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Cardiac arrhythmias occur frequently in patients with acute stroke, with atrial fibrillation (AF) being the most common. Newly detected AF may lead to increased risk of ischemic stroke, which in turn generates stroke recurrence and adverse outcomes. Currently, most studies are focusing on the role of AF in ischemic stroke and attributing cryptogenic ischemic stroke to previously undetected AF. However, in these studies, subjects used to have neither symptoms of palpitation nor evidence of AF. A better understanding of this association will contribute to the management and therapy for patients after clinical decisions regarding stroke patients. Currently, the definition of newly detected AF has not come to an agreement, and the pathophysiology remains incompletely understood, possibly involving complex alterations in both the autonomic network and humoral regulation. Therefore, this review aims to introduce the definition and epidemiology of newly detected AF after stroke with updated information and elucidate the potential pathophysi-ology, such as autonomic imbalance, catecholamine surge, poststroke systematic inflammation, and microvesicles and microRNAs. [ABSTRACT FROM AUTHOR]

New-onset atrial fibrillation (AF) is frequently observed following acute stroke. The aim of this study was to investigate the effects of the brain-stellate ganglion-atrium network on AF vulnerability in a canine model with acute middle cerebral artery occlusion (MCAO). Twenty-six dogs were randomly divided into the sham-operated group (n = 6), acute stroke (AS) group (n = 7), stellate ganglion ablation (SGA) group (n = 6) and clodronate liposome (CL) group (n = 7). In the sham-operated group, dogs received craniotomy without MCAO. Cerebral ischemic model was established in AS dogs by right MCAO. Right MCAO along with SGA and CL injection into the atrium was performed in SGA and CL dogs, respectively. After 3 days, atrial electrophysiology, neural activity, and the phenotype and function of macrophages in the atrium were studied in all the dogs. Higher AF inducibility (24.4 ± 4.4% versus 4.4 ± 2.2%, P < 0.05) and AF duration (15.7 ± 3.8 s versus 2.6 ± 1.1 s, P < 0.05) were observed in the AS group compared with the sham-operated group, and were associated with increased left stellate ganglion activity, higher macrophage infiltration and higher levels of inflammatory cytokines in the atrium. SGA or CL injection sharply suppressed AF inducibility (5.5 ± 2.7% versus 24.4 ± 4.4%; 5.3 ± 3.2% versus 24.4 ± 4.4%, both P < 0.05) and AF duration (2.9 ± 1.2 s versus 15.7 ± 3.8 s; 3.6 ± 1.0 s versus 15.7 ± 3.8 s, both P < 0.05) in canines with acute stroke. A brain-stellate ganglion-atrium network may increase AF vulnerability through macrophage activation after acute stroke. [ABSTRACT FROM AUTHOR]

Purpose. The aim of this study was to investigate the role of the medium-conductance calcium-activated potassium channel (KCNN4, KCa3.1) in the secretion of proinflammatory exosomes by atrial myocytes. Methods. Eighteen beagles were randomly divided into the sham group (n = 6), pacing group (n = 6), and pacing+TRAM-34 group (n = 6). Electrophysiological data, such as the effective refractory period, atrial fibrillation (AF) induction, and AF duration, were collected by programmed stimulation. Atrial tissues were subjected to hematoxylin and eosin, Masson's trichrome, and immunofluorescence staining. The expression of KCa3.1 and Rab27a was assessed by immunohistochemistry and western blotting. The downstream signaling pathways involved in KCa3.1 were examined by rapid pacing or overexpressing KCNN4 in HL-1 cells. Results. Atrial rapid pacing significantly induced electrical remodeling, inflammation, fibrosis, and exosome secretion in the canine atrium, while TRAM-34 (KCa3.1 blocker) inhibited these changes. Compared with those in control HL-1 cells, the levels of exosome markers and inflammatory factors were increased in pacing HL-1 cells. Furthermore, the levels of CD68 and iNOS in macrophages incubated with exosomes derived from HL-1 cells were higher in the pacing-exo group than in the control group. More importantly, KCa3.1 regulated exosome secretion through the AKT/Rab27a signaling pathway. Similarly, inhibiting the downstream signaling pathway of KCa3.1 significantly inhibited exosome secretion. Conclusions. KCa3.1 promotes proinflammatory exosome secretion through the AKT/Rab27a signaling pathway. Inhibiting the KCa3.1/AKT/Rab27a signaling pathway reduces myocardial tissue structural remodeling in AF. [ABSTRACT FROM AUTHOR]