
Iron deficiency (ID) is prevalent and adverse in chronic heart failure (CHF), but few human studies have explored the myocardial mechanism(s) that potentially underlie this adversity. Because mitochondrial oxidative phosphorylation (OXPHOS) provides over 90% of the heart's adenosine triphosphate (ATP), and iron is critical for OXPHOS, the study hypothesized that patients with CHF and ID would harbour more significant cardiac energetic impairments than patients without ID. Therefore, suppression of cardiac mitochondrial function might be a mechanism via which ID worsens human CHF.
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