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ASSA13-08-10 Effects of the Remote Ischemic Preconditioning on Inflammatory Response in Patients Undergoing the Aortic Valve Replacement
  1. Andrei Bautin,
  2. Sergey Datsenko,
  3. Dmitriy Tashkhanov,
  4. Mikhail Gordeev,
  5. Alexandr Marichev,
  6. Alexandr Najmushin,
  7. Vladimir Etin,
  8. Mikhail Galagudza
  1. Almazov Federal Heart, Blood and Endocrinology Centre


Objective This 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.

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