Abstract

Extracellular vesicles (EVs) are defined as a heterogenic group of lipid bilayer vesicular structures with a size in the range of 30–4000 nm that are released by all types of cultured cells. EVs derived from platelets, mononuclears, endothelial cells, and adipose tissue cells significantly increase in several cardiovascular diseases, including in atrial fibrillation (AF). EVs are engaged in cell-to-cell cooperation, endothelium integrity, inflammation, and immune response and are a cargo for several active molecules, such as regulatory peptides, receptors, growth factors, hormones, and lipids. Being transductors of the intercellular communication, EVs regulate angiogenesis, neovascularization, coagulation, and maintain tissue reparation. There is a large amount of evidence regarding the fact that AF is associated with elevated levels of EVs derived from platelets and mononuclears and a decreased number of EVs produced by endothelial cells. Moreover, some invasive procedures that are generally performed for the treatment of AF, i.e., pulmonary vein isolation, were found to be triggers for elevated levels of platelet and mononuclear EVs and, in turn, mediated the transient activation of the coagulation cascade. The review depicts the role of EVs in thrombogenicity in connection with a risk of thromboembolic complications, including ischemic stroke and systemic thromboembolism, in patients with various forms of AF.

Highlights

  • Atrial fibrillation (AF) is the most common form of cardiac arrhythmia amongst older people and patients with cardiovascular (CV) diseases (CVD) and continues to demonstrate steady growth in the general population [1]

  • Electroanatomic and adverse cardiac remodeling resulting in natural CVD evolution and AF persistence is considered to be a substrate for the development of cardiac dysfunction, heart failure (HF) occurrence, and thromboembolic complications, which sufficiently reduce life span duration and quality of life in patients affected by this condition [4]

  • We focus on original articles addressing Extracellular vesicles (EVs) and AF

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Summary

Introduction

Atrial fibrillation (AF) is the most common form of cardiac arrhythmia amongst older people and patients with cardiovascular (CV) diseases (CVD) and continues to demonstrate steady growth in the general population [1]. At least 65% of senior citizens in the European Union will have AF in 2060, and paroxysmal, persistent, and permanent forms of AF are projected to be diagnosed in approximately 5,989,000, approximately 2,833,000, and approximately 5,579,000 of older people, respectively [3]. Despite the numerous benefits of CVD prevention therapy and its wide implementation in routine practice, there remains an unacceptably high risk of potentially devastating complications associated with catheter pulmonary vein isolation (PVI), such as stroke/transient ischemic attack and systemic thromboembolism during persistent AF or the occurrence of its permanent form [9]. The prevention of thromboembolic complications remains the focus of pragmatic strategy development for AF therapy [13,14]

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