Atrial fibrillation (AF) is characterised by an increased risk of pathological thrombus formation due to a disruption of physiological haemostatic mechanisms that are better understood by reference to Virchow’s triad of ‘abnormal blood constituents’, ‘vessel wall abnormalities’ and ‘abnormal blood flow’. First, there is increased activation of the coagulation cascade, platelet reactivity and impaired fibrinolysis as a result of AF per se, and these processes are amplified with pre-existing comorbidities. Several prothrombotic biomarkers including platelet factor 4, von Willebrand factor, fibrinogen, β-thromboglobulin and D-dimer have been implicated in this process. Second, structural changes such as atrial fibrosis and endothelial dysfunction are linked to the development of AF which promote further atrial remodelling, thereby providing a suitable platform for clot formation and subsequent embolisation. Third, these factors are compounded by the presence of reduced blood flow secondary to dilatation of cardiac chambers and loss of atrial systole which have been confirmed using various imaging techniques. Overall, an improved understanding of the various factors involved in thrombus formation will allow better clinical risk stratification and targeted therapies in AF.

The possibilities and implementation of wearable cardiac monitoring beyond atrial fibrillation are increasing continuously. This review focuses on the real-world use and evolution of these devices for other arrhythmias, cardiovascular diseases and some of their risk factors beyond atrial fibrillation. The management of nonatrial fibrillation arrhythmias represents a broad field of wearable technologies in cardiology using Holter, event recorder, electrocardiogram (ECG) patches, wristbands and textiles. Implementation in other patient cohorts, such as ST-elevation myocardial infarction (STEMI), heart failure or sleep apnea, is feasible and expanding. In addition to appropriate accuracy, clinical studies must address the validation of clinical pathways including the appropriate device and clinical decisions resulting from the surrogate assessed.

Atrial fibrillation (AF) and chronic kidney disease (CKD) are closely related conditions with shared risk factors. The growing prevalence of both AF and CKD indicates that more patients will suffer from concurrent conditions. There are various complex interlinking mechanisms with important implications for the management of these patients. Furthermore, there is uncertainty regarding the use of oral anticoagulation (OAC) in AF and CKD that is reflected by a lack of consensus between international guidelines. Therefore, the importance of understanding the implications of co-existing AF and CKD should not be underestimated. In this review, we discuss the pathophysiology and association between AF and CKD, including the underlying mechanisms, risk of thrombo-embolic and bleeding complications, influence on stroke management, and evidence surrounding the use of OAC for stroke prevention.

The prothrombotic state in atrial fibrillation (AF) occurs as a result of multifaceted interactions, known as Virchow’s triad of hypercoagulability, structural abnormalities, and blood stasis. More recently, there is emerging evidence that lipoproteins are implicated in this process, beyond their traditional role in atherosclerosis. In this review, we provide an overview of the various lipoproteins and explore the association between lipoproteins and AF, the effects of lipoproteins on haemostasis, and the potential contribution of lipoproteins to thrombogenesis in AF. There are several types of lipoproteins based on size, lipid composition, and apolipoprotein category, namely: chylomicrons, very low-density lipoprotein, low-density lipoprotein (LDL), intermediate-density lipoprotein, and high-density lipoprotein. Each of these lipoproteins may contain numerous lipid species and proteins with a variety of different functions. Furthermore, the lipoprotein particles may be oxidized causing an alteration in their structure and content. Of note, there is a paradoxical inverse relationship between total cholesterol and LDL cholesterol (LDL-C) levels, and incident AF. The mechanism by which this occurs may be related to the stabilizing effect of cholesterol on myocardial membranes, along with its role in inflammation. Overall, specific lipoproteins may interact with haemostatic pathways to promote excess platelet activation and thrombin generation, as well as inhibiting fibrinolysis. In this regard, LDL-C has been shown to be an independent risk factor for thromboembolic events in AF. The complex relationship between lipoproteins, thrombosis and AF warrants further research with an aim to improve our knowledge base and contribute to our overall understanding of lipoprotein-mediated thrombosis.

The ‘Atrial fibrillation Better Care’ (ABC) pathway has been proposed to streamline a more holistic or integrated care approach to atrial fibrillation (AF) management. We aimed to analyse the impact of adherence to the ABC pathway on the risk of major adverse outcomes in a contemporary prospective global cohort of patients with AF. Patients enrolled Phase II and III of the GLORIA-AF Registry with complete data on ABC pathway adherence and follow-up were included in this post-hoc analysis between November 2011 and December 2014 for Phase II, and between January 2014 and December 2016 for Phase III. The primary outcome was the composite of all-cause death and major adverse cardiovascular events (MACEs). Multivariable Cox-regression and delay of event (DoE) analyses were used to evaluate the association between adherence to the ABC pathway and the risk of outcomes. We included 24,608 patients in this analysis (mean age: 70.2 (10.3) years, 10,938 (44.4%) females). Adherence to the ABC pathway was associated with a significant risk reduction for the primary outcome, with greatest magnitude observed for full ABC pathway adherence (adjusted Hazard Ratio [aHR] 0.54, 95% Confidence Interval [CI]: 0.44–0.67, p < 0.0001). ABC pathway adherence was also associated with reduced risk of mortality (aHR: 0.89, 95% CI: 0.79–1.00, p = 0.048), thromboembolism (aHR: 0.78, 95% CI: 0.65–0.94, p = 0.0078), and MACE (aHR: 0.82, 95% CI: 0.71–0.95, p = 0.0071). An increasing number of ABC criteria attained was associated with longer event-free survival in the DoE analysis. Adherence to the ABC pathway in patients with AF was associated with a reduced risk of major adverse events, including mortality, thromboembolism and MACE. This underlines the importance of using the ABC pathway in the clinical care of patients with AF. This study was funded by Boehringer Ingelheim.

Objective: To assess the efficacy and safety of catheter ablation (CA) compared with antiarrhythmic drugs (AADs) as first-line treatment for symptomatic paroxysmal atrial fibrillation (AF). Methods: Systematic review and meta-analysis of randomised controlled trials identified using MEDLINE, Cochrane Library and Embase published between 01/01/2000 and 19/03/2021. The primary efficacy endpoint was the first documented recurrence of atrial arrhythmias following the blanking period. The primary safety endpoint was a composite of all serious adverse events (SAEs). Results: From 441 records, 6 studies met the inclusion criteria. 609 patients received CA, while 603 received AAD therapy. 212/609 patients in the CA group had a recurrence of atrial arrhythmias as compared with 318/603 in the AADs group resulting in a 36% relative risk reduction (risk ratio: 0.64, 95% CI 0.51 to 0.80, p<0.01). The risk of all SAEs was not statistically different between CA and AAD (0.87, 0.58 to 1.30, p=0.49); 107/609 SAE in the CA group vs 126/603 in the AAD group. Both recurrence of symptomatic atrial arrhythmias (109/505 vs 186/504) and healthcare utilisation (126/397 vs 185/394) were significantly lower in the CA group (0.53, 0.35 to 0.79 and 0.65, 0.48 to 0.89, respectively). There was a 79% reduction in the crossover rate during follow-up among patients randomised to CA compared with AAD (0.21, 0.13 to 0.32, p<0.01). Conclusions: First-line treatment with CA is superior to AAD therapy in patients with symptomatic paroxysmal AF, as it significantly reduces the recurrence of any atrial arrhythmias and symptomatic atrial arrhythmias, and healthcare resource utilisation with comparable safety profile.