Obesity promotes atrial fat deposition independent of myocardial infarction in Göttingen minipigs.

BACKGROUND

Atrial fibrillation 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 atrial fibrillation.

OBJECTIVE

This study aimed to understand whether 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 4 distinct left and right atrial sites for histologic analysis.

RESULTS

Obese animals have a significantly higher amount of atrial adipose tissue than lean animals at all 4 sites (right atrium [RA] P = .0008; RA appendage [RAA] P = .002; left atrium [LA] P = .04; LA appendage [LAA] P = .0002). Obese animals also showed a higher level of intramyocardial adipose tissue in the LA and both appendages (RAA P = .03; LA P = .004; LAA P = .001). No significant fibrotic remodeling was detected under any condition or atrial site. MI pigs exhibited a trend toward smaller epicardial adipocytes, whereas obesity was associated with larger adipocytes in the RAA and free wall. Finally, obesity significantly increased PR interval duration by 13.7% in MI pigs (P = .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.