Iron Deficiency in Chronic Heart Failure Patients at the University Teaching Hospital in Lusaka, Zambia
Background: Iron plays a key role in oxygen uptake, transport, and storage, as well as oxidative metabolism in the muscle including myocardium and is essential for the formation of haemoglobin, myoglobin, cytochromes, cytochrome oxidase, peroxidase, and catalase. Iron deficiency (ID) often develop in chronic heart failure (CHF) patients due to depletion of iron stores, iron malabsorption and/or reduced availability of iron recycled in the reticuloendothelial system. Indeed iron content and transferrin receptor levels have been reported to be decreased in the myocardium of patients with ID. A cardinal manifestation of heart failure (both heart failure with reduced ejection fraction. HFrEF and heart failure with preserved ejection fraction, HFpEF) is impaired exercise capacity that is exaggerated in iron deficient patients. This easy fatigability is said to be a result of the reduced oxygen transport that is associated with the ID. ID leads to mitochondria and sarcomere dysfunction which reduces left ventricular functioning and hence reducing cardiac output. Reduced peak oxygen uptake has also been reported in patients withHFrEF.
Objective: To determine iron status of CHF patients at University Teaching Hospital (UTH) in Lusaka.
Methods: The study was conducted at UTH from May to August 2019. Using purposive sampling, data was collected from patients with CHF of New York Heart Association (NYHA) functional class II to IV. Information obtained included sex, age, height, weight and ejection fraction (reduced ifless than 45%). From the blood samples collected, serum iron levels, transferrin levels and ferritin concentration tests were done. The chi square test and logistic regression were used to analyze iron status in CHF patients.
Results: Forty (40) patients were enrolled, 18 male and 22 female. The average age was 45.5 (19 to 60). 24 patients (60%) had (HFrEF) and 16 patients (40%) had (HFpEF). 22 patients (55%) had transferrin saturation of less than 20%, while 8 (20%) had ferritin concentration of less than l00ng/ml. Based on both factors, a total of22(55%) patients were iron deficient. Iron deficiency was negatively associated withHFrEF (p = 0.015).
Conclusion: More than 55% of the participants in this study were iron deficient. However, ID may not be the primary cause of myocardial dysfunction as patients with HFrEF were less likely to be iron deficient. However, correction of ID in CHF patients in other studies has been reported to have clinical benefits. The observations of this study require further triangulation especially that the sample size was rather small.
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