What question did this study set out to answer?

To characterize hyperacute blood-based neurobiomarker kinetics of neuron specific enolase (NSE) and S100B during a model of brief global cerebral hypoperfusion and reperfusion.

March 21, 2026ResuscitationOpen Access

Post-Cardiac Arrest Brain Injury Model: Neurobiomarker Kinetics Following Global Cerebral Hypoperfusion-Reperfusion

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Key result

Controlled low-flow episodes during TAVI induce clinically silent elevations in neurobiomarkers NSE and S100B.

Why the study?

Hyperacute blood-based neurobiomarker kinetics after precisely defined (very) low-flow intervals in post-cardiac arrest brain injury remain poorly characterized.

Does rapid ventricular pacing-induced transient global cerebral hypoperfusion during TAVI alter the hyperacute kinetics of serum neurobiomarkers NSE and S100B in adults with severe aortic stenosis?

Key Points

To characterize hyperacute blood-based neurobiomarker kinetics of neuron specific enolase (NSE) and S100B during a model of brief global cerebral hypoperfusion and reperfusion.
Enrolled 76 adult patients undergoing transcatheter aortic valve implantation (TAVI) in a single-center, prospective, self-controlled cohort study between February 2024 and March 2025.
Applied rapid ventricular pacing (120–200 bpm) to induce transient pulseless ventricular tachycardia, functionally mimicking brief cardiac arrest.
Recorded invasive aortic blood pressure and carotid/middle cerebral artery flow, and collected serum samples at baseline (T0) and 20, 65, 110, and 200 minutes post-pacing to measure NSE and S100B concentrations.
Patients experienced a median cumulative rapid ventricular pacing duration of 60 s (IQR 41–92), causing a very low-flow state and a drop in aortic pressure below the autoregulatory threshold.
NSE increased progressively from T0 (10.6 [9.1–13.0] mg/L) to T200 (17.0 [14.2–20.5] mg/L), whereas S100B showed an inverse U-shaped pattern peaking at T65 (0.14 [0.11–0.23] mg/L) before falling to 0.08 [0.06–0.12] mg/L at T200.
No patient developed neurological deficits, and no significant monotonic correlation emerged between pacing duration and serum levels of S100B or NSE at any timepoint (all p > 0.05).

Structured PICO

Does rapid ventricular pacing-induced transient global cerebral hypoperfusion during TAVI alter the hyperacute kinetics of serum neurobiomarkers NSE and S100B in adults with severe aortic stenosis?

Population

76 adult patients (median age 79, 63% female) with severe symptomatic aortic stenosis at high surgical risk undergoing transcatheter aortic valve implantation (TAVI) with perioperative cerebral performance category 1. Excluded: history of central nervous system pathology (malignancy, epilepsy, ischemic stroke) and pre-analytical laboratory errors.

Intervention

Rapid ventricular pacing (RVP) at 120-200 beats/min during TAVI balloon predilatation or valve deployment to induce transient pulseless ventricular tachycardia (median cumulative duration 60 seconds).

Comparator

Self-controlled (baseline measurements obtained within 20 minutes prior to the TAVI procedure).

Outcome

Hyperacute kinetics of serum neurobiomarkers (Neuron Specific Enolase [NSE] and S100B) measured at 20, 65, 110, and 200 minutes after the end of rapid ventricular pacing.surrogate

Controlled, very low-flow episodes during TAVI induce measurable but clinically silent elevations in neurobiomarkers NSE and S100B, reflecting distinct ischemia and reperfusion kinetics.

Limitations

The induced arrest reflects a brief, very low-flow cardiac arrest rather than a complete no-flow, so extrapolation to prolonged cardiac arrest situations should be cautious.
Appropriate input for detailed waveform analysis was available only for a subset of patients.

Implication

Reassures on short-term neurological safety of TAVI rapid pacing; extends knowledge of cerebral ischemia-reperfusion biomarker kinetics.

Abstract

BACKGROUNDPost-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 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 minutes (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]g/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]g/L).No patient developed neurological deficits. CONCLUSIONSControlled (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.

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Cite This Study

Papp et al. (2026) studied this question. Controlled low-flow episodes during TAVI induced clinically silent elevations of NSE (10.6 to 17.0 g/L) and S100B (0.05 to 0.14 g/L) over 200 minutes without neurological deficits.

synapsesocial.com/papers/69be34886e48c4981c672bc5 https://doi.org/10.1016/j.resuscitation.2026.111063

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Implication

Reassures on short-term neurological safety of TAVI rapid pacing; extends knowledge of cerebral ischemia-reperfusion biomarker kinetics.

Post-Cardiac Arrest Brain Injury Model: Neurobiomarker Kinetics Following Global Cerebral Hypoperfusion-Reperfusion

Key Points

Structured PICO

Limitations

Implication

Abstract

Discussion

Cite This Study

Post-Cardiac Arrest Brain Injury Model: Neurobiomarker Kinetics Following Global Cerebral Hypoperfusion-Reperfusion

Key Points

Structured PICO

Limitations

Implication

Abstract

Discussion

Cite This Study

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