Obesity, Exercise, Obstructive Sleep Apnea, and Modifiable Atherosclerotic Cardiovascular Disease Risk Factors in Atrial Fibrillation

Abstract

Classically, the 3 pillars of atrial fibrillation (AF) management have included anticoagulation for prevention of thromboembolism, rhythm control, and rate control. In both prevention and management of AF, a growing body of evidence supports an increased role for comprehensive cardiac risk factor modification (RFM), herein defined as management of traditional modifiable cardiac risk factors, weight loss, and exercise. In this narrative review, we summarize the evidence demonstrating the importance of each facet of RFM in AF prevention and therapy. Additionally, we review emerging data on the importance of weight loss and cardiovascular exercise in prevention and management of AF.

The associations between atrial fibrillation and parameters of nutritional status assessment in the general hospital population — a cross-sectional analysis of medical documentation

“…Undernutrition, as a component of cardiac cachexia syndrome, may potentially be linked to the risk of AF; however, these relationships are less well documented, mainly due to the exclusion of underweight patients from analysis concerning associations between obesity and CVD [2,6]. The proposed pathophysiological mechanisms linking overnutrition status with risk of AF are: (a) the effect of chronic inflammatory status associated with an imbalance in pro-and anti-inflammatory substances (adipokines, mainly adiponectin, and cytokines) produced by extra-cardiac, cardiac, and perivascular fatty tissue [6][7][8][9][10]; (b) left atrial enlargement [11]; (c) a decreased effect of atrial natriuretic factor, the blood concentration of which is inversely related to body mass index (BMI) [12]; (d) electromechanical dysfunction and adiponectin levels, both of which are positively correlated with BMI [11,13]; (e) haemodynamic changes associated with obesity, and related increased pre-and afterload [13]; (f) autonomic nervous system imbalance and/or sympathetic overactivity in the course of coexisting coronary artery disease or heart failure [11,14,15]; (g) obstructive sleep apnoea [15]; (h) diabetes mellitus, insulin resistance [11]; (i) metabolic syndrome [16,17]; and (j) gastroesophageal reflux disease [18]. Whereas, undernutrition may lead to cardiac arrhythmia via the following: (a) a decrease in fatty and fat-free body mass (sarcopaenia) due to the importance of muscle mass as a regulator of autonomic nervous system and metabolic balances; (b) an increase in pro-inflammatory cytokines, such as interleukin-6 and tumour necrosis factor-alpha, particularly in patients with cardiac cachexia; (c) a decrease in lipoprotein levels and their activity binding pro-inflammatory cytokines and endotoxins; (d) energetic deficit; (e) lipolysis acceleration; and (f) deficiency in electrolytes, antioxidants, vitamins, and proteinaceous components responsible for building the heart [19].…”

Ablation of Atrial Fibrillation

“…Additional data support the importance of modifiable risk factors in AF situations other than ablation. 83 There are other potential pharmacological means of reducing recurrences after AF ablation, including antiarrhythmic drugs, colchicine, and steroids. In a large national claims database, patients on antiarrhythmic drugs had a significantly lower readmission rate at 90 days (11.6% versus 16.2%; P=0.009).…”

Activin Receptor‐Like Kinase 4 Haplodeficiency Mitigates Arrhythmogenic Atrial Remodeling and Vulnerability to Atrial Fibrillation in Cardiac Pathological Hypertrophy

“…Currently, hypertension is estimated to be responsible for 22% of incident AF cases6 and is considered the most widespread and modifiable risk factor for AF 4. The increased afterload may lead to increased risk of AF and worsen outcomes of AF via left ventricular (LV) diastolic dysfunction, left atrial (LA) overload, and remodeling 7. In our study we chose the suitable animal model that could best resemble AF in human hypertensive pathophysiological conditions to uncover potential molecular mechanisms of AF that have not yet been studied in patients with AF.…”