Atrial inflammation in different atrial fibrillation subtypes and its relation with clinical risk factors

Wu, Linghe; Emmens, Reindert W.; Wezenbeek, Jessie van; Stooker, Wim; Allaart, C P; Vonk, Alexander B.A.; Rossum, Albert C. van; Niessen, Hans W.M.; Krijnen, Paul A.J.

doi:10.1007/s00392-020-01619-8

Cited by 19 publications

(22 citation statements)

References 28 publications

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“…Although we did not analyse atrial arrhythmia or contractility in this study, increases in immune cell infiltration and fibrosis have been described repeatedly in the atria of patients with AF 5,6 . Moreover, infiltrated lymphocytes were shown to induce altered atrial contractility, including dysrhythmia and a decrease in tension, in mice with autoimmune myocarditis 16 .…”

Section: Discussionmentioning

confidence: 76%

“…8 Although we did not analyse atrial arrhythmia or contractility in this study, increases in immune cell infiltration and fibrosis have been described repeatedly in the atria of patients with AF. 5,6 Moreover, infiltrated lymphocytes were shown to induce altered atrial contractility, including dysrhythmia and a decrease in tension, in mice with autoimmune myocarditis. 16 Lastly, we have shown recently that CVB3-induced VM led to transient changes in myocardial electrical conduction that were strongly associated with the ventricular cellular inflammatory infiltrate.…”

Section: Discussionmentioning

confidence: 99%

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Transient atrial inflammation in a murine model of Coxsackievirus B3‐induced myocarditis

Fiet

Raaijmakers

et al. 2022

Int J Experimental Path

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Atrial dysfunction is a relatively common complication of acute myocarditis, although its pathophysiology is unclear. There is limited information on myocarditis-associated histological changes in the atria and how they develop in time. The aim of this study therefore was to investigate inflammation, fibrosis and viral genome in the atria in time after mild CVB3-induced viral myocarditis (VM) in mice. C3H mice (n = 68) were infected with 10 5 PFU of Coxsackievirus B3 (CVB3) and were compared with uninfected mice (n = 10). Atrial tissue was obtained at days 4, 7, 10, 21, 35 or 49 post-infection. Cellular infiltration of CD45+ lymphocytes, MAC3+ macrophages, Ly6G+ neutrophils and mast cells was quantified by (immuno)histochemical staining. The CVB3 RNA was determined by in situ hybridization, and fibrosis was evaluated by elastic van Gieson (EvG) staining. In the atria of VM mice, the numbers of lymphocytes on days 4 and 7 (p < .05) and days 10 (p < .01); macrophages on days 7 (p < .01) and 10 (p < .05); neutrophils on days 4 (p < .05); and mast cells on days 4 and 7 (p < .05) increased significantly compared with control mice and decreased thereafter to basal levels. No cardiomyocyte death was observed, and the CVB3 genome was detected in only one infected mouse on Day 4 post-infection. No significant changes in the amount of atrial fibrosis were found between VM and control mice. A temporary increase in inflammation is induced in the atria in the acute phase of CVB3induced mild VM, which may facilitate the development of atrial arrhythmia and contractile dysfunction.

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Section: Discussionmentioning

confidence: 76%

Section: Discussionmentioning

confidence: 99%

Transient atrial inflammation in a murine model of Coxsackievirus B3‐induced myocarditis

Fiet

Raaijmakers

et al. 2022

Int J Experimental Path

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“…A recent study regarding CD45 + and CD3 + cell infiltrates in the atria from patients with AF indicated that inflammatory cell infiltrates were significantly higher in patients with paroxysmal or non‐paroxysmal AF, being greater in the adipose tissue rather than in the myocardium. In addition, inflammation was more related to age and C‐reactive protein (CRP) blood levels than gender or diabetes 106 . The pro‐inflammatory cytokine, IL‐6, and CCRP are correlated with P wave variations in patients with different inflammation‐related diseases.…”

Section: Pathophysiological Mechanisms Of Af Related To Eatmentioning

confidence: 99%

Updates on epicardial adipose tissue mechanisms on atrial fibrillation

et al. 2021

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Summary Obesity is a well‐known risk factor for atrial fibrillation (AF). Local epi‐myocardial or intra‐myocardial adiposity caused by aging, obesity, or cardiovascular disease (CVD) is considered to be a better predictor of the risk of AF than general adiposity. Some of the described mechanisms suggest that epicardial adipose tissue (EAT) participates in structural remodeling owing to its endocrine activity or its infiltration between cardiomyocytes. Epicardial fat also wraps up the ganglionated plexi that reach the myocardium. Although the increment of volume/thickness and activity of EAT might modify autonomic activity, autonomic system dysfunction might also change the endocrine activity of epicardial fat in a feedback response. As a result, new preventive therapeutic strategies are focused on reducing adiposity and weight loss before AF ablation or inhibiting autonomic neurotransmitter secretion on fat pads during open‐heart surgery to reduce the recurrence or postoperative risk of AF. In this manuscript, we review some of the novel findings regarding the pathophysiology and associated risk factors of AF, with special emphasis on the role of EAT in the electrical, structural, and molecular mechanisms of AF initiation and maintenance. In addition, we have included a brief note provided on epicardial fat preclinical models that could be useful for identifying new therapeutic targets.

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“…Viral infection may be another trigger for AF development. Infections with multiple viruses, including influenza virus, hepatitis viruses, human immunodeficiency virus and human herpes viruses, have been shown to be significantly associated with AF development [3][4][5][6][7]. Moreover, the increased expression of Toll-like receptor 2 on monocytes [8] and high enrichment of viral response genes in lymphocytes [9], which have been found in AF patients, suggest an involvement of (chronic) viral infection in AF pathogenesis.…”

Section: Introductionmentioning

confidence: 99%

“…AF progression is associated with structural atrial remodelling, typified by increased atrial fibrosis and fatty infiltration, which disrupts electrical signal conduction, thus facilitating atrial arrhythmia. Inflammation may be a key driver of this process and inflammatory cell infiltration is indeed commonly observed in the atria of AF patients [ 2 , 3 ].…”

Section: Introductionmentioning

confidence: 99%

The presence of cardiotropic viral genomes is not increased in atrial tissue of atrial fibrillation patients

Emmens

Wezenbeek

et al. 2022

Neth Heart J

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Background Infections with potentially cardiotropic viruses are associated with the development of atrial fibrillation (AF). However, whether direct viral infection of the atria is involved in the pathogenesis of AF is unclear. We have therefore analysed the presence of cardiotropic viral genomes in AF patients. Methods Samples of left atrial tissue were obtained from 50 AF patients (paroxysmal, n = 20; long-standing persistent/permanent, n = 30) during cardiac surgery and from autopsied control patients (n = 14). Herein, the presence of PVB19, EBV, CMV, HHV‑6, adenovirus and enterovirus genomes was determined by polymerase chain reaction. The densities of CD45+ and CD3+ cells and fibrosis in the atria were quantified by (immuno)histochemistry. Results Of the tested viruses only the PVB19 genome was detected in the atria of 10% of patients, paroxysmal AF (2 of 20) and long-standing persistent/permanent AF (3 of 30). Conversely, in 50% of controls (7 of 14) PVB19 genome was found. No significant association was found between PVB19 and CD45+ and CD3+ cells, or between the presence of PVB19 and fibrosis, in either control or AF patients. Conclusion The presence of viral genomes is not increased in the atria of AF patients. These results do not support an important role for viral infection of the atria in the pathogenesis of AF.

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Atrial inflammation in different atrial fibrillation subtypes and its relation with clinical risk factors

Cited by 19 publications

References 28 publications

Transient atrial inflammation in a murine model of Coxsackievirus B3‐induced myocarditis

Transient atrial inflammation in a murine model of Coxsackievirus B3‐induced myocarditis

Updates on epicardial adipose tissue mechanisms on atrial fibrillation

The presence of cardiotropic viral genomes is not increased in atrial tissue of atrial fibrillation patients

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