Supplemental vitamin D and calcium in the management of African Americans with heart failure having hypovitaminosis D.

Introduction: A dyshomeostasis of macro- and micronutrients, including vitamin D and oxidative stress, are common pathophysiologic features in patients with congestive heart failure (CHF). In African Americans (AA) with CHF, reductions in plasma 25(OH) D are of moderate-to-marked severity (<20 ng/mL) and may be accompanied by ionized hypocalcemia with compensatory increases in serum parathyroid hormone (PTH). The management of hypovitaminosis D in AA with CHF has not been established. Methods: Herein, a 14-week regimen: an initial 8 weeks of oral ergocalciferol (50,000 IU once weekly); followed by a 6-week maintenance phase of cholecalciferol (1400 IU daily); and a CaCO3 (1000 mg daily) supplement given throughout was designed and tested. Fourteen AA patients having a dilated (idiopathic) cardiomyopathy with reduced ejection fraction (EF, <35%) were enrolled: all completed the initial 8-week course; and 12 complied with the full 14 weeks. At baseline, 8 and/or 14 weeks, serum 25(OH) D and PTH; serum 8-isoprostane, a biomarker of lipid peroxidation, and echocardiographic EF were monitored. Results: Reduced 25(OH) D at entry (14.4 +/- 1.3 ng/mL) was improved (P < 0.05) in all patients at 8 weeks (30.7 +/- 3.2 ng/mL) and sustained (P < 0.05) at 14 weeks (30.9 +/- 2.8 ng/mL). Serum PTH, abnormally increased in 5 patients at baseline (104.8 +/- 8.2 pg/mL), was reduced at 8 and 14 weeks (74.4 +/- 18.3 and 73.8 +/- 13.0 pg/mL, respectively). Plasma 8-isoprostane at entry (136.1 +/- 8.8 pg/mL) was reduced at 14 weeks (117.8 +/- 7.8 pg/mL; P < 0.05), whereas baseline EF (24.3 +/- 1.7%) was improved (31.3 +/- 4.3%; P < 0.05). Conclusions: Thus, the 14-week course of supplemental vitamin D and CaCO3 led to healthy 25(OH) D levels in AA with heart failure having vitamin D deficiency of moderate-to-marked severity. Albeit a small patient population, the findings suggest that this regimen may attenuate the accompanying secondary hyperparathyroidism and oxidative stress and improve ventricular function.