Evidence map›Paper›PMID 38631187›Full record

ArticleJournal of biomechanics2024

Multi-scaled temporal modeling of cardiovascular disease progression: An illustration of proximal arteries in pulmonary hypertension.

Young-Dae Shim, Mei-Cen Chen, Seongmin Ha, Hyuk-Jae Chang, Seungik Baek, Eun-Ho Lee

Open access · greenAbstract read
In one paragraph

Article in Journal of biomechanics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

1 citing paper in PubMed, 7 citations in OpenAlex.

  1. Article
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 at 3 institutions in 2 countries.

Young-Dae ShimDepartment of Smart Fabrication Technology, Sungkyunkwan University, Suwon-si, Gyeonggi-do 16419, Republic of Korea. Electronic address: ydshim92@g.skku.edu.
Mei-Cen ChenDepartment of Smart Fabrication Technology, Sungkyunkwan University, Suwon-si, Gyeonggi-do 16419, Republic of Korea. Electronic address: chen98@g.skku.edu.
Seongmin HaBiomedical Engineering, Yonsei University College of Medicine 250, Seoul, Republic of Korea. Electronic address: seongminha@yonsei.ac.kr.
Hyuk-Jae ChangDivision of Cardiology, Yonsei University College of Medicine 250, Seoul, Republic of Korea. Electronic address: hjchang@yuhs.ac.
Seungik BaekDepartment of Mechanical Engineering, Michigan State University, East Lansing, MI 48824, United States. Electronic address: sbaek@msu.edu.
Eun-Ho LeeDepartment of Smart Fabrication Technology, Sungkyunkwan University, Suwon-si, Gyeonggi-do 16419, Republic of Korea; School of Mechanical Engineering, Sungkyunkwan University, Suwon-si, Gyeonggi-do 16419, Republic of Korea; Department of Intelligent Robotics, Sungkyunkwan University, Suwon-si, Gyeonggi-do 16419, Republic of Korea. Electronic address: ehlee@skku.edu.
Sungkyunkwan University · KRYonsei University · KRMichigan State University · US

Funding

Image-based Multi-scale Modeling Framework of the Cardiopulmonary System: Longitudinal Calibration and Assessment of Therapies in Pediatric Pulmonary HypertensionU01HL135842 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI BAEK, SEUNGIK, DORFMAN, ADAM LEE · 2017 to 2020
$2.3M
NHLBI NIH HHS U01 HL135842
6 · The paper itself

Abstract

The progression of cardiovascular disease is intricately influenced by a complex interplay between physiological pathways, biochemical processes, and physical mechanisms. This study aimed to develop an in-silico physics-based approach to comprehensively model the multifaceted vascular pathophysiological adaptations. This approach focused on capturing the progression of proximal pulmonary arterial hypertension, which is significantly associated with the irreversible degradation of arterial walls and compensatory stress-induced growth and remodeling. This study incorporated critical characteristics related to the distinct time scales for the deformation, thus reflecting the impact of mean pressure on artery growth and tissue damage. The in-silico simulation of the progression of pulmonary hypertension was realized based on computational code combined with the finite element method (FEM) for the simulation of disease progression. The parametric studies further explored the consequences of these irreversible processes. This computational modeling approach may advance our understanding of pulmonary hypertension and its progression.

Indexed as

Computer SimulationDisease ProgressionHypertension, PulmonaryModels, CardiovascularPulmonary ArteryFinite Element AnalysisHumansArtery degradationPulmonary artery hypertensionStress-driven growthThermodynamic modeling

Identifiers

PMID38631187
PMCPMC11096051
OpenAlexW4393132200

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.