Investigation of silent neurological ischemia in patients with pacemaker implanted with atrial high speed episodes (AHRE)

Objective: Atrial high rate episodes (AHRE) are tachyarrhythmia attacks that can only be detected by implantable cardiac devices and have recently been included in the guidelines. It is generally asymptomatic and different definitions have been made in many studies regarding its definition and duration. In the European Society of Cardiology (ESC) 2020 AF guideline, the AHRE device-programmed rate criterion is defined as ≥ 175 bpm and the duration criterion is ≥ 5 minutes. Although AHRE has been shown to increase the risk of ischemic stroke, embolism and clinical AF, it has not yet been clearly demonstrated. In our study, we aimed to show the relationship between NSE (neuron specific enolase) levels, which are indicators of silent neurological ischemia, and AHRE. Patient and Method: Our study is a prospective case-control study. Our study included 80 AHRE patients who applied to the Ondokuz Mayıs University Faculty of Medicine Cardiology Arrhythmia Polyclinic between January 2021 and June 2022, and who had a permanent pacemaker implanted at any time before and met the inclusion and exclusion criteria determined by us. For the control group, patients who applied to the Ondokuz Mayıs University Faculty of Medicine Cardiology Arrhythmia Polyclinic, who had previously had a permanent pacemaker implanted at any time, and who met the inclusion and exclusion criteria determined by us and did not have any arrhythmia, including AHRE, were included. NSE (neuron specific enolase) levels of patients with AHRE detected in the last 6 months and those who had an AHRE attack within the last 72 hours were examined. The relationship between increasing AHRE duration and NSE level was examined. Results: Individuals included in the study were divided into subgroups according to AHRE duration. There were group 1 (non-AHRE) 80 (50,0%), Group 2 (<5 min) 24 (15,0%), Group 3 (≥5 min - <1h) 33 (20,6%), 19 (11,9%) Group 4 (≥1 h - <24 h) and 4 (2,5%) patients in Group 5 (≥24 h). When patients with AHRE were compared to the control group without AHRE, mean age (67,49 ± 16,6 vs. 65,00 ± 13,1; p=0,046), sPAP (27,16 ± 10,51 vs. 23,74 ± 6,86; p=0,049), transmitral E/A ratio (1,38 ± 0,23 vs. 1,12 ± 0,35; p=<0,001), ap-vp percentage (27, 59 ± 26,64 vs 15,03 ± 17,26; p=<0,001) was statistically significant. The relationship between NSE levels of patients with AHRE and between themselves and the control group was examined. There was a statistically significant difference in NSE median values between groups (p=<0,001). In further analysis (Mann Whitney U test with Bonferronni correction), it was determined that only the median values of group 1 and group 2 and group 4 and group 5 were not significantly different, but the median values of all other groups were significantly different from each other (p=<0,001). In the correlational analysis, it was determined that there was a statistically significant positive relationship between AHRE duration and NSE values (r=0,842; p=<0,001). A statistically significant correlation was also observed between AHRE duration and age (r=0,235; p=0,036), CHA2DS2-VASc score (r=0,226; p=0,044) and LA diameter (r=0,300; p=0,007). NSE levels were positively correlated with AHRE duration (r=0,842; p=<0,001) and LA diameter (r=0,242; p=0,030). Conclusion: The results of our study were consistent with other literature studies. NSE can be used as an effective biomarker to indicate silent neurological ischemia in patients with AHRE. AHRE duration was longer in patients who were older, had higher CHA2DS2-VASc scores, and had increased LA diameter. This may play a role in explaining the underlying pathophysiological changes in AHRE before AF develops. Since NSE levels are related to LA diameter as well as AHRE duration, it can be thought that increasing LA diameter contributes to thrombus development.