{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,12,29]],"date-time":"2025-12-29T18:47:42Z","timestamp":1767034062183,"version":"3.48.0"},"reference-count":54,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2025,10,14]],"date-time":"2025-10-14T00:00:00Z","timestamp":1760400000000},"content-version":"vor","delay-in-days":13,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Pulm. circ."],"published-print":{"date-parts":[[2025,10]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    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\u2010operatively. We developed a multiscale, structure\u2010based model of the pulmonary circulation using patient\u2010specific 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\u2010 and post\u2010PEA boundary conditions. Model predictions of post\u2010PEA mPAP and PVR were in reasonable agreement with measured outcomes, especially when Postoperative boundary conditions were applied. Predicted changes in mPAP (\u2206mPAP) strongly correlated with clinical values (\n                    <jats:italic>R<\/jats:italic>\n                    \u2009=\u20090.81,\n                    <jats:italic>p<\/jats:italic>\n                    \u2009=\u20090.002), improving further with post\u2010PEA flow parameters (\n                    <jats:italic>R<\/jats:italic>\n                    \u2009=\u20090.84,\n                    <jats:italic>p<\/jats:italic>\n                    \u2009=\u20090.001). The model captured variable haemodynamic responses to PEA, even among patients with similar Postoperative mPAP. This preliminary investigation demonstrates the feasibility of personalized computational modeling to non\u2010invasively estimate the extent of microvascular disease and simulate postsurgical haemodynamic outcomes in CTEPH. The findings support the potential for this approach to serve as a clinical decision\u2010making tool, with future validation in larger cohorts and integration of spatial remodeling and longitudinal data.\n                  <\/jats:p>","DOI":"10.1002\/pul2.70176","type":"journal-article","created":{"date-parts":[[2025,10,15]],"date-time":"2025-10-15T05:29:51Z","timestamp":1760506191000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Patient\u2010Specific Haemodynamic Modeling to Estimate the Extent of Microvascular Disease and Response to Pulmonary Endarterectomy in Chronic Thromboembolic Pulmonary Hypertension"],"prefix":"10.1002","volume":"15","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-6254-6226","authenticated-orcid":false,"given":"Behdad Shaarbaf","family":"Ebrahimi","sequence":"first","affiliation":[{"name":"Auckland Bioengineering Institute University of Auckland Auckland New 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