to elucidate predictors of development of chronic thromboembolic pulmonary hypertension (CTEPH) after acute pulmonary artery thromboembolism (PTE).

We included in this study 210 patients hospitalized with diagnosis of submassive and massive PTE from 2013 to 2017. In 1 to 3 years after initial hospitalization these patients were invited for control examination. According to results of this examination patients were divided into two groups: with (group 1, n=45) and without (group 2, n=165) signs of CTEPH. Severity of pulmonary artery vascular bed involvement was assessed by multislice computed tomography (MSCT) angiography and lung scintigraphy. For detection of thrombosis in the inferior vena cava system we used ultrasound angioscanning.   Examination also included echocardiography.

In the process of mathematical analysis, the following risk factors for the development of CTEPH embolism were determined: duration of thrombotic history (group 1 - 13.70±2.05 days, group 2- 16.16±1.13 days, p=0.015), localization of venous thrombosis in the lower extremities (the most favorable - shin veins, popliteal, and common femoral veins, unfavorable - superficial femoral vein). The choice of the drug for thrombolytic and anticoagulant therapy: streptokinase and urokinase were significantly more effective than alteplase, rivaroxaban was superior to the combination of unfractionated or low molecular weight heparins with warfarin. Also, risk factors for the development of CTEPH were the initial degree of pulmonary hypertension and tricuspid insufficiency, as well as the positive dynamics of these indicators at the background of thrombolytic or anticoagulant therapy. Of concomitant diseases, significant risk factors for development of CTEPH were grade 3 hypertensive disease, diabetes mellitus, post-infarction cardiosclerosis. On the other hand, age, gender, degree of severity at the time of admission, presence of infarction pneumonia, surgical prevention of recurrent pulmonary embolism, number of pregnancies and deliveries, history of trauma and malignancies, cardiac arrhythmias produced no significant impact on the development of CTEPH.