Key result
Atrial high-rate episodes linked to ~66% higher neuron-specific enolase levels versus controls.
Why the study?
Does the presence and duration of atrial high-rate episodes increase neuron-specific enolase levels as a surrogate for silent neurological ischemia in pacemaker-implanted patients?
Observational (n=160)
No
Does the presence and duration of atrial high-rate episodes increase neuron-specific enolase levels as a surrogate for silent neurological ischemia in pacemaker-implanted patients?
Answers are grounded in this paper and cite their sources.
Atrial high-rate episodes in pacemaker patients are associated with elevated neuron-specific enolase levels, suggesting a potential dose-dependent link to silent neurological ischemia.
Background and Objectives: An atrial high-rate episode (AHRE) is defined according to the European Society of Cardiology (ESC) guidelines as a heart rate of ≥175 bpm lasting at least 5 min. This study aimed to evaluate whether neuron-specific enolase (NSE) levels, an indicator of neurological impact, could serve as a surrogate biomarker for silent neurological ischemia in patients with atrial high-rate episodes (AHREs). Materials and Methods: Patients with AHRE detected in a pacemaker analysis and a control group without any arrhythmias were included. Patients with AHRE were divided into subgroups according to AHRE duration—Group 1: AHRE < 5 min, Group 2: AHRE ≥ 5 min–<1 h, Group 3: AHRE ≥ 1 h–<24 h, Group 4: AHRE ≥ 24 h. Neuron-specific enolase (NSE) levels were measured using a double-antibody enzyme-linked immunosorbent assay (ELISA) with a sensitivity of 0.05 ng/mL. Imaging techniques were not employed in this study, and NSE was used as an indirect measure of potential neurological impact. Results: There were 160 patients, including 80 (50.0%) in the AHRE group and 80 (50.0%) in the control group. According to AHRE duration, there were 24 (30.0%) patients in Group 1, 33 (41.2%) in Group 2, 19 (23.8%) in Group 3, and 4 (5.0%) in Group 4. Patients with AHRE had statistically significant differences in age, sPAP, transmitral E/A ratio, and NSE levels. The mean NSE levels of all groups were significantly different (p < 0.001). A correlation analysis in patients with AHRE showed a very strong positive correlation between AHRE duration and NSE values as well as correlations with age, virtual CHA2DS2-VASc score, and LA diameter. NSE levels were positively correlated with AHRE duration and LA diameter. AHRE duration was an independent predictor of elevated NSE levels. Conclusions: It was shown that AHRE is associated with silent neurological ischemia and that NSE levels can be used to demonstrate these neurological effects. Future studies can contribute to the development of more effective treatment strategies based on these findings by investigating the neurological effects of AHRE in more detail.
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Çınar et al. (2025) conducted an observational in Atrial high-rate episodes (AHRE) (n=160). Atrial high-rate episodes (AHRE) vs. No arrhythmias detected during pacemaker interrogation was evaluated on Mean Neuron-Specific Enolase (NSE) levels (ng/mL) (p=<0.001). Atrial high-rate episodes were associated with higher neuron-specific enolase levels compared to controls, and episode duration independently predicted NSE elevation.
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