ReviewFrontiers in cardiovascular medicine2021
Chronic Thromboembolic Pulmonary Hypertension - What Have We Learned From Large Animal Models.
Review in Frontiers in cardiovascular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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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.
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Who cites it
7 citing papers in PubMed, 14 citations in OpenAlex.
- Minimally Invasive Porcine Model for Chronic Thromboembolic Pulmonary Hypertension.Pulmonary circulation · 2026Article
- Large animal models of right heart failure due to pulmonary hypertension: a bridge to translational success.European respiratory review : an official journal of the European Respiratory Society · 2026Review
- Animal models of chronic thromboembolic pulmonary hypertension.Animal models and experimental medicine · 2026Review
- Is Inducible Nitric Oxide Synthase (iNOS) Promising as a New Target Against Pulmonary Hypertension?Antioxidants (Basel, Switzerland) · 2025Review
- Artificial intelligence-driven quantitative analysis of CT morphological differences between chronic thromboembolic pulmonary hypertension and chronic thromboembolic disease.Quantitative imaging in medicine and surgery · 2025Article
- SPHK1-mediated M2 macrophage polarization drives TGF-β1-dependent thrombus fibrosis.Frontiers in immunology · 2025Article
- A swine model of severe chronic thromboembolic pulmonary hypertension induced by repeated pulmonary artery long suture injection.Frontiers in cardiovascular medicine · 2025Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic thrombo-embolic pulmonary hypertension (CTEPH) develops in a subset of patients after acute pulmonary embolism. In CTEPH, pulmonary vascular resistance, which is initially elevated due to the obstructions in the larger pulmonary arteries, is further increased by pulmonary microvascular remodeling. The increased afterload of the right ventricle (RV) leads to RV dilation and hypertrophy. This RV remodeling predisposes to arrhythmogenesis and RV failure. Yet, mechanisms involved in pulmonary microvascular remodeling, processes underlying the RV structural and functional adaptability in CTEPH as well as determinants of the susceptibility to arrhythmias such as atrial fibrillation in the context of CTEPH remain incompletely understood. Several large animal models with critical clinical features of human CTEPH and subsequent RV remodeling have relatively recently been developed in swine, sheep, and dogs. In this review we will discuss the current knowledge on the processes underlying development and progression of CTEPH, and on how animal models can help enlarge understanding of these processes.
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Registered trials
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.