Abstract 16241: Fat Infiltration Within Myocardial Infarction is Initiated by Macrophage Foam Cell Formation in the Scar Regions Containing Persistent Iron Deposits
Introduction: Fat deposition in old myocardial infarct scar is a common finding. The mechanism of this fatty infiltration has conventionally been attributed to the process of “lipomatous metaplasia”. It has been believed now for almost 30 years that scar collagen becomes replaced by metaplastic adipose tissue as part of the healing cascade after myocardial infarction (MI). To date, the trigger for fat deposition within old MI is unknown.
Hypothesis: Given that iron plays a critical role in creating a self-amplifying loop in macrophage foam cell formation, we hypothesized that fatty degeneration of myocardial scar following MI can in part be attributed to macrophage foam cell formation in the scar regions containing persistent iron deposits.
Methods: Canines (n=10) were subjected to 3-hour occlusion of the LAD artery, followed by reperfusion. Animals were recovered and followed for 6 months post MI at which time the hearts were explanted for histopathological analysis of macrophage markers within iron and fat-laden scar tissue.
Results: All dogs exhibited the presence of iron deposition and fatty infiltration within chronic myocardial infarctions. Sparse fat deposits within scar tissue showed strong positive staining for CD36 (indicating foam cell formation) and were exclusively co-localized with iron deposits and CD163+ macrophages (indicating iron-specific macrophage activation) (Figure 1).
Conclusions: Herein, we demonstrate that formation of fat deposits within old MIs begins with macrophage foam cell accumulation in the regions of persistent iron deposits. Our findings form the first evidence that fat infiltration within old MIs can be driven by processes other than lipomatous metaplasia.
Author Disclosures: I. Cokic: None. A. Kali: None. H. Yang: None. R. Tang: None. J. Francis: None. R. Dharmakumar: None.
- © 2016 by American Heart Association, Inc.