Purpose Congestive heart failure (CHF) features a disabling systemic illness that includes oxidative stress and a proinflammatory phenotype. Endogenous antioxidant defenses, integral to combating superoxide and H2O2, include cytosolic superoxide dismutase and glutathione peroxidase and which are Zn and Se dependent, respectively. Serum Zn and Se balance in patients with CHF remain uncertain. Urinary Zn excretion is increased in hyperparathyroidism (HPT) as well as in response to treatment with an angiotensin-converting enzyme inhibitor (ACEI), an AT1 receptor antagonist (AT1Ra), and a thiazide but not loop diuretic. We therefore hypothesized a deficiency of Zn and Se in CHF.
Methods We monitored serum Zn, Se, and parathyroid hormone (PTH) in 25 AA (50.6 6 2.3 yrs; 16 men) with systolic dysfunction (EF < 35%) due to ischemic or dilated (idiopathic) cardiomyopathy; 20 were hospitalized because of signs and symptoms of CHF, who were further stratified on historical grounds as having decompensated (D) failure of long ($ 4 wks) or short (1-2 wks) duration in 11 and 9, respectively, despite medical care that included ACEI or AT1Ra, a loop diuretic and spironolactone; and 5 were outpatients with treated, compensated failure (Comp). Results (mean 6 SEM):
Conclusions In AA, either hospitalized with CHF or followed as outpatients with compensated heart failure, all of whom were treated with an ACEI or AT1Ra, we found hypozincemia and hyposelenemia. It remains to be determined if the observed fall in serum Zn and Se reflects increased renal and/or colonic excretion of these micronutrients related to secondary HPT and/or medications, a dietary deficiency, and/or their redistribution within tissues related to up-regulated expression of binding proteins. A role for dietary supplementation of Zn and Se in AA patients with CHF remains to be addressed.
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