Cardiopulmonary bypass (CPB) is a common procedure to maintain body perfusion during cardiac surgery. It is associated with a systemic inflammatory response, hemostasis and circulatory dysfunction that can lead to organ dysfunction and seldomly to death. O-GlcNAcylation is a post-translational modification modulated in response to stress in different acute and chronic situations.

Decipher if blood O-GlcNAc levels are modified during CPB induced stress.

Vingt adult patients with CPB time >60minutes were included. Blood samples were collected on EDTA at (i) anesthesia induction (Ind), (ii) aortic declamping (AD) and (iii) 5hours post-declamping (AD+5). Whole blood and plasma were recovered from samples. O-GlcNAc levels in blood were evaluated by western blot while plasmatic biological markers were measured on automatic laboratory analysis system to correlate O-GlcNAc level with systemic response to CPB. Demographics and One-Way ANOVA analysis were performed with RStudio.

CPB induced an early increase of plasmatic inflammatory marker IL-6 (Ind: 5.7±3.2, AD: 120.0±26.5pg/mL, P<0.01) that was sustained after 5hrs. Systemic stress was confirmed via an increase in Creatine Kinase (Ind: 95.2±12.2, AD: 271.9±41.1U/L, P<0.001) and Lactate Dehydrogenase (AD: 316.3±32.2, AD+5: 541.2±64.3U/L, P<0.001) release. Heart and renal markers demonstrated a dysfunction with Troponin T (AD: 656±148, AD+5: 1899±568pg/mL, P<0.05) and Creatinine (AD: 94.8±6.6, AD+5:106.0±7.14μM, P<0.05) respectively. CPB induced a significant 20% increase in O-GlcNAc levels (P<0.01).

In this preliminary study, we highlighted that the inflammation and tissue stress consecutive to CPB are associated with an increase in blood O-GlcNAc levels 5hours after CPB. Inclusion of more patients and correlations between O-GlcNAc level variation and demographics and/or patients’ outcome might reveal a new biomarker of risk after CPB.