15 research outputs found
ΠΠΏΠΈΠ΄Π΅ΠΌΠΈΠΎΠ»ΠΎΠ³ΠΈΡΠ΅ΡΠΊΠΈΠ΅ Π°ΡΠΏΠ΅ΠΊΡΡ ΡΠ½ΡΠ΅ΡΠΎΠ²ΠΈΡΡΡΠ½ΠΎΠΉ ΠΈΠ½ΡΠ΅ΠΊΡΠΈΠΈ Π² Π ΠΎΡΡΠΈΠΉΡΠΊΠΎΠΉ Π€Π΅Π΄Π΅ΡΠ°ΡΠΈΠΈ Π·Π° ΠΏΠ΅ΡΠΈΠΎΠ΄ 2018β2019 Π³Π³.
Aim: Analysis of enterovirus infection morbidity and characteristics of the etiological agents of this infection on some territories of Russia in 2017.Materials and methods: We investigated 7858 samples of the biological material from the patients suffering from enterovirus infection. The isolation and identification of enteroviruses were conducted by virological and molecular methods.Results: The epidemic process and the clinical picture of enterovirus infection on different territories had some peculiarities. On some territories enterovirus meningitis was the predominant form of infection, on other territories enterovirus infection with exanthema prevailed. In Saint-Petersburg, Archangel and Saratov regions the percentage of enterovirus infection cases with the clinical picture of enterovirus meningitis was significantly higher than the percentage of enterovirus infection with exanthema. In the Komi Republic, Leningrad and Murmansk regions the percentage of infection with exanthema was statistically higher than the enterovirus meningitis portion. Enteroviruses of 30 serotypes were detected in the samples of patients suffering from enterovirus infection. We determined the etiology of sporadic and epidemic cases of enterovirus infection represented by different clinical forms. On some territories the epidemic foci of enterovirus infection among children were revealed. The etiological agents of enterovirus meningitis foci in Saint-Petersburg, Murmansk and Saratov regions were Coxsackievirus B5, Coxsackievirus B4 and Echovirus 30. The foci of enterovirus infection with exanthema in Archangel, Leningrad, Murmansk and Novgorod regions were caused by Coxsackieviruses A10, A16 and A6.Conclusion: The clinical forms of enterovirus infection on some territories were provoked by enteroviruses which dominated in the circulation on one or other territory. Enteroviruses of species B, mainly Echovirus 30, Echovirus 6 and Coxsackieviruses B1β6 were the etiological agents of enterovirus meningitis. The etiological factors of enterovirus infection with exanthema were Enteroviruses of species A, mainly Coxsackieviruses of different serotypes as well as Enterovirus 71.Π¦Π΅Π»Ρ: Π°Π½Π°Π»ΠΈΠ· Π·Π°Π±ΠΎΠ»Π΅Π²Π°Π΅ΠΌΠΎΡΡΠΈ ΡΠ½ΡΠ΅ΡΠΎΠ²ΠΈΡΡΡΠ½ΠΎΠΉ ΠΈΠ½ΡΠ΅ΠΊΡΠΈΠ΅ΠΉ ΠΈ Ρ
Π°ΡΠ°ΠΊΡΠ΅ΡΠΈΡΡΠΈΠΊΠ° Π΅Π΅ ΡΡΠΈΠΎΠ»ΠΎΠ³ΠΈΡΠ΅ΡΠΊΠΈΡ
Π°Π³Π΅Π½ΡΠΎΠ² Π½Π° ΡΡΠ΄Π΅ ΡΠ΅ΡΡΠΈΡΠΎΡΠΈΠΉ Π ΠΎΡΡΠΈΠΉΡΠΊΠΎΠΉ Π€Π΅Π΄Π΅ΡΠ°ΡΠΈΠΈ Π² 2018β2019 Π³Π³.ΠΠ°ΡΠ΅ΡΠΈΠ°Π»Ρ ΠΈ ΠΌΠ΅ΡΠΎΠ΄Ρ: ΠΈΡΡΠ»Π΅Π΄ΠΎΠ²Π°Π½ΠΎ 7858 ΠΏΡΠΎΠ± Π±ΠΈΠΎΠ»ΠΎΠ³ΠΈΡΠ΅ΡΠΊΠΎΠ³ΠΎ ΠΌΠ°ΡΠ΅ΡΠΈΠ°Π»Π° ΠΎΡ Π±ΠΎΠ»ΡΠ½ΡΡ
ΡΠ½ΡΠ΅ΡΠΎΠ²ΠΈΡΡΡΠ½ΠΎΠΉ ΠΈΠ½ΡΠ΅ΠΊΡΠΈΠ΅ΠΉ. ΠΡΠ΄Π΅Π»Π΅Π½ΠΈΠ΅ ΠΈ ΠΈΠ΄Π΅Π½ΡΠΈΡΠΈΠΊΠ°ΡΠΈΡ ΡΠ½ΡΠ΅ΡΠΎΠ²ΠΈΡΡΡΠΎΠ² ΠΏΡΠΎΠ²ΠΎΠ΄ΠΈΠ»ΠΈ Π²ΠΈΡΡΡΠΎΠ»ΠΎΠ³ΠΈΡΠ΅ΡΠΊΠΈΠΌ ΠΈ ΠΌΠΎΠ»Π΅ΠΊΡΠ»ΡΡΠ½ΠΎ-Π³Π΅Π½Π΅ΡΠΈΡΠ΅ΡΠΊΠΈΠΌ ΠΌΠ΅ΡΠΎΠ΄Π°ΠΌΠΈ.Π Π΅Π·ΡΠ»ΡΡΠ°ΡΡ: ΡΠ΅ΡΠ΅Π½ΠΈΠ΅ ΡΠΏΠΈΠ΄Π΅ΠΌΠΈΡΠ΅ΡΠΊΠΎΠ³ΠΎ ΠΏΡΠΎΡΠ΅ΡΡΠ° ΠΈ ΠΊΠ»ΠΈΠ½ΠΈΡΠ΅ΡΠΊΠΈΠ΅ ΠΏΡΠΎΡΠ²Π»Π΅Π½ΠΈΡ ΡΠ½ΡΠ΅ΡΠΎΠ²ΠΈΡΡΡΠ½ΠΎΠΉ ΠΈΠ½ΡΠ΅ΠΊΡΠΈΠΈ Π½Π° ΡΠ°Π·Π½ΡΡ
ΡΠ΅ΡΡΠΈΡΠΎΡΠΈΡΡ
ΠΈΠΌΠ΅Π»ΠΈ ΠΎΡΠ»ΠΈΡΠΈΡ. ΠΠ° ΠΎΠ΄Π½ΠΈΡ
ΡΠ΅ΡΡΠΈΡΠΎΡΠΈΡΡ
ΠΏΡΠ΅ΠΎΠ±Π»Π°Π΄Π°Π»ΠΈ Π·Π°Π±ΠΎΠ»Π΅Π²Π°Π½ΠΈΡ Ρ ΠΊΠ»ΠΈΠ½ΠΈΠΊΠΎΠΉ ΡΠ½ΡΠ΅ΡΠΎΠ²ΠΈΡΡΡΠ½ΠΎΠ³ΠΎ ΠΌΠ΅Π½ΠΈΠ½Π³ΠΈΡΠ°, Π½Π° Π΄ΡΡΠ³ΠΈΡ
ΡΠ΅ΡΡΠΈΡΠΎΡΠΈΡΡ
ΠΏΡΠ΅Π²Π°Π»ΠΈΡΠΎΠ²Π°Π»ΠΈ ΡΠΊΠ·Π°Π½ΡΠ΅ΠΌΠ½ΡΠ΅ ΡΠΎΡΠΌΡ Π·Π°Π±ΠΎΠ»Π΅Π²Π°Π½ΠΈΡ. Π Π‘Π°Π½ΠΊΡ-ΠΠ΅ΡΠ΅ΡΠ±ΡΡΠ³Π΅, ΠΡΡ
Π°Π½Π³Π΅Π»ΡΡΠΊΠΎΠΉ ΠΈ Π‘Π°ΡΠ°ΡΠΎΠ²ΡΠΊΠΎΠΉ ΠΎΠ±Π»Π°ΡΡΡΡ
ΡΠ΄Π΅Π»ΡΠ½ΡΠΉ Π²Π΅Ρ ΡΠ»ΡΡΠ°Π΅Π² ΡΠ½ΡΠ΅ΡΠΎΠ²ΠΈΡΡΡΠ½ΠΎΠΉ ΠΈΠ½ΡΠ΅ΠΊΡΠΈΠΈ Ρ ΠΊΠ»ΠΈΠ½ΠΈΡΠ΅ΡΠΊΠΎΠΉ ΠΊΠ°ΡΡΠΈΠ½ΠΎΠΉ ΡΠ½ΡΠ΅ΡΠΎΠ²ΠΈΡΡΡΠ½ΠΎΠ³ΠΎ ΠΌΠ΅Π½ΠΈΠ½Π³ΠΈΡΠ° Π΄ΠΎΡΡΠΎΠ²Π΅ΡΠ½ΠΎ ΠΏΡΠ΅Π²ΡΡΠ°Π» Π°Π½Π°Π»ΠΎΠ³ΠΈΡΠ½ΡΠΉ ΠΏΠΎΠΊΠ°Π·Π°ΡΠ΅Π»Ρ Π΄Π»Ρ ΡΠΊΠ·Π°Π½ΡΠ΅ΠΌΠ½ΡΡ
ΡΠΎΡΠΌ ΡΠ½ΡΠ΅ΡΠΎΠ²ΠΈΡΡΡΠ½ΠΎΠΉ ΠΈΠ½ΡΠ΅ΠΊΡΠΈΠΈ. Π Π Π΅ΡΠΏΡΠ±Π»ΠΈΠΊΠ΅ ΠΠΎΠΌΠΈ, ΠΠ΅Π½ΠΈΠ½Π³ΡΠ°Π΄ΡΠΊΠΎΠΉ ΠΈ ΠΡΡΠΌΠ°Π½ΡΠΊΠΎΠΉ ΠΎΠ±Π»Π°ΡΡΡΡ
Π΄ΠΎΠ»Ρ ΡΠ»ΡΡΠ°Π΅Π² ΡΠ½ΡΠ΅ΡΠΎΠ²ΠΈΡΡΡΠ½ΠΎΠΉ ΠΈΠ½ΡΠ΅ΠΊΡΠΈΠΈ Ρ ΡΠΊΠ·Π°Π½ΡΠ΅ΠΌΠ½ΡΠΌΠΈ ΠΏΡΠΎΡΠ²Π»Π΅Π½ΠΈΡΠΌΠΈ Π±ΡΠ»Π° Π΄ΠΎΡΡΠΎΠ²Π΅ΡΠ½ΠΎ Π²ΡΡΠ΅, ΡΠ΅ΠΌ Π΄ΠΎΠ»Ρ Π·Π°Π±ΠΎΠ»Π΅Π²Π°Π½ΠΈΠΉ ΡΠ½ΡΠ΅ΡΠΎΠ²ΠΈΡΡΡΠ½ΡΠΌ ΠΌΠ΅Π½ΠΈΠ½Π³ΠΈΡΠΎΠΌ. ΠΠ½ΡΠ΅ΡΠΎΠ²ΠΈΡΡΡΡ 30 ΡΠ΅ΡΠΎΡΠΈΠΏΠΎΠ² Π±ΡΠ»ΠΈ Π΄Π΅ΡΠ΅ΠΊΡΠΈΡΠΎΠ²Π°Π½Ρ Π² ΠΏΡΠΎΠ±Π°Ρ
ΠΎΡ Π±ΠΎΠ»ΡΠ½ΡΡ
ΡΠ½ΡΠ΅ΡΠΎΠ²ΠΈΡΡΡΠ½ΠΎΠΉ ΠΈΠ½ΡΠ΅ΠΊΡΠΈΠ΅ΠΉ. ΠΡΠ»Π° ΡΡΡΠ°Π½ΠΎΠ²Π»Π΅Π½Π° ΡΡΠΈΠΎΠ»ΠΎΠ³ΠΈΡ ΡΠΏΠΎΡΠ°Π΄ΠΈΡΠ΅ΡΠΊΠΈΡ
ΠΈ Π³ΡΡΠΏΠΏΠΎΠ²ΡΡ
Π·Π°Π±ΠΎΠ»Π΅Π²Π°Π½ΠΈΠΉ ΡΠ½ΡΠ΅ΡΠΎΠ²ΠΈΡΡΡΠ½ΠΎΠΉ ΠΈΠ½ΡΠ΅ΠΊΡΠΈΠ΅ΠΉ Ρ ΡΠ°Π·Π½ΡΠΌΠΈ ΠΊΠ»ΠΈΠ½ΠΈΡΠ΅ΡΠΊΠΈΠΌΠΈ ΡΠΎΡΠΌΠ°ΠΌΠΈ. ΠΠ° Π½Π΅ΠΊΠΎΡΠΎΡΡΡ
ΡΠ΅ΡΡΠΈΡΠΎΡΠΈΡΡ
Π±ΡΠ»ΠΈ Π²ΡΡΠ²Π»Π΅Π½Ρ ΠΎΡΠ°Π³ΠΈ Π³ΡΡΠΏΠΏΠΎΠ²ΡΡ
Π·Π°Π±ΠΎΠ»Π΅Π²Π°Π½ΠΈΠΉ ΡΡΠ΅Π΄ΠΈ Π΄Π΅ΡΠ΅ΠΉ. ΠΡΠΈΠΎΠ»ΠΎΠ³ΠΈΡΠ΅ΡΠΊΠΈΠΌΠΈ Π°Π³Π΅Π½ΡΠ°ΠΌΠΈ Π³ΡΡΠΏΠΏΠΎΠ²ΡΡ
Β Π·Π°Π±ΠΎΠ»Π΅Π²Π°Π½ΠΈΠΉ ΡΠ½ΡΠ΅ΡΠΎΠ²ΠΈΡΡΡΠ½ΡΠΌ ΠΌΠ΅Π½ΠΈΠ½Π³ΠΈΡΠΎΠΌ Π² Π‘Π°Π½ΠΊΡ-ΠΠ΅ΡΠ΅ΡΠ±ΡΡΠ³Π΅, ΠΡΡΠΌΠ°Π½ΡΠΊΠΎΠΉ ΠΈ Π‘Π°ΡΠ°ΡΠΎΠ²ΡΠΊΠΎΠΉ ΠΎΠ±Π»Π°ΡΡΡΡ
Π±ΡΠ»ΠΈ ΡΠ½ΡΠ΅ΡΠΎΠ²ΠΈΡΡΡΡ ΠΠΎΠΊΡΠ°ΠΊΠΈ Π5, ΠΠΎΠΊΡΠ°ΠΊΠΈ Π4 ΠΈ Π²ΠΈΡΡΡ ECHO30. ΠΡΡΠΏΠΏΠΎΠ²ΡΠ΅ Π·Π°Π±ΠΎΠ»Π΅Π²Π°Π½ΠΈΡ Ρ ΠΊΠ»ΠΈΠ½ΠΈΠΊΠΎΠΉ Π²ΠΈΡΡΡΠ½ΠΎΠΉ ΡΠΊΠ·Π°Π½ΡΠ΅ΠΌΡ Π² ΠΡΡ
Π°Π½Π³Π΅Π»ΡΡΠΊΠΎΠΉ, ΠΠ΅Π½ΠΈΠ½Π³ΡΠ°Π΄ΡΠΊΠΎΠΉ, ΠΡΡΠΌΠ°Π½ΡΠΊΠΎΠΉ ΠΈ ΠΠΎΠ²Π³ΠΎΡΠΎΠ΄ΡΠΊΠΎΠΉ ΠΎΠ±Π»Π°ΡΡΡΡ
Π±ΡΠ»ΠΈ ΠΎΠ±ΡΡΠ»ΠΎΠ²Π»Π΅Π½Ρ ΡΠ½ΡΠ΅ΡΠΎΠ²ΠΈΡΡΡΠ°ΠΌΠΈ ΠΠΎΠΊΡΠ°ΠΊΠΈ Π10, Π16 ΠΈ Π6.ΠΠ°ΠΊΠ»ΡΡΠ΅Π½ΠΈΠ΅: ΠΊΠ»ΠΈΠ½ΠΈΡΠ΅ΡΠΊΠΈΠ΅ ΡΠΎΡΠΌΡ ΡΠ½ΡΠ΅ΡΠΎΠ²ΠΈΡΡΡΠ½ΠΎΠΉ ΠΈΠ½ΡΠ΅ΠΊΡΠΈΠΈ Π½Π° ΠΎΡΠ΄Π΅Π»ΡΠ½ΡΡ
ΡΠ΅ΡΡΠΈΡΠΎΡΠΈΡΡ
Π±ΡΠ»ΠΈ ΠΎΠ±ΡΡΠ»ΠΎΠ²Π»Π΅Π½Ρ ΡΠ½ΡΠ΅ΡΠΎΠ²ΠΈΡΡΡΠ°ΠΌΠΈ, ΠΊΠΎΡΠΎΡΡΠ΅ Π΄ΠΎΠΌΠΈΠ½ΠΈΡΠΎΠ²Π°Π»ΠΈ Π² ΡΠΈΡΠΊΡΠ»ΡΡΠΈΠΈ Π½Π° ΡΠΎΠΉ ΠΈΠ»ΠΈ ΠΈΠ½ΠΎΠΉ ΡΠ΅ΡΡΠΈΡΠΎΡΠΈΠΈ. ΠΡΠΈΠΎΠ»ΠΎΠ³ΠΈΡΠ΅ΡΠΊΠΈΠΌΠΈ Π°Π³Π΅Π½ΡΠ°ΠΌΠΈ ΡΠ½ΡΠ΅ΡΠΎΠ²ΠΈΡΡΡΠ½ΠΎΠ³ΠΎ ΠΌΠ΅Π½ΠΈΠ½Π³ΠΈΡΠ° Π±ΡΠ»ΠΈ ΡΠ½ΡΠ΅ΡΠΎΠ²ΠΈΡΡΡΡ Π²ΠΈΠ΄Π° Π, ΡΠ°ΡΠ΅ Π²ΡΠ΅Π³ΠΎ ECHO30, ECHO6 ΠΈ ΠΠΎΠΊΡΠ°ΠΊΠΈ Π1β6. ΠΡΠΈΠΎΠ»ΠΎΠ³ΠΈΡΠ΅ΡΠΊΠΈΠΌΠΈ Π°Π³Π΅Π½ΡΠ°ΠΌΠΈ ΡΠΊΠ·Π°Π½ΡΠ΅ΠΌΠ½ΡΡ
ΡΠΎΡΠΌ ΡΠ½ΡΠ΅ΡΠΎΠ²ΠΈΡΡΡΠ½ΠΎΠΉ ΠΈΠ½ΡΠ΅ΠΊΡΠΈΠΈ ΡΠ²Π»ΡΠ»ΠΈΡΡ ΡΠ½ΡΠ΅ΡΠΎΠ²ΠΈΡΡΡΡ Π²ΠΈΠ΄Π° Π (Π² ΠΎΡΠ½ΠΎΠ²Π½ΠΎΠΌ, Π²ΠΈΡΡΡΡ ΠΠΎΠΊΡΠ°ΠΊΠΈ Π ΡΠ°Π·Π½ΡΡ
ΡΠ΅ΡΠΎΡΠΈΠΏΠΎΠ² ΠΈ ΡΠ½ΡΠ΅ΡΠΎΠ²ΠΈΡΡΡ 71 ΡΠΈΠΏΠ°)
Fatty acid and carbohydrate metabolism in acute myocardial ischemia
Fatty acid metabolism (FA) requires 60-70% of O2 coming to myocardium. In O2 deficit, FA and carbohydrate metabolism declines. Reversible and irreversible ischemic damage is caused by unoxydated metabolitesβ storage. Medicament therapy-induced carbohydrate metabolism is perspective, due to its less O2 demand
Radiation Damping of Surface Plasmons in a Pair of Nanoparticles and in Nanoparticles near Interfaces
A theory of surface plasmon radiation damping in a system
of coupled
spherical metallic nanoparticles is developed, and a simple formula
for the radiation line width is obtained for the first time. It is
shown that as a result of surface plasmon frequency redshift, a notable
reduction of the radiation damping rate takes place. For small separations,
the radiation line width narrows by a factor of 3 as compared to large
separations. The theory is expanded to the case of a spherical metallic
nanoparticle placed near an interface of two dielectric media. The
dependence of the redshift of surface plasmon frequency and the radiation
damping rate on the particleβinterface separation are calculated.
It is revealed that in both cases, a decrease of refractive index
of the surrounding media also leads to a decrease of the damping rate
REMODELING OF THE RIGHT HEART AND THE LEVEL OF BRAIN NATRIURETIC PEPTIDE IN PATIENTS WITH CHRONIC THROMBOEMBOLIC PULMONARY HYPERTENSION: A COMPARATIVE CROSS-SECTIONAL OBSERVATIONAL STUDY
Aim. To study the right heart remodeling and level of N-terminal brain natriuretic peptide (Nt-proBNP) in patients with chronic thromboembolic pulmonary hypertension (CTEPH). Material and methods. Patients (n=79) after pulmonary embolism were included into the study. The main group consisted of patients (n=43) with an increase in systolic pulmonary artery pressure (SPAP) >30 mm Hg: 30 (37.9%) Β patients had pulmonary hypertension (PH) degree I, and 13 (16.5%) Β β PH degree IIβIII. Group of comparison con- sisted of 36 patients expired pulmonary embolism and having SPAP <30 mm Hg. The control group consisted of 20 people. 6-minute walk test (6-MWT) and Doppler echocardiography were performed in all patients. Besides myocardial tissue Doppler echocardiography and assessment of Nt-proBNP level were performed in 38 and 71 patients, respectively. Results. Dyspnea occurred in 90.7% of patients with various degrees of PH and 80.5% of patients with normal SPAP. Patients without PH and with PH I complained of palpitations, weakness, fatigue, and dizziness with similar frequency. Patients with PH I were comparable with ones of comparison group in 6-MWT distance that dramatically decreased in patients with PH IIβIII. Enlargement of the right atrium (RA) and/or right ventricular (RV) was observed in 76.7% of patients with PH I and 100% of patients with PH IIβIII. RV diastolic function abnormalities (E/A<1 and E/A>2) were detected in 19.4%, 16.7% and 61.5% of patients of comparison group, PH I and PH IIβIII patients, respectively. According to myocardial tissue Doppler echocardiography Em/Am<1 was observed in 8 (72.7%) patients of the comparison group and in 13 (76.4%) patients with PH. Nt-proB-NP level was 17.3 [2.3, 33.9] fmol/ml in PH I patients and 142.1 [62.1, 171.8] fmol/ml in PH IIβIII patients. Nt-proBNP level was 6.5 [3.1, 18.3] fmol/mL in patients of the comparison group, and it was higher than this in patients of the control group (3.5 [1.8, 7.5 fmol/ml]. Conclusion. Various indicators of heart remodeling and RV diastolic dysfunction were found in the majority of patients after pulmonary embolism, including those with nor- mal SPAP. Elevation of Nt-proBNP level adequately reflects the severity of RV dysfunction in CTEPH patients only in PH IIβIII. This marker has low diagnostic value in patients with- out CTEPH and PH I patients
REMODELING OF THE RIGHT HEART AND THE LEVEL OF BRAIN NATRIURETIC PEPTIDE IN PATIENTS WITH CHRONIC THROMBOEMBOLIC PULMONARY HYPERTENSION: A COMPARATIVE CROSS-SECTIONAL OBSERVATIONAL STUDY
Aim. To study the right heart remodeling and level of N-terminal brain natriuretic peptide (Nt-proBNP) in patients with chronic thromboembolic pulmonary hypertension (CTEPH). Material and methods. Patients (n=79) after pulmonary embolism were included into the study. The main group consisted of patients (n=43) with an increase in systolic pulmonary artery pressure (SPAP) >30 mm Hg: 30 (37.9%) Β patients had pulmonary hypertension (PH) degree I, and 13 (16.5%) Β β PH degree IIβIII. Group of comparison con- sisted of 36 patients expired pulmonary embolism and having SPAP <30 mm Hg. The control group consisted of 20 people. 6-minute walk test (6-MWT) and Doppler echocardiography were performed in all patients. Besides myocardial tissue Doppler echocardiography and assessment of Nt-proBNP level were performed in 38 and 71 patients, respectively. Results. Dyspnea occurred in 90.7% of patients with various degrees of PH and 80.5% of patients with normal SPAP. Patients without PH and with PH I complained of palpitations, weakness, fatigue, and dizziness with similar frequency. Patients with PH I were comparable with ones of comparison group in 6-MWT distance that dramatically decreased in patients with PH IIβIII. Enlargement of the right atrium (RA) and/or right ventricular (RV) was observed in 76.7% of patients with PH I and 100% of patients with PH IIβIII. RV diastolic function abnormalities (E/A<1 and E/A>2) were detected in 19.4%, 16.7% and 61.5% of patients of comparison group, PH I and PH IIβIII patients, respectively. According to myocardial tissue Doppler echocardiography Em/Am<1 was observed in 8 (72.7%) patients of the comparison group and in 13 (76.4%) patients with PH. Nt-proB-NP level was 17.3 [2.3, 33.9] fmol/ml in PH I patients and 142.1 [62.1, 171.8] fmol/ml in PH IIβIII patients. Nt-proBNP level was 6.5 [3.1, 18.3] fmol/mL in patients of the comparison group, and it was higher than this in patients of the control group (3.5 [1.8, 7.5 fmol/ml]. Conclusion. Various indicators of heart remodeling and RV diastolic dysfunction were found in the majority of patients after pulmonary embolism, including those with nor- mal SPAP. Elevation of Nt-proBNP level adequately reflects the severity of RV dysfunction in CTEPH patients only in PH IIβIII. This marker has low diagnostic value in patients with- out CTEPH and PH I patients