Faculty Bibliography

Diabetic patients with coronary artery disease (CAD) are more likely to develop heart failure (HF) than nondiabetic patients, but the mechanism responsible is unclear. Evidence suggests that infarct size and accompanying remodeling may not explain this difference. We used cardiac magnetic resonance (CMR) imaging to compare degree of left ventricular (LV) myocardial scar and remodeling in diabetic and nondiabetic patients with CAD. We evaluated 85 patients (39 diabetic, 46 nondiabetic) who underwent coronary angiography showing obstructive CAD and CMR imaging within 6 months of each other. Myocardial scar was measured by late gadolinium enhancement on CMR imaging and was graded according to spatial and transmural extents on a semiquantitative scale. More diabetic than nondiabetic patients had HF (69% vs 43%, p <0.03); however, groups did not differ in total scar burden (0.94 +/- 0.60 vs 1.17 +/- 0.74, p = NS), spatial extent of scar, or extent of transmural scar. Diabetes remained an independent predictor of HF after adjustment for CAD and other variables. LV ejection fraction (36 +/- 12% vs 37 +/- 14%, p = NS) and end-diastolic volume (215 +/- 56 vs 217 +/- 76 ml, p = NS) were similar for diabetic and nondiabetic patients, respectively. In conclusion, although diabetic patients with CAD had a higher prevalence of HF than nondiabetic patients, there was no difference in myocardial scar, LV volume, or LV ejection fraction. These findings support the theory that mechanisms other than extent of myocardial injury and negative remodeling play a significant role in the development of HF in diabetic patients with CAD

Iron-deficiency anemia is common in patients with heart failure (HF), but the optimum diagnostic tests to detect iron deficiency and the treatment options to replete iron have not been fully characterized. Recent studies in patients with HF indicate that intravenous iron can rapidly replenish iron stores in patients having iron-deficiency anemia, with resultant increased hemoglobin levels and improved functional capacity. Preliminary data from a subgroup analysis also suggest that supplemental intravenous iron therapy can improve functional capacity even in those subjects without anemia. The mechanisms responsible for this observation are not fully characterized, but may be related to beneficial effects of iron supplementation on mitochondrial respiration in skeletal muscle. The long-term safety of using intravenous iron supplementation in HF populations is not known. Iron is a known pro-oxidant factor that can inhibit nitric oxide signaling and irreversibly injury cells. Increased iron stores are associated with vascular endothelial dysfunction and increased risk of coronary heart disease events. Additional clinical trials are needed to more fully characterize the therapeutic potential and safety of intravenous iron in HF patients

Iron deficiency is a common cause of anemia in otherwise healthy individuals and plays an important role in the development of anemia within the heart failure patient population. Iron-deficient heart failure patients experience worse symptoms and are less exercise tolerant than those without iron deficiency. These symptoms may occur even before clinical anemia is evident. This article reviews studies of the benefits of the use of intravenous iron to treat iron deficiency in anemic and nonanemic heart failure patients and an overview of the physiology and pathophysiology of iron metabolism in chronic heart failure