Obesity Results in Progressive Atrial Electrical and Structural Remodeling: Implications for Atrial Fibrillation

Abstract

Background: Obesity has been associated with the development of atrial fibrillation (AF); however the mechanisms by which it results in a pro-arrhythmic substrate remain unknown.Methods: Thirty sheep were studied at baseline, four months and eight months, following an ad libitum calorie dense diet. Ten were sampled at each time point for cardiac MRI, invasive haemodynamic evaluation (left atrial and arterial pressure) and detailed electrophysiologic study. An additional six maintenance-fed control sheep were sampled at four and eight months to control for time/age-related effects. A custom made 128-electrode plaque applied to the right and left atria was used to quantify; bi-atrial effective refractory periods (ERP); conduction velocity (CV); conduction heterogeneity index (CHI) at four pacing cycle lengths (PCL) from four sites; and AF inducibility. Quantitative myocardial histology was performed for myocardial fibrosis, inflammation and lipidosis.Results: Weight increased from 58 ± 7 kg to 77 ± 5 kg to 105 ± 13 kg (P < 0.001). With increasing weight there was: progressive decrement in atrial CV (P = 0.01), increasing atrial volumes (P = 0.01), atrial fibrosis (P = 0.007) and lipidosis (P = 0.049). There was regional variation in conduction heterogeneity (P = 0.04) with increasing weight. Electrophysiologic disturbances persisted after adjusting for haemodynamic variables. No changes were observed in the control cohort (ERP; P = 0.5, CV; P = 0.8, CHI; P = 0.9). With increasing adiposity, AF event number (P = 0.001) and duration (P < 0.001) significantly increased. No significant change was observed in ERP with increasing adiposity (P = 0.198).Conclusion: Obesity induces early and progressive atrial structural and electrophysiological remodelling. These electrophysiological abnormalities were independent of adverse haemodynamic changes and occurred with a step-wise increase in AF burden.

Effectiveness and safety of simultaneous hybrid thoracoscopic endocardial catheter ablation of atrial fibrillation in obese and non-obese patients

“…J Thorac Dis 2017;9(9):3087-3096 jtd.amegroups.com with increasing atrial volume, fibrosis and lipidosis (31). Weight gain can also induce structural and histological changes in cardiomyocytes, which may predispose patients to chaotic rhythms such as AF (31,32).…”

“…Weight gain can also induce structural and histological changes in cardiomyocytes, which may predispose patients to chaotic rhythms such as AF (31,32). Furthermore, obesity may also be associated with pericardial fat, causing increased inflammation and local atrial infiltration, leading to increased risk of AF (30).…”

The Clinical Profile and Pathophysiology of Atrial Fibrillation

“…206 Autonomic activity is required to elicit ectopic firing in the setting of chronic atrial coronary artery obstruction. 206 Obesity causes atrial structural remodeling, 207 as well as left ventricular diastolic dysfunction that induces acute left atrial dilation and stretch on volume loading. 208 Acute OSA is associated with strongly negative intrathoracic pressures that increase venous return and thereby induce AF-promoting left atrial volume loading.…”

Diffuse Ventricular Fibrosis Measured by T 1 Mapping on Cardiac MRI Predicts Success of Catheter Ablation for Atrial Fibrillation

“…[12][13][14] Alternatively, there are a range of clinical conditions such as hypertension, heart failure, obesity, and ageing which are associated with AF and a propensity to tissue fibrosis. [15][16][17] Cardiac MRI with gadolinium contrast provides a noninvasive assessment of myocardial fibrosis with LGE representative of focal scar and postcontrast T 1 mapping sequences quantifying diffuse fibrosis. Postcontrast ventricular T 1 time provides a sensitive qualitative index of tissue as a measure of bimodal clinical variables.…”