Abstract

Objective: The most common reason of arrhythmia onset nowadays is hypertensive desease. The aim of the study is to compare the subpopulations of lymphocytes (LCTs) and monocytes (MCTs) in blood of patients (pts) with paroxysmal and persistent forms of AF or atrial flutter (AFL) associated with arterial hypertension. Design and method: The study involved 103 patients with atrial fibrillation and flutter that occurred on the backdround of hypertension. Depending on the form of arrhythmia, patients were divided into three main groups: group I – with paroxysmal form of atrial fibrillation, group II – with a persistent form of atrial fibrillation, group III – with a persistent form of atrial flutter. The control groups included patients with hypertension, but without these arrhythmias and healthy individuals who entered groups IV and V, respectively. The lymphocytes and monocytes subpopulation in peripheral blood was assessed by flow cytometry. Results: Analyzing the lymphocyte subpopulations in peripheral blood of patients with atrial fibrillation and flutter (groups I, II and III), it was found that the number of cells with cytotoxic activity (NK and NKT) in both absolute count and percentage values was significantly higher than in healthy individuals. A statistically significant decrease of T-regulatory cells number was found in patients with arrhythmias compared to control groups (p < 0.05). In patients with AF and AFL associated with hypertension, compared to patients with hypertension without these rhythm disturbances or healthy individuals, there is an increased number of classical and intermediate monocytes subpopulations. Conclusions: 1. In patients with atrial fibrillation or atrial flutter associated with hypertension, compared to patients with hypertension without these rhythm disturbances or healthy people, there is an increased number of classical and intermediate monocytes fraction and a decreased content of T-regulatory cells in peripheral blood, an increased number of cells with cytotoxic activity (NK and NKT) compared to healthy individuals. These changes can be one of the factors for the activation of systemic and local inflammatory processes that can lead to fibrosis in the myocardium and the associated electrical and structural remodeling typical for AF and AFL.

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