Acute cardiac care & resuscitationCohort study
Post-cardiac arrest brain injury model: neurobiomarker kinetics following global cerebral hypoperfusion-reperfusion
- single-center, prospective, self-controlled cohort study
Authors' conclusion
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.
Study context
- Population
- Adults undergoing transcatheter aortic valve implantation (TAVI) with rapid ventricular pacing (RVP) inducing transient very low-flow state
- Participants
- 76 enrolled patients
- Exposure
- Serum neurobiomarkers before vs 20, 65, 110 and 200 min after RVP
Main finding
As reported in the abstract
Cumulative RVP duration
median cumulative RVP duration
60 s (IQR 41-92)
Observational data: associations, not effects.
Further findings
Middle cerebral artery (MCA) and common carotid (CCA) flow and aortic pressure during RVP
- MCA and CCA flow showed a very low-flow state while aortic pressure fell below the presumed autoregulatory threshold
Neuron specific enolase (NSE) concentrations (µg/L) · 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]
- increased progressively
S100B concentrations (µg/L) · baseline to 200 min
- 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]
- inverse U-shaped profile
Original publication
Post-cardiac arrest brain injury model: neurobiomarker kinetics following global cerebral hypoperfusion-reperfusion. Resuscitation. Published 17 March 2026. doi:10.1016/j.resuscitation.2026.111063
Summarised from the published abstract; every number is checked against it