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Hypertension not controlled by 26 ng of Vitamin D (50,000 IU bi-weekly A-A) – RCT Nov 2017

Abstract 20556: Randomized Controlled Trial of Vitamin D Adjunct Therapy for African American Patients With Left Ventricular Hypertrophy

Circulation. 2017;136:A20556
Phillip D Levy, Aaron Brody, Tao Li, Rachelle Dawood, Lynn Marie Mango, Laura Gowland, Michael Twiner, Greg Gandits, Kenneth Svendsen, Cheryl Courage, John Flack


Vitamin D is rarely provides benefit if the level is less than 30 nanograms/mL
It appears that this African-American group needed a more frequent dosing than once every 14 days.
Perhaps weekly

Introduction: Left ventricular hypertrpophy (LVH) is a consequence of uncontrolled hypertension (HTN). Vitamin D helps regulate multiple, cardiac neurohormonal pathways, and its deficiency may contribute to heart disease. Vitamin D deficiency, HTN, and LVH are all more prevelent among African Americans (AAs); however, few trials have evaluated the direct impact of vitamin D supplementation on LVH in AAs who have uncontrolled HTN.

Hypothesis: We hypothesized that, in a cohort of vitamin D deficient AAs with uncontrolled HTN and subclinical hypertensive heart disease, the addition of vitamin D to evidence-based antihypertensive therapy would lead to greater regression of LV mass at one year compared to placebo.

Methods: African American patients with uncontrolled HTN (SBP > 160 mm Hg), increased LV mass index (LVMI > 73 g/m2 for females and > 89 g/m2 for males by cardiac MRI [CMR]), and vitamin D deficiency (< 20 ng/mL) were randomized to receive antihypertensive therapy plus 50,000 IU vitamin D3 or placebo bi-weekly for one year. To detect a 7 g/m2 difference in LVMI by CMR at one year, 96 patients were needed. To account for dropouts, we oversampled by 15% but all data were analyzed by intention to treat.

Results: A total of 113 patients (55 vitamin D, 58 placebo) were randomized. Mean age was 46 years, and 54% were female. Mean randomization BP was 161/102 mm Hg, and mean LVMI was 97 g/m2. Baseline variables were balanced between groups, with the exception of female gender (67% vs. 41%; p<0.01), and tobacco use (57% vs. 35%, p=0.02), both of which were more common in the vitamin D arm. Most patients (43 [78%] vitamin D; 49 [84%] placebo) completed the protocol, with a significant increase in median vitamin D concentration in the treatment arm 26 ng/ml vs. 13 ng/ml; p<0.01 ), and substantial but equivalent reductions in SBP for both groups (vitamin D: -25.6 ± 4.9 mm Hg; placebo: -25.7 ± 3.6 mm Hg; p = 0.99). Although meaningful reductions in LVMI were achieved in vitamin D (-14.1 g/m2 ) and placebo groups (-16.9 g/m2), the difference was non-significant (2.8 g/m2; p=0.34).

Conclusions: When combined with evidence-based antihyptensive therapy, vitamin D supplementation provided no added benefit on LVH in this cohort of vitamin D deficient AAs with subclinical heart disease.

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