ObjectiveThis study was carried out to assess whether the remote ischemic preconditioning (RIPC) affects the inflammatory response in patients undergoing the aortic valve replacement. Methods Twenty seven patients were included into the prospective randomised study. In all cases the aortic valve replacement was performed due to the aortic stenosis under cardiopulmonary bypass (CPB). 13 patients of main group received RIPC and 14 patients formed control group. Anaesthesia was maintained either by propofol and fentanyl (7 patients in the control group, 8 patients in the RIPC group) or by sevoflurane and fentanyl (7 patients in the control group, 5 patients in the RIPC group). RIPC was induced by three 5-min cycles of lower limb ischemia and reperfusion after anaesthesia induction. Cytokines (interleukin-8 (IL-8), interleukin-6 (IL-6)) were analysed at baseline, 30 min, 12 h, 24 h and 48 h after CPB completion. Quantitative data were presented as median (25th–75th percentile). According to nonparametrically distribution, data were assessed by the Mann-Whitney U-test, a P value < 0.05 was considered as significant. Results Our study displayed the significant increase in cytokines levels after CPB completion in both groups. There were no statistical differences in IL-8 and IL-6 concentrations between groups at 30 min and 12 h after CPB. Unexpectedly we found the significantly higher IL-8 activity in the RIPC group at 24 h and 48 h after CPB: it was 12.3 (7.9; 16.5) pg/mL vs. 6.5 (5.5; 10.4) pg/mL in the control group, p = 0.03 at 24 h and 10.6 (5.8; 13.2) pg/mL vs. 5.5 (4.5; 6.1) pg/mL in the control group, p = 0.02 at 48 h. The same tendency was found in IL-6 activity, however statistical significance between the RIPC group and the control one was not confirmed: 27.6 (15.1; 38.5) pg/mL vs. 15.3 (10.5; 28.8) pg/mL, respectively (p = 0.32) at 24 h and 17.1 (13.0; 27.3) pg/mL vs. 9.9 (6.8; 17.2) pg/mL, respectively (p = 0.14) at 48 h. Conclusions This pilot study indicates surprisingly that RIPC may enhance inflammatory response after CPB. Our data suggest that large clinical trials assessing the effects of RIPC on the inflammatory response should be performed in order to study the underlying mechanisms.

Background. Recently, transcatheter pulmonary artery (PA) ablation aiming at sympathetic denervation has been proposed in pulmonary arterial hypertension (PAH). This pilot feasibility study aimed to assess the feasibility of selective radiofrequency PA ablation based on response to high-frequency stimulation mapping. Methods. The study comprised 3 female patients with idiopathic PAH (IPAH). The following reactions to PA stimulation were noted and marked by color points on the three-dimensional map: sinus bradycardia (heart rate decrease ≥15%), tachycardia (heart rate increase ≥15%), phrenic nerve capture, and cough. Since the most appropriate ablation strategy was unknown, two approaches were suggested, according to stimulation results: ablation at points with any heart rate response (either bradycardia or tachycardia)—this approach was applied in patient #1 (IPAH long-term responder to calcium channel blockers); segmental ablation at points with no response and with tachycardia response (one IPAH long-term responder to calcium channel blockers patient and one–IPAH with negative vasoreactive testing). Hemodynamic measurements were performed before and after denervation. Follow-up visits were scheduled at 6 and 12 months. Results. Six-months follow-up was uneventful for patients #1 and 3; patient #2 had one syncope and reduced 6-minute walk test distance and peak VO2 consumption. At 12 months, there was a normalization of mean PA pressure and pulmonary vascular resistance (PVR) in patient #1. Patient #2 had no change in PA pressure and PVR at 12 months. Patient #3 remained in II functional class; however, there was an increase in mean PA pressure and loss of vasoreactivity. Conclusions. Electrical high-frequency stimulation of the PA identifies several types of evoked reactions: heart rate slowing, acceleration, phrenic nerve capture, and cough. The improvement in clinical and hemodynamic parameters following targeted PA ablation in the IPAH patient with positive vasoreactive testing should be confirmed in larger studies.

The purpose of our prospective, consistent, non-randomized study was to analyze the results of vasoreactivity tests (VRT) performed with nitric oxide (NO) or inhaled Iloprost in heart transplant candidates. 72 VRTs were done in 58 candidates for heart transplantation. All patients had heart failure III-IV NYHA and pulmonary hypertension (PH) with pulmonary vascular resistance (PVR) over 2.5 WU. 43 patients received NO, 80 ppm for 20 min. 29 patients inhaled 20 g of Iloprost (Ventavis, Bayer). Hemodynamic parameters were measured at baseline, 20 min after NO inhalation and 15 min following the completion of Iloprost inhalation. There were no between-group differences in the severity of patient's condition and baseline hemodynamic indicators. Both vasodilators caused statistically significant reduction in mean PAP: in the NO group it dropped (p = 0.002), in the Iloprost group the mean PAP decreased (p<0.0001). A more than 20% decrease in PAP was recorded in 13 cases (30.2%) in the NO group and in 16 cases (55.2%) in the Iloprost group (p = 0.03). A more than 20% decrease in PVR was noted in 24 cases (55.8%) in the NO group and in 24 cases (82.8%) in the Iloprost group (p<0.02). We found some differences in the effect of NO and Iloprost on LV efficiency. There were no changes in the stroke volume index (SVI) in the NO group, while inhaled Iloprost increased SVI (p<0.001). A probable cause of the increase in LV efficiency might have been the reduction of total peripheral vascular resistance (p<0.0001). There were no differences in SVI during NO inhala-tion. It should be noted in conclusion that Iloprost is more effective in decreasing mean PAP and PVR in heart transplant candidates. Inhaled Iloprost causes favorable changes in preload and afterload of the impaired LV and increases its performance.

Background: Fixed pulmonary hypertension (PH) in heart transplant candidates is a risk factor for right ventricular failure in the postoperative period and early mortality. Patients with fixed PH are not included in the waiting list. Thus, the correct assessment of the pulmonary circulation before the operation affects both clinical management and prognosis. Aim: To reduce the risk of incorrect patient non-inclusion to the waiting list by reduction of false negative test results for PH reversibility.Materials and methods: Fourteen heart transplant candidates were included in this retrospective cohort single center study. Fixed PH with pulmonary vascular resistance (PVR) exceeding 3.5 Wood's units was found in all these patients using right heart catheterization and pulmonary vasoreactivity tests. Initially, these patients had not been put into the waiting list. Pulmonary catheterization was performed in the intensive care unit with a Swan-Ganz catheter and pre-pulmonary thermodilution technique. To perform pulmonary vasoreactivity tests, inhaled iloprost (n = 12) or nitric oxide (n = 2) were used. Subsequently all patients received levosimendan infusion at a dose of 12.5 (0.05–0.2) mg/kg/min, with repeated pulmonary artery catheterization and pulmonary vasoreactivity tests at 72 hours after the infusion. Pulmonary vasoreactivity tests results allowed 13 patients to be included into the waiting list. Heart transplantation was performed in 8 recipients, with postoperative assessment of their hemodynamic and clinical parameters. Data are presented as median [25th percentile; 75th percentile].Results: After the levosimendan infusion, there was a decrease in the pulmonary artery mean pressure from 45 [36; 47] to 29.5 [23; 37] mm Hg (p < 0.01), and in PVR from 6.9 [4.9; 8.9] to 3.6 [2.9; 5.9] Wood's units (p <0.01). In 7 patients, PVR decreased to less than 3.5 Wood's units: the rest of the patients underwent pulmonary vasoreactivity tests. As a result, 13 of 14 patients showed reversible PH and were included into the waiting list. By the date of the manuscript submission, heart transplantation has been performed in 8 patients. Their PVR 6 hours after surgery was 2.2 [2; 3.1] Wood's units; there were no cases of fixed PH and right heart failure. There was a single death associated to a hemorrhagic stroke at day 6 after heart transplantation. The sensitivity of pre-operative pulmonary vasoreactivity tests with the use of levosimendan was 87.5%.Conclusion: Levosimendan infusion may increase the sensitivity of the pulmonary vasoreactivity tests before patients' inclusion into the waiting list for heart transplantation.

Цель. Сравнить воздействие оксида азота (NO) и ингаляционного илопроста (ИИ) на гемодинамику пациентов с легочной гипертензией (ЛГ), ассоцииро-ванной с выраженной систолической дисфункцией левого желудочка (ЛЖ). Материал и методы. Проведено ретроспективное описательное исследова-ние результатов 158 последовательно выполненных тестов на обратимость ЛГ с применением NO и ИИ у 124 кандидатов на трансплантацию сердца, имею-щих легочное сосудистое сопротивление (ЛСС) более 2,5 ед. Вуда. Обследо-вано 32 женщины и 92 мужчины (средний возраст 48,9±11,2 года) с сердечной недостаточностью (СН) ишемического (n=59) и некоронарогенного (n=65) генеза, имеющих фракцию выброса левого желудочка (ФВ ЛЖ) 22,5±5,2%. Ингаляция NO с концентрацией 80 ppm применялась в 47 случаях (39 пациен-тов), ИИ в дозе 20 мкг -в 111 случаях (93 пациента). Измерение давления в легочной артерии (ЛА) и показателей гемодинамики выполняли с примене-нием катетера Сван-Ганца. Данные представлены в виде среднее ± стандарт-ное отклонение. Результаты. Отмечено снижение среднего давления в легочной артерии (ДЛАср.): на фоне NO с 34,7±8,4 до 32,7±9,7 мм рт.ст. (p=0,015), ИИ с 36,7±10 до 31,1±9,2 мм рт.ст. (p<0,001). ЛСС снизилось на фоне NO с 4,8±1,7 до 3,6±1,6 ед. Вуда (p<0,001) и на фоне ИИ -с 4,9±2 до 3,1±1,4 ед. Вуда (p<0,001 98Повышение давления в малом круге кровообра-щения закономерно сопровождает систолическую дисфункцию левого желудочка (ЛЖ) и, в соответ-ствии с современной классификацией, относится ко второму типу легочной гипертензии (ЛГ) [1]. Глав-ной причиной ЛГ в этом случае является увеличение конечно-диастолического давления с развитием левопредсердной и легочной венозной гипертензии. По мере прогрессирования сердечной недостаточно-сти (СН) дополнительно к описанному посткапил-лярному пассивному компоненту развивается актив-ный прекапиллярный, связанный с эндотелиальной дисфункцией, которая проявляется снижением про-дукции основной вазодилататорной субстанции оксида азота (NO) и ростом продукции вазокон-стрикторной субстанции эндотелина-1 [1, 2]. По мере прогрессирования левожелудочковой СН доля боль-ных с прекапиллярным компонентом ЛГ увеличива-ется. Так, среди кандидатов на трансплантацию серд ца (ТС), находившихся на лечении в СЗФМИЦ им. В. А. Алмазова, у 67,8% был отмечен повышен-ный (более 2,5 ед. Вуда) уровень легочного сосудис-того сопротивления (ЛСС) [3]. До определенного времени вазоконстрикция артерий и артериол малого круга кровообращения остается обратимой и разре-шается при коррекции левожелудочковой недоста-точности. Однако постепенно пролиферация интимы и гипертрофия/гиперплазия медии трансформируют функциональный характер прекапиллярной гипер-тензии в морфологический, делая ее необратимой [2].В настоящее время установлено, что ЛГ значи-тельно утяжеляет течение хронической СН и явля-ется независимым фактором риска экстренных госпитализаций и летальности [1,2].Методы коррекции посткапиллярной пассивной ЛГ при систолической дисфункции ЛЖ хорошо известны и утверждены в международных руковод-ствах [1]. Эти подходы направлены на сниж...