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- Open Access
Role of iron chelation in hemorrhagic myocardial infarction: a quantitative CMR study
© Ghugre et al; licensee BioMed Central Ltd. 2012
- Published: 1 February 2012
- Acute Myocardial Infarction
- Cardiovascular Magnetic Resonance
- Acute Myocardial Infarction
- Iron Chelation
Reperfusion hemorrhage is an independent predictor of adverse left-ventricular remodeling following acute myocardial infarction. Iron chelation may potentially alleviate the toxic and pro-inflammatory effects of iron degradation products. CMR can provide insights into the interaction between hemorrhage and iron chelator.
It has been speculated that iron chelation may be beneficial in acute myocardial infarction (AMI) and that early treatment can limit ischemia-reperfusion injury and also reduce infarct size. However, the role of iron chelation in hemorrhagic myocardial infarction, where it would be most suited, has not yet been explored. Reperfusion hemorrhage results in accumulation of iron degradation products of hemoglobin that may be pro-inflammatory as free iron is toxic in nature. The purpose of the study was to investigate the interaction between iron chelating agent deferiprone (DFP) and hemorrhage in a porcine model of myocardial infarction and monitor remodeling by cardiovascular magnetic resonance (CMR).
The study involved two groups of animals that were subjected to a 90 min balloon occlusion of the LAD followed by reperfusion - untreated (N=2) and DFP treated (N=2). DFP (supported by ApoPharma Inc., Toronto, ON) was administered (orally) a few hours before the procedure (pre-loading) and treatment was continued with a daily dose of 100 mg/kg. Imaging was performed on a 3T MRI scanner (MR 750, GE Healthcare) pre-AMI (healthy) and day 2-week 4 post-AMI. Edema was evaluated by T2 quantification using a T2-prepared spiral sequence and hemorrhage was identified by T2* determined using a multi-echo gradient-echo acquisition. Infarct assessment was performed by delayed hyperenhancement (DHE) using an IR-GRE sequence.
Hemorrhage may be a source of iron toxicity and a mediator of inflammation, directly contributing to adverse remodeling in the setting of AMI. DFP was able to penetrate the infarct zone and was also effective in neutralizing hemorrhagic byproducts. Elimination of hemorrhage resulted in faster resolution of edema and normal ventricular volumes, representing a beneficial remodeling process. Iron chelation could potentially serve as an adjunctive therapy in hemorrhagic AMI.
We would like to acknowledge funding support from the Ontario Research Fund, the Canadian Institutes of Health Research and GE Healthcare.
This article is published under license to BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.