Abstract
Introduction - The most dangerous complication of acute venous thrombosis is pulmonary embolism (PE), which results directly in mortality in most cases. In non-fatal cases of massive pulmonary embolism, when thrombolytic therapy or embolectomy is not possible or ineffective, there is severe chronic thromboembolic pulmonary hypertension (CTEPH). The purpose of our study was to develop clinical, laboratory and instrumental criteria to characterize the development of varying CTEPH intensity after the earlier is PE. Methods - The study is based on a retrospective material comprising 26 patients with the pulmonary embolism arteries and survived it. At different times (1-5 years) after the event and discharge from the hospital, the patients were summoned and examined. All patients were performed to an ultrasonography of the lower limbs, echocardiography, and some patients had pulmonary perfusion scintigraphy and CT angiography. In case of high pulmonary hypertension, which was detected with echocardiography, the right heart catheterization was used for the immediate detection of pulmonary pressure. In the course of our study, we compared the patients' findings received in the initial hospital admissions with the findings of clinical and instrumental methods we had received in the long term after the pulmonary embolism (PE). Results - According to our study, there is a certain trend towards the development of severe CTEPH forms, depending on the following primary clinical and instrumental characteristics. The following factors have been recognized as favorable factors resulting in the incidence of milder CTEPH forms or its total absence in the long term: effective thrombolytic therapy, relative “freshness” of thrombotic masses, distal lesion level of the lower extremity veins (up to the popliteal veins inclusive), young age of patients. It is worth mentioning separately the adequate anticoagulant therapy, which is prescribed following the thrombolysis or in automedication. As a rule, patients followed two regimens of anticoagulant therapy after the thrombolytic therapy: unfractionated heparin during the first 24 hours, with the subsequent transition to warfarin, rivaroxaban immediately at the end of the thrombolysis. Two regimens of anticoagulant therapy: low molecular heparins followed by the transition to warfarin and rivaroxaban from the first days of treatment were also present when the thrombolytic therapy was not possible or not necessary. In the long term, we observed the best pulmonary artery recanalization by combination of the thrombolytic therapy and rivaroxaban, although there were patients who were not treated with the thrombolysis due to the developed allergic reaction in the massive PE, but on the top of administered rivaroxaban there was detected a full pulmonary channel permeability one year after the treatment onset. The effect of the pulmonary artery recanalization in the warfarin treatment was much weaker. Negative factors in the CTEPH development could include the proximal level of deep vein lesions, the elderly age of patients, not "fresh" thrombotic masses. After 10 days of their formation, each consecutive day affected negatively the efficiency forecast of the thrombolytic and anticoagulant therapy in terms of pulmonary artery recanalization. Conclusion - There are certain clinical and instrumental parameters that allow for a certain degree of prediction of the CTEPH development following the earlier PE, but further studies are required to have more reliable statistics.
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More From: European Journal of Vascular and Endovascular Surgery
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