title: The importance of lost minerals in heart failure.
abstract: The clinical syndrome congestive heart failure (CHF) has its origins rooted in a salt-avid state mediated largely by effector hormones of the renin-angiotensin-aldosterone system (RAAS). In addition, a systemic illness accompanies chronic RAAS activation. Its features include: the presence of oxidative stress in diverse tissues coupled with a reduction in activity of endogenous oxidoreductases, such as Cu/Zn-superoxide dismutase and Se-glutathione peroxidase; a proinflammatory phenotype with activated immune cells and increased circulating levels of proinflammatory cytokines; and a catabolic state with loss of soft tissues and bone that eventuates in a wasting syndrome termed cardiac cachexia. Pathogenic mechanisms and pathophysiologic expressions of this illness are under active investigation. In this context and less well appreciated is the importance of a dyshomeostasis of various minerals, including Ca2+, Mg2+, Zn, and Se, and their impact on the systemic and progressive nature of CHF. A convergence of multiple factors, some hormonal (e.g., aldosteronism, secondary hyperparathyroidism, hypovitaminosis D), others pharmacologic (e.g., loop diuretics, angiotensin-converting enzyme inhibitors), predispose to the heightened excretion of these minerals in urine and feces while parathyroid hormone promotes intracellular Ca2+ overloading in diverse tissues. The importance of these macro- and micronutrients to the appearance of oxidative stress, compromised antioxidant defenses, an immunostimulatory state and tissue wasting needs to be critically addressed. So, too, must the potential for nutriceuticals, complementary to today's pharmaceuticals, to assist in the overall management of CHF.
authors.affiliation: Division of Cardiovascular Diseases, Department of Medicine, University of Tennessee Health Science Center, 920 Madison Ave., Suite 300, Memphis, TN 38163, USA. KNewman@utmem.edu
authors.forename: Kevin P
authors.initials: KP
authors.lastname: Newman
authors.forename: Matthew T
authors.initials: MT
authors.lastname: Neal
authors.forename: Matthew
authors.initials: M
authors.lastname: Roberts
authors.forename: Kayla D
authors.initials: KD
authors.lastname: Goodwin
authors.forename: Elizabeth A
authors.initials: EA
authors.lastname: Hatcher
authors.forename: Syamal K
authors.initials: SK
authors.lastname: Bhattacharya
mesh_terms: D000450:Aldosterone / Q000502:physiology; D002118:Calcium / Q000378:metabolism; D006333:Heart Failure / Q000188:drug therapy / Q000378:metabolism* / Q000503:physiopathology*; D006801:Humans; D006929:Hyperaldosteronism / Q000503:physiopathology*; D008274:Magnesium / Q000378:metabolism; D010281:Parathyroid Hormone / Q000378:metabolism; D012084:Renin-Angiotensin System; D012643:Selenium / Q000378:metabolism; D014807:Vitamin D / Q000378:metabolism; D015032:Zinc / Q000378:metabolism
chemical_list: D010281:Parathyroid Hormone; D014807:Vitamin D; D000450:Aldosterone; D012643:Selenium; D008274:Magnesium; D015032:Zinc; D002118:Calcium