Recruitment of Immune Cells Across Atrial Endocardium in Human Atrial Fibrillation

Yamashita, Takeshi; Sekiguchi, Akiko; Iwasaki, Yu‐ki; Date, Taro; Sagara, Koichi; Tanabe, Hiroaki; Suma, Hisayoshi; Sawada, Hitoshi; Aizawa, Tadanori

doi:10.1253/circj.cj-09-0644

Cited by 171 publications

(139 citation statements)

References 38 publications

Supporting

Mentioning

129

Contrasting

Order By: Relevance

“…These inflammatory cytokines play a pivotal role in the pathogenesis of AF. 24,25 Finally, there is evidence to say that chronic GERD may induce an autoimmune response that contributes to AF. Autoantibodies against myosin heavy chain have been detected in the sera of patients with lone AF.…”

Section: Mechanism Of Af With Acid Refluxmentioning

confidence: 99%

Atrial Fibrillation and Acid Reflux Disease

Velagapudi

Turagam

Leal

et al. 2012

Clinical Cardiology

View full text Add to dashboard Cite

To date, the precise mechanism of atrial fibrillation (AF) as a possible cause of reflux disease remains uncertain, although some possibilities can be postulated. Inflammation and vagal stimulation may have a key role linking these 2 common diseases. There is some evidence in the form of case reports and limited observational studies reporting that reflux disease, and more specifically esophagitis, can cause paroxysmal AF, and various mechanisms have been proposed. Some studies have demonstrated that acid suppressive therapy by proton pump inhibitors (PPIs) may help ameliorate symptoms associated with AF and also facilitate conversion to normal sinus rhythm in a subset of patients. Further prospective studies are needed to determine if a true causal mechanism exists between the two and assess whether the mechanism is dependent on a specific subtype of AF. In addition, the response of AF‐related symptoms to PPI therapy and the potential for PPI therapy to reduce the development of AF merits further investigation. Clin. Cardiol. 2011 DOI: 10.1002/clc.21969The authors have no funding, financial relationships, or conflicts of interest to disclose.

show abstract

Section: Mechanism Of Af With Acid Refluxmentioning

confidence: 99%

Atrial Fibrillation and Acid Reflux Disease

Velagapudi

Turagam

Leal

et al. 2012

Clinical Cardiology

View full text Add to dashboard Cite

show abstract

“…One possible mechanism is that paracrine release of inflammatory mediators from peri-atrial EAT could traverse the atrial wall by diffusion from "outside-to-inside" or via small channels to interact with atrial cells. On the other hand, Yamashita et al 10 showed that the distribution of immune cells was heterogeneous and atrial endomyocardium and subendomyocardium were more subject to infiltration by immune cells than the midmyocardium in AF patients. They suggested recruitment of immune cells across the atrial endocardium as a possible mechanism for inflammation in AF.…”

Section: Article P 2748mentioning

confidence: 99%

Role of Epicardial Adipose Tissue in Atrial Fibrillation

Soeki

Sata

2012

Circ J

View full text Add to dashboard Cite

“…Relevant to the present study is the fact that atrial fibrillation has been shown to be associated with significant inflammation (e.g. macrophage infiltration and pro‐inflammatory cytokine up‐regulation) and atrial fibrosis 14, 15. Cardiac macrophages are increasingly recognized as key regulators of inflammation, tissue injury, and fibrosis in small animal models.…”

Section: Discussionmentioning

confidence: 70%

Recovery free of heart failure after acute coronary syndrome and coronary revascularization

et al. 2017

View full text Add to dashboard Cite

AimsPrevious studies have examined risk factors for the development of heart failure (HF) subsequent to acute coronary syndrome (ACS). Our study seeks to clarify the clinical variables that best characterize patients who remain free from HF after coronary artery bypass grafting (CABG) surgery for ACS to determine novel biological factors favouring freedom from HF in prospective translational studies.Methods and resultsNova Scotia residents (1995–2012) undergoing CABG within 3 weeks of ACS were included. The primary outcome was freedom from readmission to hospital due to HF. Descriptive statistics were generated, and a Cox proportional hazards model assessed outcome with adjustment for clinical characteristics. Of 11 936 Nova Scotians who underwent isolated CABG, 3264 (27%) had a recent ACS and were included. Deaths occurred in 210 (6%) of subjects prior to discharge. A total of 3054 patients were included in the long‐term analysis. During follow‐up, HF necessitating readmission occurred in 688 (21%) subjects with a hazard ratio of 12% at 2 years. The adjusted Cox model demonstrated significantly better freedom from HF for younger, male subjects without metabolic syndrome and no history of chronic obstructive pulmonary disease, renal insufficiency, atrial fibrillation, or HF.ConclusionsOur findings have outlined important clinical variables that predict freedom from HF. Furthermore, we have shown that 12% of patients undergoing CABG after ACS develop HF (2 years). Our findings support our next phase in which we plan to prospectively collect blood and tissue specimens from ACS patients undergoing CABG in order to determine novel biological mechanism(s) that favour resolution of post‐ACS inflammation.

show abstract

Recruitment of Immune Cells Across Atrial Endocardium in Human Atrial Fibrillation

Cited by 171 publications

References 38 publications

Atrial Fibrillation and Acid Reflux Disease

Atrial Fibrillation and Acid Reflux Disease

Role of Epicardial Adipose Tissue in Atrial Fibrillation

Recovery free of heart failure after acute coronary syndrome and coronary revascularization

Contact Info

Product

Resources

About