Evidence map›Paper›PMID 26583449›Full record

ArticleComputer methods in biomechanics and biomedical engineering2016

Computational modeling of acute myocardial infarction.

P Sáez, E Kuhl

Open access · greenAbstract read
In one paragraph

Article in Computer methods in biomechanics and biomedical engineering, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

9 citing papers in PubMed, 31 citations in OpenAlex.

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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

2 authors at 2 institutions in 2 countries.

P Sáeza Mathematical Institute, University of Oxford , Oxford , UK .
E Kuhlb Department of Mechanical Engineering , Stanford University , Stanford , CA , USA .
Stanford University · USUniversity of Oxford · GB

Funding

Multi-Scale Laws of Myocardial Growth and RemodelingU01HL119578 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI GUCCIONE, JULIUS MATTEO, KASSAB, GHASSAN S · 2014 to 2018
$3.8M
NHLBI NIH HHS U01 HL119578
6 · The paper itself

Abstract

Myocardial infarction, commonly known as heart attack, is caused by reduced blood supply and damages the heart muscle because of a lack of oxygen. Myocardial infarction initiates a cascade of biochemical and mechanical events. In the early stages, cardiomyocytes death, wall thinning, collagen degradation, and ventricular dilation are the immediate consequences of myocardial infarction. In the later stages, collagenous scar formation in the infarcted zone and hypertrophy of the non-infarcted zone are auto-regulatory mechanisms to partly correct for these events. Here we propose a computational model for the short-term adaptation after myocardial infarction using the continuum theory of multiplicative growth. Our model captures the effects of cell death initiating wall thinning, and collagen degradation initiating ventricular dilation. Our simulations agree well with clinical observations in early myocardial infarction. They represent a first step toward simulating the progression of myocardial infarction with the ultimate goal to predict the propensity toward heart failure as a function of infarct intensity, location, and size.

Indexed as

Computer SimulationModels, CardiovascularCell DeathCollagenHeart VentriclesHumansMyocardial InfarctionMyocardiumMyocytes, CardiacCollagenBiomechanicsfinite element methodgrowthhypertensionsmooth muscle cells

Identifiers

PMID26583449
PMCPMC4828331
OpenAlexW2281670211

What OpenQuestion holds

Textmetadata
LicenceTDM
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.