![]() ![]() Some patients suffer from symptomatic chronic thromboembolic pulmonary disease without pulmonary hypertension at rest, and they may also benefit from pulmonary endarterectomy (PEA). ![]() ĭiagnosis of CTEPH requires ≥3 months of effective anticoagulation and a mean pulmonary arterial pressure (mPAP) >25 mmHg with a pulmonary capillary wedge pressure ≤15 mmHg, and at least one (segmental) perfusion defect. Registry data indicate a prevalence of CTEPH of 3–30 per million in the general population. Įvidence suggests that the incidence of CTEPH after pulmonary embolism is ∼1.5%. Not all patients with CTEPH have a history of acute pulmonary embolism. Consequently, pressure and vascular resistance in the pulmonary vasculature are increased, leading eventually to right heart failure and premature mortality. Other controversies discussed in this article include eligibility for PEA versus balloon pulmonary angioplasty, the new treatment algorithm in the European Society of Cardiology/European Respiratory Society guidelines and the definition of an “expert centre” for the management of this condition.Ĭhronic thromboembolic pulmonary hypertension (CTEPH) is a type of pulmonary hypertension resulting from fibrotic transformation of pulmonary artery clots causing chronic obstruction of pulmonary arteries and associated vascular remodelling in the microvasculature. Therefore, treatment of patients with CTEPH depends largely on subjective judgements of eligibility for surgery by the CTEPH team. However, PEA, is a complex procedure and relies on a multidisciplinary CTEPH team led by an experienced surgeon to decide on an individual's operability, which is determined primarily by lesion location and the haemodynamic parameters. Current in-hospital mortality rates are 90% at 1 year and >70% at 10 years. Pulmonary endarterectomy (PEA) offers the best chance of symptomatic and prognostic improvement in eligible patients in expert centres, it has excellent results. ![]() Chronic thromboembolic pulmonary hypertension (CTEPH) is a type of pulmonary hypertension, resulting from fibrotic transformation of pulmonary artery clots causing chronic obstruction in macroscopic pulmonary arteries and associated vascular remodelling in the microvasculature. ![]()
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