SUMMARY
Hepcidin, the iron-regulatory hormone and acute phase reactant, is proposed to contribute to the pathogenesis of atherosclerosis by promoting iron accumulation in plaque macrophages, leading to increased oxidative stress and inflammation in the plaque (the “iron hypothesis”). Hepcidin and iron may thus represent modifiable risk factors in atherosclerosis. We measured hepcidin expression in Apoe−/− mice with varying diets and ages. To assess the role of macrophage iron in atherosclerosis, we generated Apoe−/− mice with macrophage-specific iron accumulation by introducing the ferroportin ffe mutation. Macrophage iron loading was also enhanced by intravenous iron injection. Contrary to the iron hypothesis, we found that hepatic hepcidin expression was not increased at any stage of the atherosclerosis progression in Apoe−/− or Apoe/ffe mice and the atherosclerotic plaque size was not increased in mice with elevated macrophage iron. Our results strongly argue against any significant role of macrophage iron in atherosclerosis progression in mice.
months, 336 patients were included. Patients with history of DM and/or pre-LVAD HbA1c ≥6.5 comprised the DM group (n=142), while those with no history of DM and a pre-LVAD HbA1c <6.5 comprised the non-DM group (n=194). Diabetics with a pre-LVAD HbA1c <7 were considered well-controlled (n=72) and those with a pre-LVAD HbA1c ≥7 not well-controlled (n=70). Relative changes between pre-and post-LVAD LVEF and LVEDD, were calculated. Cardiac recovery was defined as post-LVAD LVEF ≥40% and LVEDD <6.0cm. Results: Baseline characteristics of the 2 groups are shown in the Table . Cardiac functional and structural improvement, as evidenced by relative LVEF and LVEDD changes, was more prominent in non-DM compared to DM patients, and in well-compared to not well-controlled DM patients (Figure). Overall, DM patients were less likely to experience cardiac recovery (8.4% vs 17.5%; p=0.032), while on LVAD support. This remained significant in a multivariate logistic regression after controlling for potential confounders.
Conclusion:The presence of DM, and notably not well-controlled DM, appears to negatively affect the potential for LVAD-induced myocardial recovery. Further research is needed to investigate the dynamic cardiac metabolism in HF with DM.
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