Author + information
- Ivan Cokic,
- Kolja Wawrowsky,
- Avinash Kali,
- Hsin-Jung Yang,
- Richard Tang,
- Joseph Francis and
- Rohan Dharmakumar
Background: Upon phagocytosis of oxidized red blood cells (oxRBC), macrophages tend to transform into foam cells (FC) and produce autofluorescent pigment with the characteristics of ceroid (CR). The process of FC formation following erythrophagocytosis involves exocytosis of iron. Phagocytosis of this iron by new macrophages can lead to a self-perpetuating and amplifying cycle of FC and CR accumulation. In this study, we hypothesized that fatty degeneration of hemorrhagic myocardial infarctions (MI) has its origin in perpetual oxRBC-iron recycling and FC formation.
Methods: Canines (n=10) were subjected to 3-hour occlusion of the LAD artery, followed by reperfusion. All dogs underwent T2* and LGE CMR on day 7 post-MI. Animals were sacrificed 6 months post-MI. Explanted hearts underwent histopathological analysis. Sections stained with Prussian Blue were examined for autofluorescence of CR under confocal microscope.
Results: Reperfusion hemorrhage in acute MI was evident in all dogs by MRI (Figure 1). Histopathological studies demonstrated both iron and FCs within all MIs. Moreover, fat depots within scars exclusively co-localized with autofluorescent CR and iron deposits (Figure 2).
Conclusions: Our results indicate that iron deposits from hemorrhagic MIs are being persistently recycled in a self-amplified loop of foam cell formation with perpetual production and deposition of intra-and extracellular ceroid. We conclude that iron is a key player in adverse myocardial remodeling post-MI.
Poster Hall, Hall C
Saturday, March 18, 2017, 3:45 p.m.-4:30 p.m.
Session Title: Emerging Basic Science in Ischemic Heart Disease
Abstract Category: 1. Acute and Stable Ischemic Heart Disease: Basic
Presentation Number: 1251-297
- 2017 American College of Cardiology Foundation