Author + information
- Received January 25, 2002
- Revision received August 19, 2002
- Accepted September 13, 2002
- Published online January 1, 2003.
- Armin Zittermann, PhD*,* (, )
- Stefanie Schulze Schleithoff*,
- Gero Tenderich, MD†,
- Heiner K Berthold, MD, PhD‡,
- Reiner Körfer, MD† and
- Peter Stehle, PhD*
- ↵*Reprint requests and correspondence:
Dr. Armin Zittermann, Associate Professor, Department of Nutrition Science, University of Bonn, Endenicher Allee 11-13, 53115 Bonn, Germany.
Objectives This study was designed to evaluate the association between vitamin D status and congestive heart failure (CHF).
Background Impaired intracellular calcium metabolism is an important factor in the pathogenesis of CHF. The etiology of CHF, however, is not well understood.
Methods Twenty patients age <50 years and 34 patients age ≥50 years with New York Heart Association classes ≥2 and 34 control subjects age ≥50 years were recruited. N-terminal pro-atrial natriuretic peptide (NT-proANP), a predictor of CHF severity; vitamin D metabolites; and parameters of calcium metabolism were measured in fasting blood samples collected between November 2000 and March 2001.
Results Both groups of CHF patients had markedly increased serum levels of NT-proANP (p < 0.001), increased serum phosphorus levels (p < 0.001), and reduced circulating levels of both 25-hydroxyvitamin D (p < 0.001) and calcitriol (p < 0.001). Albumin-corrected calcium levels were reduced and parathyroid hormone levels were increased in the younger CHF patients compared with the controls (both p values <0.001). Moreover, parathyroid hormone levels tended to be higher in the elderly CHF patients than in the controls (p = 0.074). In a nonlinear regression analysis 25-hydroxyvitamin D and calcitriol were inversely correlated with NT-proANP (r2= 0.16; p < 0.001 and r2= 0.12; p < 0.01, respectively). The vitamin D genotype at the BmsI restriction site did not differ between the study groups.
Conclusions The low vitamin D status can explain alterations in mineral metabolism as well as myocardial dysfunction in the CHF patients, and it may therefore be a contributing factor in the pathogenesis of CHF.
☆ This study was supported by the Pinguin Stiftung, Düsseldorf, Germany.
- Received January 25, 2002.
- Revision received August 19, 2002.
- Accepted September 13, 2002.
- American College of Cardiology Foundation