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Shadwan Alsafwah, MD, Division of Cardiovascular Diseases, Department of Medicine, University of Tennessee Health Science Center, Memphis, Tennessee
Stephen P. LaGuardia, MD, Division of Cardiovascular Diseases, Department of Medicine, University of Tennessee Health Science Center, Memphis, Tennessee
Maximiliano Arroyo, MD, Division of Cardiovascular Diseases, Department of Medicine, University of Tennessee Health Science Center, Memphis, Tennessee
Brian K. Dockery, MD, Division of Cardiovascular Diseases, Department of Medicine, University of Tennessee Health Science Center, Memphis, Tennessee
Syamal K. Bhattacharya, PhD, Division of Cardiovascular Diseases, Departments of Medicine and Surgery, University of Tennessee Health Science Center, Memphis, Tennessee
Robert A. Ahokas, PhD, Department of Obstetrics & Gynecology, University of Tennessee Health Science Center, Memphis, Tennessee
Kevin P. Newman, MD, Division of Cardiovascular Diseases, Department of Medicine, University of Tennessee Health Science Center, Memphis, Tennessee
Reprint Requests: Kevin P. Newman, MD, Division of Cardiovascular Diseases, University of Tennessee Health Science Center, 920 Madison Avenue, Suite 300, Memphis, TN 38163, Tel: 901-448-5314, Fax: 901-448-8084, Email: KNewman{at}utmem.edu
Congestive heart failure (CHF) is a clinical syndrome that features a failing heart together with signs and symptoms arising from renal retention of salt and water, mediated by attendant neurohormonal activation, and which prominently includes the renin-angiotensin-aldosterone system. More than this cardiorenal perspective, CHF is accompanied by a systemic illness whose features include an altered redox state in diverse tissues and blood, an immunostimulatory state with proinflammatory cytokines and activated lymphocytes and monocytes, and a wasting of tissues that includes muscle and bone. Based on experimental studies of aldosteronism and clinical findings in patients with CHF, there is an emerging body of evidence that secondary hyperparathyroidism is a covariant of CHF. The aldosteronism of CHF predisposes patients to secondary hyperparathyroidism because of a chronic increase in Ca2+ and Mg2+ losses in urine and feces, with a fall in their serum ionized levels and consequent secretion of parathyroid hormone. Secondary hyperparathyroidism accounts for bone resorption and contributes to a fall in bone strength that can lead to nontraumatic fractures.The long-term use of a loop diuretic with its attendant urinary wasting of Ca2+ and Mg2+ further predisposes patients to secondary hyperparathyroidism and attendant bone loss. Aberrations in minerals and micronutrient homeostasis that includes Ca2+, Mg2+, vitamin D, zinc and selenium appear to be an integral component of pathophysiologic expressions of CHF that contributes to its systemic and progressive nature. This broader perspective of CHF, which focuses on the importance of secondary hyperparathyroidism and minerals and micronutrients, raises the prospect that dietary supplements could prove remedial in combination with the current standard of care.
Key Words: Aldosteronism Congestive heart failure Hyposelenemia Hypovitaminosis D Hypozincemia Secondary hyperparathyroidism
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T Sugimoto, T Tanigawa, K Onishi, N Fujimoto, A Matsuda, S Nakamori, K Matsuoka, T Nakamura, T Koji, and M Ito Serum intact parathyroid hormone levels predict hospitalisation for heart failure Heart, March 1, 2009; 95(5): 395 - 398. [Abstract] [Full Text] [PDF] |
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