maternal iron deficiency impairs postpartum reversal of pregnancy-related cardiac remodelling.
Background-
The maternal heart remodels during pregnancy to adapt to increased haemodynamic load. This involves hypertrophy of the left ventricle. The maternal heart reverse-remodels back to pre-pregnancy state rapidly in postpartum. Inadequate reverse-remodelling of the maternal heart is now emerging as a precursor to heart failure. However, the risk factors that impair reverse remodelling are not fully understood, The aim of his study is to explore the role of maternal iron status in maternal heart adaptations during pregnancy and postpartum.
Methods
We placed wild type female mice on iron-replete (200ppm) or iron-deficient diets (5ppm) for 10 weeks prior to mating. They were maintained on these diets throughout pregnancy and postpartum. We examined heart function by Cine MRI, and quantified myocardial and systemic iron levels.
Results
In both iron-replete and iron-deficient mothers, the hearts responded to pregnancy by increasing LV mass, LV end diastolic and end-systolic volumes. By 3 weeks postpartum, the hearts of iron-replete mothers had returned to pre-pregnancy levels. However, the hearts of iron-deficient mothers remained hypertrophied. This was preceded by profound depletion of systemic and myocardial iron, myocardial upregulation of the iron exporter ferroportin, and suppression of hepcidin.
Conclusion-
These data identify maternal iron deficiency and in particular myocardial iron depletion as a risk factor for impaired postpartum reverse remodelling, and as such a new female-specific risk factor for heart failure. These findings have the potential to improve maternal outcomes, because therapies that replenish systemic and myocardial iron rapidly are available.
The maternal heart remodels during pregnancy to adapt to increased haemodynamic load. This involves hypertrophy of the left ventricle. The maternal heart reverse-remodels back to pre-pregnancy state rapidly in postpartum. Inadequate reverse-remodelling of the maternal heart is now emerging as a precursor to heart failure. However, the risk factors that impair reverse remodelling are not fully understood, The aim of his study is to explore the role of maternal iron status in maternal heart adaptations during pregnancy and postpartum.
Methods
We placed wild type female mice on iron-replete (200ppm) or iron-deficient diets (5ppm) for 10 weeks prior to mating. They were maintained on these diets throughout pregnancy and postpartum. We examined heart function by Cine MRI, and quantified myocardial and systemic iron levels.
Results
In both iron-replete and iron-deficient mothers, the hearts responded to pregnancy by increasing LV mass, LV end diastolic and end-systolic volumes. By 3 weeks postpartum, the hearts of iron-replete mothers had returned to pre-pregnancy levels. However, the hearts of iron-deficient mothers remained hypertrophied. This was preceded by profound depletion of systemic and myocardial iron, myocardial upregulation of the iron exporter ferroportin, and suppression of hepcidin.
Conclusion-
These data identify maternal iron deficiency and in particular myocardial iron depletion as a risk factor for impaired postpartum reverse remodelling, and as such a new female-specific risk factor for heart failure. These findings have the potential to improve maternal outcomes, because therapies that replenish systemic and myocardial iron rapidly are available.