Congestive heart failureHow does vitamin D work?

One mechanism whereby vitamin D may reduce the risk of CHF is through effects on the the renin-angiotensin-aldosterone system (RAAS), which affects blood pressure1.

A disturbance of the RAAS leads to further complications including increases in proinflammatory cytokines and disruption of trace mineral balance:

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 CHF2.

There are also likely effects on the heart:

In adults, almost all patients with heart failure exhibit reduced 25-hydroxyvitamin D levels, which are used to classify the vitamin D status. In prospective studies, vitamin D deficiency was an independent risk factor for mortality, deaths due to heart failure and sudden cardiac death. Several vitamin D effects on the electrophysiology, contractility, and structure of the heart suggest that vitamin D deficiency might be a causal factor for myocardial diseases3.

A review discusses the current understanding of the role of vitamin D in heart failure:

Vitamin D, indeed, stimulates the synthesis of various contractile proteins and activates crucial intracellular mechanisms that manage calcium metabolism and energy production. These functions can be altered once vitamin D deficiency develops. This review focuses on the relationship between vitamin D deficiency, asymptomatic changes in left ventricular geometry and function, and heart failure syndrome through a recall of the myocardial metabolic processes regulated by vitamin D. The analysis of the available data from the literature leads to raise some questions that, at present, have no answer. Future prospective studies are needed to assess the effect of treatment of vitamin D deficiency on cardiac function4.

A recent review had this summary:

The steroid hormone vitamin D regulates gene expression of many genes that play a prominent role in the progression of heart failure, such as cytokines and hormones. Specifically, vitamin D is a negative regulator of the hormone renin, the pivotal hormone of the renin-angiotensin system. Mechanistic insights were gained by studying mice deficient for the vitamin D receptor, which develop hypertension and adverse cardiac remodeling mediated via the renin-angiotensin system. Furthermore, vitamin D receptor is expressed in the heart and regulated under pro-hypertrophic stimuli and vitamin D has receptor has been associated with the expression of other hypertrophic genes such as natriuretic peptides. So, epidemiological data and mechanistic studies have provided strong support for a potentially cardioprotective effect of vitamin D. It remains unclear if vitamin D supplementation is beneficial in preventing heart failure or if it could be a therapeutic addendum in the treatment of heart failure. This review summarizes current knowledge on vitamin D and its biology in heart failure5.

Page last edited: 06 May 2011

References

  1. Rostand, S. G. Vitamin D, blood pressure, and African Americans: toward a unifying hypothesis. Clin J Am Soc Nephrol. 2010 Sep; 5 (9): 1697-703.
  2. Newman, K. P. Neal, M. T. Roberts, M. Goodwin, K. D. Hatcher, E. A. Bhattacharya, S. K. The importance of lost minerals in heart failure. Cardiovasc Hematol Agents Med Chem. 2007 Oct; 5 (4): 295-9.
  3. Pilz, S. Henry, R. M. Snijder, M. B. van Dam, R. M. Nijpels, G. Stehouwer, C. D. Kamp, O. Tomaschitz, A. Pieber, T. R. Dekker, J. M. Vitamin D deficiency and myocardial structure and function in older men and women: the Hoorn study. J Endocrinol Invest. 2010 Oct; 33 (9): 612-7.
  4. Cioffi, G. Gatti, D. Adami, S. [Vitamin D deficiency, left ventricular dysfunction and heart failure]. Giornale italiano di cardiologia. 2010 Sep; 11 (9): 645-53.
  5. Meems, L. M. van der Harst, P. van Gilst, W. H. de Boer, R. A. Vitamin D biology in heart failure: molecular mechanisms and systematic review. Curr Drug Targets. 2011 Jan; 12 (1): 29-41.