Do myocardial infarction and obesity have a synergistic impact on atrial remodeling in a minipig model?
Obesity, rather than myocardial infarction, is the primary driver of atrial adipose tissue remodeling in a minipig model.
AbstractBackground Atrial fibrillation (AF) often follows myocardial infarction (MI) and is associated with increased risks of adverse cardiovascular outcomes. Obesity is a potent risk factor for both MI and AF. Objective To understand if MI and obesity have a synergistic impact on atrial remodeling. Methods Lean (sham n=3, MI n=12) and obese (sham n=3, MI n=9) Göttingen minipigs (MI group) underwent a 120-minute balloon occlusion of the left anterior descending coronary artery. After 8 weeks, myocardial tissue was collected from four distinct left and right atrial sites for histological analysis. Results Obese animals have a significantly higher amount of atrial adipose tissue compared to lean at all four sites (RA: p=0.0008, RAA: p=0.002, LA: p=0.04, LAA p=0.0002). Obese animals also showed a higher level of intramyocardial adipose tissue in the left atrial free wall and both appendages (RAA: p=0.03, LA: p=0.004, LAA p=0.001). No significant fibrotic remodeling was detected under any condition or atrial site. MI pigs exhibited a trend towards smaller epicardial adipocytes, while obesity was associated with larger adipocytes in the right atrial appendage and free wall. Finally, obesity significantly increased PR interval duration by 13.7 % in MI pigs (p=0.037). Conclusion Obesity is the primary driver of atrial adipose tissue remodeling both in and around the atria. MI had no effect on atrial remodeling at any site in either lean or obese animals.
Dannesboe et al. (Thu,) studied this question.
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