Chronic thromboembolic pulmonary hypertension (CTEPH) is a life-threatening disease due to pulmonary artery obstruction by persistent organised clots related to one or more episodes of acute pulmonary embolism. To date, the pathogenesis of CTEPH remains unexplained. Pulmonary endarterectomy removes obstruction from pulmonary vessels and can cure patients. However, some unreachable distal pulmonary obstruction and/or associated distal pulmonary vasculopathy could induce persistent pulmonary hypertension, the main postoperative complication.The pathophysiology of CTEPH is not fully understood and improving knowledge of this disease could improve our future surgical and medical management. Many attempts, conducted over several decades, have failed to reproduce this chronic disease in animals. However, several animal models have provided insights into the pathophysiology and pathogenesis of CTEPH. Here, we review all the animal models that have improved the comprehension of CTEPH and hold promise for further investigations. This short review analyses strengths and weaknesses of all animal models available to study the pathophysiology of CTEPH. , chronic thromboembolic pulmonary hypertension (CTEPH) is a type-4 subtype of pulmonary hypertension (PH), in which pulmonary endarterectomy (PEA) [2] is effective in preventing death by right ventricle (RV) failure. CTEPH is due to obstruction of pulmonary arteries by persistent organised clots formed during one or more episodes of acute pulmonary embolism. The reason for clot persistence is unknown and the pathogenesis of CTEPH remains unexplained. To date, the lack of risk factors predicting the evolution from acute pulmonary embolism to CTEPH does not allow the development of preventive care and/or screening programmes.The increase in pulmonary vascular resistance is believed to result from a combination of proximal pulmonary artery obstruction and distal pulmonary vasculopathy [3,4], which have to be quantified before PEA to estimate risks and predict surgical success. However, the mechanisms underlying lesion development in the obstructed and unobstructed peripheral vascular beds remain unknown. Hence, medical management of inoperable CTEPH or operable CTEPH with an important distal vasculopathy remains troublesome because of a lack of efficient therapy.To elucidate the pathophysiology of CTEPH, considerable effort has been expended in attempting to develop reliable animal models. Acute pulmonary embolism is easily produced in several animal species. In contrast, the induction of a disease replicating all the components of human CTEPH has proved challenging. These