Abstract

Presents data on the pathogenesis of chronic thromboembolic pulmonary hypertension (CTEPH), which serve as a rationale for approaches to the choice of treatment. CTEPH usually begins with persistent obstruction of the large and/or medium pulmonary arteries by organized thrombi. Impaired lysis of thrombi may be associated with abnormal fibrinolysis, hematological or autoimmune diseases. The molecular processes underlying the lesions of small vessels are not fully understand. The degree of small-vessel disease has a significant impact on the severity of CTEPH and postoperative outcomes. The CTEPH treatment has evolved with the development of three directions pulmonary endarterectomy, balloon angioplasty of pulmonary arteries and the use of specific therapy used for pulmonary arterial hypertension. The paper demonstrates the possibilities of a multimodal approach in the treatment of this category of patients.

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