Arrhythmia
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26/Heart rhythm variability in patients with atrial fibrillation and atrial flutter depending on immune status, systemic inflammation and renin-angiotensin-aldosterone system activity

Published Online: October 9th 2012 European Journal of Arrhythmia & Electrophysiology. 2021;7(Suppl. 1):abstr26
Authors: OY Ilchyshyna (Presenting Author) – NSC M. D. Strazhesko Institute of cardiology NAMS of Ukraine, Kyiv; OS Sychov – NSC M. D. Strazhesko Institute of cardiology NAMS of Ukraine, Kyiv; TV Talaieva – NSC M. D. Strazhesko Institute of cardiology NAMS of Ukraine, Kyiv
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Aims: Arterial hypertension (AH) is one of the most common causes of atrial fibrillation (AF) and atrial flutter (AFl), but still the concrete reason for their onset is not known. Indication and comparison of systemic inflammation and renin-angiotensin-aldosterone system activity and heart rhythm variability differences in these patients have become the background of our study.

Methods and results: The study involved 103 patients with hypertension and arrhythmias, who were divided into three main groups: Group 1 (n=35) – with paroxysmal AF; Group 2 (n=38) – with persistent form of AF; Group 3 (n=30) – with persistent form of AFl. For comparison, 2 control groups were formed: Group 4 (n=23) – patients with hypertension, but without a history of arrhythmias; Group 5 (n=21) – almost healthy people. The immune status of these patients was assessed by determining the level of monocytes (Mc), lymphocyte subpopulations and T-regulatory (T-reg) cells in the peripheral blood using flow cytometry. These 103 patients with arrhythmias were examined and divided into two groups according to highly specific C-reactive protein (CRP) and angiotensin converting enzyme (ACE) level in serum. It was noted that the number of classical CD14++CD16- and intermediate CD14++CD16+ Mc was significantly higher in patients with persistent AF and AFl compared with both patients without arrhythmias and healthy people (p<0.005). The amount of non-classical CD14+CD16++ Mc was significantly lower in the second group both quantitatively and in percentage (p<0.005). The count of T cells with natural killer (TNK) activity was higher in all groups compared with the normal value, so statistical significance was observed only in comparison with the fifth group. The highest quantity of T-reg cells was found in healthy people compared with the other groups and a strong mathematical significance was obtained in all cases (p<0.005), both comparing the values in percentage and in μL. Assessing the activity of ACE in the vast majority of patients with arrhythmias, its increased level was observed in 82% (85/103) vs 27% (12/44) among patients in the control groups (p<0.05). Overall, 83% of patients (86/103) with AF and AFl had a significantly increased CRP rate vs 9% of patients (4/44) without arrhythmias. All patients received Holter ECG monitoring when they had sinus rhythm, and it was noted that in cases of increased CRP and ACE levels, SDNN (ms) was higher: 115 (108.4–124.2) vs 101 (97.1–108.8) (p=0.035). Also, mean heart rate was significantly higher: 82 (78.5–87.1) vs 73.1 (71.7–78.4) (p=0.048).

Conclusions: Compared with healthy people or patients with hypertension without arrhythmias, hypertensive patients with AF and AFl have increased activity of proinflammatory subpopulations of monocytes, higher levels of T-cells with natural killer activity and reduced T-reg cells, whose main function is to control the immune response. According to Holter ECG in patients with AF/AFl with elevated compared with normal levels of highly specific CRP and ACE, there was a statistically significant difference between mean heart rate and SDNN, indicating sympatho-adrenal system and systemic inflammation activation in these patients. 

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