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Historically, regular exercise contributed to reduce the arrhythmic burden and improve cardiovascular outcomes in the general population. However, a heightened risk of atrial fibrillation (AF) seems to occur mainly amongst endurance athletes. The exact mechanisms are not fully elucidated, but dynamic interactions between electro-anatomical changes induced by exercise, the autonomic system, variable triggers, along individual genetic predisposition are the main contributors to AF development in athletes. The type and training load of sports are also crucial in determining the arrhythmogenic milieu predisposing to AF insurgence and perpetuation. Moreover, a sex difference seems to influence an increased risk of AF only in men undergoing strenuous exercise, whereas women appear protected even during more vigorous training. In the absence of solid evidence, the advent of modern technologies could help to monitor and deep investigate the peculiar aspects of AF in these athletes. This review aims to describe the pathophysiology, diagnosis, and management of AF in athletes, shedding light on possible future strategies to face AF in this population.

Purpose of Review: Omega-3 fatty acid (O3FA) supplementation has shown conflicting evidence regarding its benefit in cardiovascular events. We performed a pairwise and network meta-analysis to elucidate the benefit of different doses of O3FA supplementation in cardiovascular prevention., Recent Findings: Fourteen studies were identified providing data on 125,763 patients. A prespecified cut-off value of < 1 g per day was set for low-dose (LD) O3FA and > 1 g per day for high-dose (HD) O3FA. The efficacy outcomes of interest were total death, cardiac death, sudden cardiac death, myocardial infarction, stroke, coronary revascularization, unstable angina, and major vascular events. Safety outcomes of interest were bleeding, gastrointestinal disturbances, and atrial fibrillation events. HD treatment was associated with a lower risk of cardiac death (IRR 0.79, 95% CI [0.65-0.96], p = 0.03 versus control), myocardial infarction (0.71 [0.62-0.82], p < 0.0001 versus control and 0.79 [0.67-0.92], p = 0.003 versus LD), coronary revascularization (0.74 [0.66-0.83], p < 0.0001 versus control and 0.74 [0.66-0.84], p < 0.0001 versus LD), unstable angina (0.73 [0.62-0.86], p = 0.0001 versus control and 0.74 [0.62-0.89], p = 0.002 versus LD), and major vascular events (0.78 [0.71-0.85], p < 0.0001 versus control and 0.79 [0.72-0.88], p < 0.0001 versus LD). HD treatment was associated with increased risk for bleeding events (1.49 [1.2-1.84], p = 0.0002 versus control and 1.63 [1.16-2.3], p = 0.005 versus LD) and increased atrial fibrillation events compared to control (1.35 [1.1-1.66], p = 0.004). HD O3FA treatment was associated with lower cardiovascular events compared to LD and to control, but increased risk for bleeding and atrial fibrillation events.

Recent findings in atrial fibrillation (AF) patients receiving oral anticoagulation showed that diabetes without insulin therapy has a thromboembolic risk comparable to nondiabetic patients, whereas only diabetic patients on insulin have a heightened thromboembolic risk. We explored possible pathophysiological correlates of such finding on 90 AF patients on oral anticoagulation, divided according to diabetes status (n = 30 without diabetes; n = 29 with diabetes on oral antidiabetic drugs; n = 31 with insulin-requiring diabetes). We assessed von Willebrand Factor (VWF) concentration (VWF:Ag) and activity (VWF R:Co) as measures of endothelial dysfunction; and thrombin-activatable fibrinolysis inhibitor (TAFI) and prothrombin fragment 1 + 2 (F1+2) levels as markers of fibrinolytic activity and thrombin generation. Values of VWF:Ag, VWF:RCo, and TAFI were similar in the 3 groups. Patients with diabetes requiring insulin had significantly higher levels of F1+2 (median 23.1 pg/ml [interquartile range 17.6; 33.5]) than those without diabetes (16.3 pg/ml [11.5; 22.5], p = 0.036) and diabetic patients on oral antidiabetic drugs (20.6 pg/ml [13.3; 29], p = 0.046). Thus, in AF patients receiving oral anticoagulation, those with diabetes, regardless of the diabetes type (with or without insulin therapy), and those without diabetes have comparable indices of the explored parameters of endothelial dysfunction and fibrinolytic activity. Despite anticoagulant therapy, thrombin generation is selectively higher in diabetic patients' on insulin than in those without diabetes or with diabetes on oral antidiabetic drugs, with no differences between these latter 2 conditions. Thrombin generation might thus be a predominant contributor to the excess of thromboembolic risk in AF patients on insulin-requiring diabetes., (Copyright © 2019 Elsevier Inc. All rights reserved.)

Abstract The autonomic nervous system (ANS) is known to play an important role in the genesis and maintenance of atrial fibrillation (AF). Biomolecular and genetic mechanisms, anatomical knowledges with recent diagnostic techniques acquisitions, both invasive and non‐invasive, have enabled greater therapeutic goals in patients affected by AF related to ANS imbalance. Catheter ablation of ganglionated plexi (GP) in the left and right atrium has been proposed in varied clinical conditions. Moreover interesting results arise from renal sympathetic denervation and vagal nerve stimulation. Despite all this, in the scenario of ANS modulation translational strategies we necessary must consider the treatment or correction of dynamic factors such as obesity, obstructive sleep apnea, lifestyle, food, and stress. Finally, new antiarrhythmic drugs, gene therapy and “ablatogenomic” could be represent exciting future therapeutic perspectives.

Antithrombotic treatment of frail patients with AF presents various challenges. The fear of bleeding often leds to a large underuse of anticoagulant agents in these patients, although more recent data indicate that oral anticoagulation (especially with the newer, direct anticoagulants) is increasingly used. While there is a need for more real world data, available evidence suggests that non-vitamin K antagonist oral anticoagulants (NOACs) are an effective alternative to warfarin in frail patients with AF for preventing thromboembolic events, with a better safety profile. Logical considerations and evidence-base data related to the reduced bleeding risk (also including major bleeding and intracranial bleeding) of NOACs make these drugs the anticoagulant agents of choice in frail patients; however, in this setting an individualised approach should be taken, taking into consideration the risk of thromboembolic and bleeding events, other comorbidities and patient-related factors, rather than a generalised "one drug fits all" approach. [ABSTRACT FROM AUTHOR]