Fig. 9: Reduction of residual iron by deferiprone in the post-MI period is accompanied by a reduction in lipomatous metaplasia in canine models of hemorrhagic MI. | Nature Communications

Fig. 9: Reduction of residual iron by deferiprone in the post-MI period is accompanied by a reduction in lipomatous metaplasia in canine models of hemorrhagic MI.

From: Intramyocardial hemorrhage drives fatty degeneration of infarcted myocardium

Fig. 9: Reduction of residual iron by deferiprone in the post-MI period is accompanied by a reduction in lipomatous metaplasia in canine models of hemorrhagic MI.The alternative text for this image may have been generated using AI.

Representative, raw and processed, short-axis late-gadolinium enhancement (depicting zone of MI), R2* (depicting iron concentration), and PDFF (depicting fat concentration) cardiac MRI images from one animal with hemorrhagic MI and receiving DFP treatment (DFP+/IMH+) and another animal with hemorrhagic MI but not receiving DFP treatment (DFP−/IMH+) (a), acquired on day 3 (D3), week 8 (Wk8) and month 6 (M6) post-MI are shown. Note the reduction in R2* within the infarction zone in the treated animal at Wk8 and M6, relative to D3. In the untreated animal, R2* was elevated on D3 and remained elevated at Wk8 and M6. Also note that in the DFP-treated animal, the deposition of fat within the MI zone was visibly reduced compared to in the untreated animal at Wk8 and M6. The residual iron concentration based on R2* in animals with hemorrhagic MI undergoing DFP treatment and no treatment (normalized to values obtained on D3) is shown in (b) at Wk8 and M6. Note the marked reduction in the residual iron at Wk8 and M6 in the treated group compared to the untreated group. The extent of fat deposition based on PDFF in animals with hemorrhagic MI undergoing DFP treatment and no treatment (normalized to values on D3) are shown in c at Wk8 and M6. Note the marked reduction in the fat content at Wk8 and M6 in the treated group compared to the untreated group. (x) represents well-known off-resonance artifacts in non-infarcted (posterior wall) regions. Evaluable canine CMR data were available in n = 12 (DFP+/IMH+) and n = 8 (DFP−/IMH+) at D3; n = 8 (DFP+/IMH+) and n = 8 (DFP−/IMH+) on Wk8; and n = 3 (DFP+/IMH+) and n = 3 (DFP−/IMH+) on M6. Evaluable canine CMR data comprising of both R2* and PDFF were available in n = 12 (DFP+/IMH+) and n = 8 (DFP−/IMH+) at D3; n = 8 (DFP+/IMH+) and n = 8 (DFP−/IMH+) on Wk8; and n = 3 (DFP+/IMH+) and n = 3 (DFP−/IMH+) on M6. All data were normally distributed by Shapiro–Wilk test and quantile-quantile plots. A two-sided t-test was performed to test for significant differences between the two groups for residual iron analysis: p = 0.000011 between DFP+/IMH+ and DFP−/IMH+ at Wk8 and p = 0.0072 at M6, p = 0.032 between DFP+/IMH+ group at Wk8 and M6, p = 0.86 between DFP+/IMH− group at Wk8 and M6. One-sided t-test was performed to test for significant differences between two groups for fat infiltration analysis: p = 0.020 between DFP+/IMH+ and DFP−/IMH+ at Wk8 and p = 0.039 at M6, p = 0.020 between DFP+/IMH+ group at Wk8 and M6, p = 0.0071 between DFP+/IMH− group at Wk8 and M6. +p < 0.05; ++p < 0.001. The data are shown as mean ± SEM. Source data are provided in the Source Data file.

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