiology Division, Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts, USA.
Mathew S MaurerDivision of Cardiology, Department of Medicine, Columbia University Irving Medical Center, New York City, New York, USA.
Muredach P ReillyDivision of Cardiology, Department of Medicine, Columbia University Irving Medical Center, New York City, New York, USA.
Yuichi J ShimadaDivision of Cardiology, Department of Medicine, Columbia University Irving Medical Center, New York City, New York, USA ys3053@cumc.columbia.edu.
Columbia University Irving Medical Center · USMassachusetts General Hospital · US

Funding

Clinical and Translational Science AwardUL1TR001873 · NCATS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI REILLY, MUREDACH P · 2016 to 2025
$99.0M
Proteomics profiling in hypertrophic cardiomyopathy and cardiac event predictionR01HL157216 · NHLBI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI SHIMADA, YUICHI · 2021 to 2025
$3.5M
Midcareer Mentoring Award for Patient Oriented Research in Geriatric CardiologyK24AG036778 · NIA · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI MAURER, MATHEW S · 2010 to 2020
$1.6M
Mentored Patient Oriented Research in Cardiometabolic DiseaseK24HL107643 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI REILLY, MUREDACH P · 2011 to 2020
$1.4M
NCATS NIH HHS UL1 TR001873NHLBI NIH HHS K24 HL107643NHLBI NIH HHS R01 HL157216NIA NIH HHS K24 AG036778
6 · The paper itself

Abstract

objectiveHypertrophic cardiomyopathy (HCM) is a heterogeneous disease, likely encompassing several subtypes of disease with distinct biological mechanisms (ie, molecular subtypes). Current models based solely on clinical data have yielded limited accuracy in predicting the risk of major adverse cardiovascular events (MACE). Our aim in this study was to derive molecular subtypes in our multicentre prospective cohort of patients with HCM using proteomics profiling and to examine their longitudinal associations with MACE.

methodsWe applied unsupervised machine learning methods to plasma proteomics profiling data of 1681 proteins from 258 patients with HCM who were prospectively followed for a median of 2.8 years. The primary outcome was MACE, defined as a composite of arrhythmia, heart failure, stroke and sudden cardiac death.

resultsWe identified four molecular subtypes of HCM. Time-to-event analysis revealed significant differences in MACE-free survival among the four molecular subtypes (p

conclusionsOur prospective plasma proteomics study not only exhibited the presence of HCM molecular subtypes but also identified pathobiological mechanisms associated with a distinct high-risk subtype of HCM.

Indexed as

Cardiomyopathy, HypertrophicHeart FailureDeath, Sudden, CardiacHumansProspective StudiesProteomicsRisk FactorsBiomarkersHeart FailureHypertrophic cardiomyopathy

Identifiers

PMID35351822
PMCPMC9741498
OpenAlexW4220689678

What OpenQuestion holds

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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.