None listed
Conditions
Brief summary
It remains unclear whether obesity itself or its accompanying co-morbidities are causative in the development of the favourable substrate for atrial fibrillation. The exact mechanisms remain the subject of current research. There is preliminary data suggesting a reversal of this substrate following interventional weight loss strategies. Intensive weight reduction strategies may play a role in reversing the adverse electromechanical substrate and thus complementing concurrent therapies, pharmacotherapy or catheter-based. In this observational clinical study, we propose to evaluate the effects of weight loss on the substrate predisposing to AF (clinically collected maps) and arrhythmia burden (during routine follow up).
Interventions
Weight loss - self directed or through weight loss clinic. Diet included any type of caloric restriction, and exercise included any type of exercise in which it was possible to quantify the recommended activity.
According to recent AHA/ACC guidelines for the management of obesity in adults, any weight loss >3% is considered meaningful reduction and compared from weight loss <3% or weight gain group. To determine the dose response effect of weight loss (WL), groups were divided into Group-1 (>1
Weight loss - self directed or through weight loss clinic. Diet included any type of caloric restriction, and exercise included any type of exercise in which it was possible to quantify the recommended activity. According to recent AHA/ACC guidelines for the management of obesity in adults, any weight loss >3% is considered meaningful reduction and compared from weight loss <3% or weight gain group. To determine the dose response effect of weight loss (WL), groups were divided into Group-1 (>10% WL), Group-2 (3-9% WL) and Group-3 (<3% WL or weight gain). For the purpose of these analyses, weight fluctuation (WF) was defined a priori as at least a 2% weight cycle (“Gain and loss” or “loss and gain”). For the assessment of the effect of WF we have divided the patients into Wide (>5% WF) Average (2-5% WF) and stable (<2% WF) during the yearly follow up for 5 years.
Sponsors
Adelaide University
Eligibility
Sex/Gender
All
Age
18 Years to 85 Years
Healthy volunteers
No
Inclusion criteria
Age: 18 – 85 years paroxysmal or persistent AF Paroxysmal AF defined as recurrent episodes that self-terminate within 7 days or persistent AF as recurrent episodes that last more than 7 days and may be terminated with cardioversion. Stable or no coronary artery disease. Risk Factors identified at initial assessment including obesity (BMI>27), hypertension, diabetes, smoking and ETOH abuse.
Exclusion criteria
Significant cardiac valvulopathy Significant left ventricular systolic dysfunction (EF less than or equal than 45% on Simpson biplane estimation or regional wall motion abnormalities), obvious LV regional wall motion abnormality, dilated LV Myocardial infraction or cardiac surgery in the previous 12 months, and previous ablation for AF Right ventricular dysfunction with or without pulmonary hypertension (resting PASP equal to 45mmHg) and/or at least moderate tricuspid regurgitation Congenital heart disease Severe coronary heart disease. Uncontrolled endocrinopathy (adrenal, thyroid, etc.) Severe medical condition such as malignancies, autoimmune or inflammatory diseases, renal failure, or hepatic failure
Outcome results
None listed