Congestive heart failureTreatment

Three studies gave congestive heart failure (CHF) patients vitamin D supplements.

In the first: One hundred twenty-three patients randomly received either 50 mug (2000 IU) vitamin D(3)/d plus 500 mg Ca/d [D(+) group] or placebo plus 500 mg Ca/d [D(-) group] for 9 months.

25-Hydroxyvitamin D increased by 26.8 ng/mL in the D(+) group but increased only by 3.6 ng/mL in the D(-) group. Compared with baseline, parathyroid hormone was significantly lower and the antiinflammatory cytokine interleukin 10 was significantly higher in the D(+) group after 9 mo. The proinflammatory cytokine tumor necrosis factor alpha increased in the D(-) group but remained constant in the D(+) group. The survival rate did not differ significantly between the study groups during the follow-up period.

CONCLUSIONS: Vitamin D(3) reduces the inflammatory milieu in CHF patients and might serve as a new antiinflammatory agent for the future treatment of the disease. Our data provide evidence for the involvement of an impaired vitamin D-parathyroid hormone axis in the progression of CHF1.

The second, which also included calcium, found that calcium alone improved biomarkers of bone turnover1.

The other found no improvement in functional capacity or quality of life in older patients2. However, it used vitamin D2 (ergocalciferol), which is not considered as effective as vitamin D3 (cholecalciferol)3. It could be the case, however, that increasing serum 25(OH)D levels once CHF reaches advanced stages has little beneficial effect since structural changes in the body from years of precursor effects cannot be changed. While there do not seem to be studies indicating that treating those with CHF improves their condition, assessment of vitamin D status and increasing blood levels of vitamin D should be encouraged4.

However, those who study vitamin D and CHF point out that no vitamin D intervention studies to date have provided good evidence that supplementation increases survival rates, and that more research is required before vitamin D supplementation can be recommended:

Recent evidence suggests a number of mechanisms whereby vitamin D may positively influence the pathophysiology of heart failure. These include actions on the renin-angiotensin system, calcium handling, reduction of proinflammatory cytokines, and improvements in endothelial function and blood pressure. Observational data suggest that low vitamin D levels are common in patients with heart failure and are associated with worse exercise capacity and natriuretic peptide levels. Little interventional data are currently available, but evidence to date does not support vitamin D supplementation, even in patients with low vitamin D levels. Further studies are needed to establish whether larger doses of vitamin D given over a longer period of time can reduce symptoms, hospitalization, and mortality in heart failure2.

An estimated 1 billion people worldwide have deficient or insufficient levels of vitamin D. Even more alarming is the association of vitamin D deficiency with many types of diseases, particularly heart failure (HF). Hypovitaminosis D has been observed to be highly prevalent in the HF community with rates varying from approximately 80% to 95%. Higher rates of deficiency have been linked to winter months, in patients with protracted decompensated HF, darker skin pigmentation, and higher New York Heart Association (NYHA) classes. In fact, some data suggest vitamin D deficiency may even be an independent predictor of mortality in patients with HF. Traditionally obtained through UV exposure and activated in the liver and then the kidneys, vitamin D is classified as a vitamin but functions as a steroid hormone. The hormone acts through the vitamin D receptor (VDR), which is expressed in vascular smooth muscle cells, renal juxtaglomerular cells, and most interestingly, cardiac myocytes. Studies have shown that the association between vitamin D deficiency and HF often manifests in the structural components of cardiac myocytes and/or through alterations of the neurohormonal cascade. In addition, vitamin D may also act rapidly through intracellular nongenomic receptors that alter cardiac contractility. Unfortunately, prospective vitamin D supplementation trials show mixed results. In rat models, successful correction of deficiency was associated with reductions in ventricular hypertrophy. In humans, however, echocardiographic dimensions did not change significantly. These results bring into questions whether vitamin D is a risk factor for HF, a marker of HF disease severity, or has a true pathologic role. This article provides a thorough review of vitamin D deficiency etiology, prevalence, and possible pathophysiologic role in HF. Furthermore, we carefully review prospective trials on vitamin D therapy in HF. We believe more trials on vitamin D therapy in HF need to be conducted before any conclusions can be drawn5.

Page last edited: 07 January 2012

References

  1. Schleithoff, S. S. Zittermann, A. Tenderich, G. Berthold, H. K. Stehle, P. Koerfer, R. Combined calcium and vitamin D supplementation is not superior to calcium supplementation alone in improving disturbed bone metabolism in patients with congestive heart failure. Eur J Clin Nutr. 2008 Dec; 62 (12): 1388-94.
  2. Witham, M. D. Crighton, L. J. Gillespie, N. D. Struthers, A. D. McMurdo, M. E. The effects of vitamin D supplementation on physical function and quality of life in older patients with heart failure: a randomized controlled trial. Circ Heart Fail. 2010 Mar; 3 (2): 195-201.
  3. Heaney, R. P. Recker, R. R. Grote, J. Horst, R. L. Armas, L. A. Vitamin D3 Is More Potent Than Vitamin D2 in Humans. J Clin Endocrinol Metab. 2010 Dec 22;
  4. Rendina, D. De Filippo, G. Strazzullo, P. Should vitamin D status be assessed in patients with congestive heart failure?. Nutr Metab Cardiovasc Dis. 2010 Nov; 20 (9): 627-32.
  5. Agarwal, M. Phan, A. Willix, R., Jr. Barber, M. Schwarz, E. R. Is Vitamin D Deficiency Associated With Heart Failure? A Review of Current Evidence. Journal of cardiovascular pharmacology and therapeutics. 2011 Feb 8;