Background: Atrial fibrillation (AF) is the commonest abnormal heart rhythm with significant related morbidity and mortality. Several pathophysiologic mechanisms have been advocated to explain the onset of AF. There has been increasing evidence that abnormalities of the autonomic nervous system (ANS) that includes sympathetic, parasympathetic and intrinsic neural network are involved in the pathogenesis of AF. This review will consider the anatomical and pathophysiological concepts of the cardiac neuronal network and discuss how it can be investigated.Design: Relevant articles for this review were selected primarily from Ovid Medline and Embase databases (see appendix). We searched for key terms “atrial fibrillation,” “AF,” “autonomic dysfunction,” “autonomic nervous system,” “heart rate variability” and “HRV” to gather relevant studies. Duplicate papers were excluded.Results: Heart is richly innervated by autonomic nerves. Both sympathetic and parasympathetic systems interact in developing AF along with cardiac ganglionated plexi (GP). Thus autonomic dysfunction is present in AF. There are methods including selective ablation that reduce autonomic innervation and show to reduce the incidence of spontaneous or induced atrial arrhythmias. Heart rate variability (HRV) is a useful tool to assess sympathetic and parasympathetic influences on disease states. HRV can be improved following intervention and is thus a useful application in assessing autonomic dysfunction in patients with AF.Conclusion: ANS plays a crucial role in the development, propagation and complexity of AF. Assessment of the autonomic involvement in the propagation of AF may help in explaining why certain patients with AF do not benefit from cardioversion or ablation.

Atrial fibrillation is the most common heart arrhythmia and is associated with poor outcomes. The adverse effects of atrial fibrillation are mediated through multiple pathways, including endothelial dysfunction, as measured by flow-mediated dilatation. Flow-mediated dilatation has demonstrated endothelial dysfunction in several conditions and is associated with poor outcomes including mortality, yet can be improved with medical therapy. It is thus a useful tool in assessing endothelial function in patients. Endothelial dysfunction is present in patients with atrial fibrillation and is associated with poor outcomes. These patients are generally older and have other co-morbidities such as hypertension, hypercholesterolaemia and diabetes. The precise process by which atrial fibrillation is affiliated with endothelial damage/dysfunction remains elusive. This review explores the endothelial structure, its physiology and how it is affected in patients with atrial fibrillation. It also assesses the utility of flow mediated dilatation as a technique to assess endothelial function in patients with AF.

The study analysed the effectiveness and safety of warfarin use compared with warfarin non-use and non-vitamin K antagonist oral anticoagulants (NOACs) in atrial fibrillation (AF) patients aged ≥65 years. after searching PubMed and the Cochrane Library, 26 studies were included, with 10 comparing warfarin with warfarin non-use and 16 comparing warfarin with NOACs, in older AF patients (≥65 years). warfarin use was superior to no antithrombotic therapy [relative risk (RR) 0.59, 95% confidence interval (CI) 0.51–0.76, I² = 12.3%, n = 8] and aspirin (RR 0.44, 95% CI 0.24–0.64, I² = 0.0%, n = 5) for stroke/thromboembolism (TE) prevention. Warfarin use was associated with a non-significant increase in risk of major bleeding compared with no antithrombotic therapy (RR 1.26, 95% CI 0.99–1.52, I² = 0.0%, n = 7) and aspirin (RR 1.20, 95% CI 0.91–1.50, I² = 0.0%, n = 5). NOACs were superior to warfarin for stroke/TE prevention [hazard ratio (HR) 0.81, 95% CI 0.73–0.89, I² = 56.6%, n = 9], and also were associated with reduced risk of major bleeding compared to warfarin (HR 0.87, 0.77–0.97, I² = 86.1%, n = 9). warfarin use was superior to warfarin non-use, aspirin and no antithrombotic therapy in reducing the risk of stroke/TE in older AF patients, but with a possible increase in major bleeding. NOACs were superior to warfarin for stroke/TE prevention, with reduced risk of major bleeding.

Background and purpose: Given the great clinical heterogeneity of atrial fibrillation (AF) patients, conventional classification only based on disease subtype or arrhythmia patterns may not adequately characterize this population. We aimed to identify different groups of AF patients who shared common clinical phenotypes using cluster analysis and evaluate the association between identified clusters and clinical outcomes. Methods: We performed a hierarchical cluster analysis in AF patients from AMADEUS and BOREALIS trials. The primary outcome was a composite of stroke/thromboembolism (TE), cardiovascular (CV) death, myocardial infarction, and/or all-cause death. Individual components of the primary outcome and major bleeding were also assessed. Results: We included 3980 AF patients treated with the Vitamin-K Antagonist from the AMADEUS and BOREALIS studies. The analysis identified four clusters in which patients varied significantly among clinical characteristics. Cluster 1 was characterized by patients with low rates of CV risk factors and comorbidities; Cluster 2 was characterized by patients with a high burden of CV risk factors; Cluster 3 consisted of patients with a high burden of CV comorbidities; Cluster 4 was characterized by the highest rates of non-CV comorbidities. After a mean follow-up of 365 (standard deviation 187) days, Cluster 4 had the highest cumulative risk of outcomes. Compared with Cluster 1, Cluster 4 was independently associated with an increased risk for the composite outcome (hazard ratio (HR) 2.43, 95% confidence interval (CI) 1.70–3.46), all-cause death (HR 2.35, 95% CI 1.58–3.49) and major bleeding (HR 2.18, 95% CI 1.19–3.96). Conclusions: Cluster analysis identified four different clinically relevant phenotypes of AF patients that had unique clinical characteristics and different outcomes. Cluster analysis highlights the high degree of heterogeneity in patients with AF, suggesting the need for a phenotype-driven approach to comorbidities, which could provide a more holistic approach to management aimed to improve patients’ outcomes.