Prevention and Treatment of Atrial Fibrillation via Risk Factor Modification

Abstract

Atrial fibrillation (AF) is the most common clinically significant arrhythmia, and it increases stroke risk. A preventive approach to AF is needed because virtually all treatments such as cardioversion, antiarrhythmic drugs, ablation, and anticoagulation are associated with high cost and carry significant risk. A systematic review was performed to identify effective lifestyle-based strategies for reducing primary and secondary AF. A PubMed search was performed using articles up to March 1, 2021. Search terms included atrial fibrillation, atrial flutter, exercise, diet, metabolic syndrome, type 2 diabetes mellitus, obesity, hypertension, stress, tobacco smoking, alcohol, Mediterranean diet, sodium, and omega-3 fatty acids. Additional articles were identified from the bibliographies of retrieved articles. The control of hypertension, ideally with a renin-angiotensin-aldosterone system inhibitor, is effective for preventing primary AF and recurrence. Obstructive sleep apnea is a common cause of AF, and treating it effectively reduces AF episodes. Alcohol increases the risk of AF in a dose-dependent manner, and abstinence reduces risk of recurrence. Sedentary behavior and chronic high-intensity endurance exercise are both risk factors for AF; however, moderate physical activity is associated with lower risk of AF. Recently, sodium-glucose cotransporter-2 inhibitors and glucagon-like peptide-1 agonists have been associated with reduced risk of AF. Among overweight/obese patients, weight loss of ≥10% is associated with reduced AF risk. Lifestyle changes and risk factor modification are highly effective for preventing AF.

Protecting against sedentary lifestyle, left atrial enlargement and atrial fibrillation

“…inactivity in contemporary obesogenic environments induces cardiac maladaptations, which causes a higher risk of atrial fibrillation (AF). 1 Light-to-moderate physical activity (PA), however, is associated with a lower incidence of AF. [1][2][3] Conversely, the long-term practice of strenuous endurance exercise increases the risk of AF in younger, middle-aged and older populations, particularly in highly competitive athletes, 4 depicting a U-shaped curve (see figure 1).…”

“…1 Light-to-moderate physical activity (PA), however, is associated with a lower incidence of AF. [1][2][3] Conversely, the long-term practice of strenuous endurance exercise increases the risk of AF in younger, middle-aged and older populations, particularly in highly competitive athletes, 4 depicting a U-shaped curve (see figure 1). 1 5 The precise causative mechanism/s of exercise-induced AF is still unknown.…”

“…6 This type of exercising produces structural and functional cardiac adaptations, higher levels of oxidative stress, inflammation and adrenergic activation, ultimately predisposing to atrial fibrosis and AF. 1 Left atrium (LA) dilation or LA enlargement (LAE) is thought to be a potential causative mechanism of exercise-related AF. 7 8 In addition, there are likely differences in the aetiology and clinical presentation of AF between endurance athletes and the general (non-athletic) population, that is, 'classical AF', 9 10 so much so that we described that 'exercise-induced' AF, which we coined as 'Paroxysmal Atrial Fibrillation in Young and Middle-Aged Athletes' syndrome, usually shows a number of features that are common to most affected athletes.…”

“…Physical inactivity in contemporary obesogenic environments induces cardiac maladaptations, which causes a higher risk of atrial fibrillation (AF) 1. Light-to-moderate physical activity (PA), however, is associated with a lower incidence of AF 1–3.…”

“…Conversely, the long-term practice of strenuous endurance exercise increases the risk of AF in younger, middle-aged and older populations, particularly in highly competitive athletes,4 depicting a U-shaped curve (see figure 1). 1 5 The precise causative mechanism/s of exercise-induced AF is still unknown 6. This type of exercising produces structural and functional cardiac adaptations, higher levels of oxidative stress, inflammation and adrenergic activation, ultimately predisposing to atrial fibrosis and AF 1…”