Evidence map›Paper›PMID 41104021›Full record

ArticlePulmonary circulation2025

Patient-Specific Haemodynamic Modeling to Estimate the Extent of Microvascular Disease and Response to Pulmonary Endarterectomy in Chronic Thromboembolic Pulmonary Hypertension.

Behdad Shaarbaf Ebrahimi, Prashanna Khwaounjoo, Ho-Fung Chan, Finbar Argus, Xiaohui Ma, Martyn P Nash, Atsuo Doi, Misha Dagan, David M Kaye, Timothy Joseph and 2 more

Abstract read
In one paragraph

Article in Pulmonary circulation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Review
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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

12 authors.

Behdad Shaarbaf EbrahimiAuckland Bioengineering Institute University of Auckland Auckland New Zealand.ORCID https://orcid.org/0000-0001-6254-6226
Prashanna KhwaounjooAuckland Bioengineering Institute University of Auckland Auckland New Zealand.
Ho-Fung ChanAuckland Bioengineering Institute University of Auckland Auckland New Zealand.ORCID https://orcid.org/0000-0002-5382-2097
Finbar ArgusAuckland Bioengineering Institute University of Auckland Auckland New Zealand.
Xiaohui MaAuckland Bioengineering Institute University of Auckland Auckland New Zealand.
Martyn P NashAuckland Bioengineering Institute University of Auckland Auckland New Zealand.
Atsuo DoiDepartment of Cardiothoracic Surgery and Transplantation The Alfred Melbourne Victoria Australia.
Misha DaganDepartment of Cardiology Heart Failure and Transplant Service, Alfred Hospital Melbourne Victoria Australia.
David M KayeDepartment of Surgery, Central Clinical School Monash University Melbourne Victoria Australia.
Timothy JosephAlfred Hospital Melbourne Victoria Australia.
David McGiffinDepartment of Cardiothoracic Surgery and Transplantation The Alfred Melbourne Victoria Australia.
Merryn H TawhaiAuckland Bioengineering Institute University of Auckland Auckland New Zealand.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic thromboembolic pulmonary hypertension (CTEPH) is a form of pulmonary hypertension that is caused by persistent obstruction of the pulmonary arteries by organized thrombi and associated microvascular disease. Pulmonary endarterectomy (PEA) is the gold standard treatment, but the extent of small vessel remodeling, which strongly influences treatment outcomes, remains difficult to quantify pre-operatively. We developed a multiscale, structure-based model of the pulmonary circulation using patient-specific vascular geometries from CT pulmonary angiography (CTPA) and haemodynamic data from right heart catheterization (RHC). Eleven CTEPH patients were included. The model estimated individual remodeling burden by fitting simulated to measured preoperative mean pulmonary artery pressure (mPAP). PEA was simulated by removing flow obstructions to predict Postoperative mPAP and pulmonary vascular resistance (PVR), both under pre- and post-PEA boundary conditions. Model predictions of post-PEA mPAP and PVR were in reasonable agreement with measured outcomes, especially when Postoperative boundary conditions were applied. Predicted changes in mPAP (∆mPAP) strongly correlated with clinical values (

Indexed as

chronic thromboembolic pulmonary hypertensioncomputational modelingmicrovascular diseasepersonalized medicinepulmonary endarterectomypulmonary haemodynamics

Identifiers

PMID41104021
PMCPMC12521630

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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.