Post-cardiac arrest brain injury model: neurobiomarker kinetics following global cerebral hypoperfusion-reperfusion.

Abstract

Post-cardiac arrest brain injury is driven by both global cerebral hypoperfusion and subsequent reperfusion. However, hyperacute blood-based neurobiomarker kinetics after precisely defined (very) low-flow intervals remain poorly characterized. During transcatheter aortic valve implantation (TAVI), rapid ventricular pacing (RVP) induces a transient pulseless ventricular tachycardia, functionally mimicking brief cardiac arrest. In this single-center, prospective, self-controlled cohort study, adults undergoing TAVI were enrolled. RVP (120-200 bpm) was applied to transiently suppress forward flow. Invasive aortic pressure, common carotid (CCA) and middle cerebral artery (MCA) flow were recorded continuously. Serum samples were obtained pre-procedure and 20, 65, 110 and 200 min after RVP. Neuron specific enolase (NSE), and S100 were measured as neurobiomarkers. In case of the 76 enrolled patients, median cumulative RVP duration was 60 s (IQR 41-92). During RVP, MCA and CCA flow showed a very low-flow state while aortic pressure fell below the presumed autoregulatory threshold. NSE concentrations increased progressively from baseline to 200 min (T0: 10.6 [9.1-13.0]; T20: 12.8 [11.6-15.5]; T65: 15.1 [13.0-18.6]; T110: 15.8 [13.8-18.6]; T200: 17.0 [14.2-20.5] µg/L). S100B concentrations showed an inverse U-shaped profile (T0: 0.05 [0.04-0.07]; T20: 0.13 [0.10-0.18]; T65: 0.14 [0.11-0.23]; T110: 0.11 [0.08-0.16]; T200: 0.08 [0.06-0.12] µg/L). No patient developed neurological deficits. Controlled (very) low-flow episodes during TAVI induce measurable, but clinically silent, elevations of NSE and S100. Neurobiomarkers reflects with distinct kinetics on ischaemia and reperfusion following a short, very low-flow cardiac arrest.