Evidence map›Paper›PMID 35076018›Full record

ArticleeLife2022

Personalized computational heart models with T1-mapped fibrotic remodeling predict sudden death risk in patients with hypertrophic cardiomyopathy.

Ryan P O'Hara, Edem Binka, Adityo Prakosa, Stefan L Zimmerman, Mark J Cartoski, M Roselle Abraham, Dai-Yin Lu, Patrick M Boyle, Natalia A Trayanova

Open access · goldAbstract read
In one paragraph

Article in eLife, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 1 pooled it
6.4field-weighted citation impact, top 3% 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

36 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.

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  8. A case of hypertrophic cardiomyopathy with untoward outcome.The British journal of cardiology · 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

9 authors at 4 institutions in 1 country.

Ryan P O'HaraDepartment of Biomedical Engineering, Johns Hopkins University, Baltimore, United States.ORCID 0000-0002-7636-1799
Edem BinkaDivision of Pediatric Cardiology, Johns Hopkins School of Medicine, Baltimore, United States.
Adityo PrakosaDepartment of Biomedical Engineering, Johns Hopkins University, Baltimore, United States.
Stefan L ZimmermanDepartment of Radiology, Johns Hopkins School of Medicine, Baltimore, United States.
Mark J CartoskiDivision of Pediatric Cardiology, Nemours/Alfred I. duPont Hospital for Children, Wilmington, United States.
M Roselle AbrahamDivision of Cardiology, University of California, San Francisco, San Francisco, United States.
Dai-Yin LuDivision of Cardiology, University of California, San Francisco, San Francisco, United States.
Patrick M BoyleDepartment of Bioengineering, University of Washington, Seattle, United States.ORCID 0000-0001-9048-1239
Natalia A TrayanovaDepartment of Biomedical Engineering, Johns Hopkins University, Baltimore, United States.ORCID 0000-0002-8661-063X
Johns Hopkins University · USUniversity of California, San Francisco · USAlfred I. duPont Hospital for Children · USUniversity of Washington · US

Funding

Infarct-related Ventricular Tachycardia Mechanisms: From Micro to ClinicalR01HL142496 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI TRAYANOVA, NATALIA A. · 2019 to 2022
$3.1M
Training for Clinician Scientists in Pediatric Critical Cardiopulmonary DiseaseT32HL125239 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI BEMBEA, MELANIA MARIA, EVERETT, ALLEN D · 2015 to 2024
$3.0M
Exploration of Arrhythmogenic Triggers and Substrates in Heart FailureR01HL126802 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI EFIMOV, IGOR R, GORELIK, JULIA · 2016 to 2019
$2.8M
NHLBI NIH HHS R01 HL126802NHLBI NIH HHS R01 HL142496NHLBI NIH HHS T32 HL125239
6 · The paper itself

Abstract

Hypertrophic cardiomyopathy (HCM) is associated with risk of sudden cardiac death (SCD) due to ventricular arrhythmias (VAs) arising from the proliferation of fibrosis in the heart. Current clinical risk stratification criteria inadequately identify at-risk patients in need of primary prevention of VA. Here, we use mechanistic computational modeling of the heart to analyze how HCM-specific remodeling promotes arrhythmogenesis and to develop a personalized strategy to forecast risk of VAs in these patients. We combine contrast-enhanced cardiac magnetic resonance imaging and T1 mapping data to construct digital replicas of HCM patient hearts that represent the patient-specific distribution of focal and diffuse fibrosis and evaluate the substrate propensity to VA. Our analysis indicates that the presence of diffuse fibrosis, which is rarely assessed in these patients, increases arrhythmogenic propensity. In forecasting future VA events in HCM patients, the imaging-based computational heart approach achieved 84.6%, 76.9%, and 80.1% sensitivity, specificity, and accuracy, respectively, and significantly outperformed current clinical risk predictors. This novel VA risk assessment may have the potential to prevent SCD and help deploy primary prevention appropriately in HCM patients.

Indexed as

Computer SimulationMagnetic Resonance ImagingAdultAgedCardiomyopathy, HypertrophicDeath, Sudden, CardiacFemaleFibrosisHumansLogistic ModelsMaleMiddle AgedMyocardiumPredictive Value of TestsRetrospective StudiesRisk Assessmentcomputational biologycomputational modelinghumanhypertrophic cardiomyopathymedicinepersonalized medicinesudden cardiac deathsystems biologyT1 mapping

Identifiers

PMID35076018
PMCPMC8789259
OpenAlexW4205281484

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.