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Impact of body iron status on myocardial perfusion, left ventricular function, and angiographic morphologic features
Ayşe Emre Say1, Metin Gursurer, Mehmet Vefik Yazicioglu
1Department of Cardiology, Siyami Ersek Thoracic and Cardiovascular Surgery Center, Istanbul, Turkey. saymer@superonline.com
Insights
In hypercholesterolemia patients, elevated iron stores correlate with impaired myocardial perfusion and function, but not coronary artery disease extent. This suggests iron-mediated oxidative stress worsens hypercholesterolemia-related endothelial dysfunction.
Area of Science:
- Cardiology
- Biochemistry
- Medical Imaging
Background:
- Iron stores influence atherogenesis via free radical formation and LDL oxidation, particularly in hypercholesterolemia (HCL).
- A synergistic link between serum ferritin, LDL cholesterol, and myocardial infarction risk exists in humans.
Purpose of the Study:
- To investigate the association between serum iron parameters and myocardial perfusion, wall motion, and coronary artery disease (CAD) extent in HCL patients.
Main Methods:
- Coronary angiography and exercise technetium-99m sestamibi SPECT imaging were performed on 68 male HCL patients and 52 normocholesterolemic controls.
- Serum iron parameters, including ferritin and total iron-binding capacity, were analyzed.
Main Results:
- Serum ferritin strongly correlated with perfusion (r=0.70), reversibility (r=0.68), and wall motion (r=0.54) indices in HCL patients.
- Total iron-binding capacity showed an inverse correlation with perfusion (r=-0.59) in HCL patients.
- No significant associations were found between iron parameters and perfusion/wall motion in normocholesterolemic individuals or with angiographic CAD extent in either group.
Conclusions:
- Increased iron stores are linked to greater myocardial perfusion and functional abnormalities in HCL patients, independent of CAD extent.
- Iron-mediated oxidative stress and LDL peroxidation may exacerbate HCL-related endothelial dysfunction, impairing myocardial function.
Background:
Previous studies have shown that the effects of iron stores on atherogenesis through promotion of free radical formation and low-density lipoprotein (LDL) oxidation largely depend on the state of hypercholesterolemia (HCL) in animal models. A synergistic association of serum ferritin and LDL cholesterol with the risk of myocardial infarction has also been observed in humans.
Methods:
We sought to assess the relationship of serum iron parameters to myocardial perfusion and wall motion abnormalities and to the extent of angiographic coronary artery disease (CAD) in patients with HCL. Sixty-eight male patients (mean age 58 +/- 9 years) with hypercholesterolemia (LDL cholesterol >130 mg/dL) who had never been treated and 52 normocholesterolemic male subjects of similar age underwent coronary angiography and exercise technetium-99m sestamibi gated single-photon emission computed tomography imaging within 10 days.
Results:
Serum ferritin had a significant correlation with the perfusion index (r = 0.70, P <.001), the reversibility index (r = 0.68, P <.01), and the wall motion index (r = 0.54, P <.05), whereas a relatively weak correlation was observed between total iron binding capacity and perfusion index (inversely) (r = -0.59, P <.01) in patients with HCL. Iron parameters were not associated with either perfusion or wall motion indices in the normocholesterolemic group. Stepwise multiple regression analysis confirmed these results. Ferritin was a strong determinant of perfusion in patients with HCL only (beta =.55, P =.002). Iron parameters were not related to the angiographic extent of CAD as defined by angiographic vessel or extent score in either group.
Conclusions:
Our data suggest that increased iron stores are closely associated with a greater extent and severity of perfusion and functional abnormalities but not with the angiographic extent of CAD in patients with HCL. Enhanced iron-mediated oxidative stress and LDL peroxidation may contribute to the hypercholesterolemia-related endothelial dysfunction and cause further impairment of myocardial perfusion and wall motion.