Key result
Addition of biweekly 50,000 IU vitamin D3 to antihypertensive therapy did not improve regression of LV mass index compared with placebo at 1 year.
Why the study?
LVH and vitamin D deficiency have been linked to HTN and cardiovascular disease in African Americans, but whether adding vitamin D to antihypertensive therapy enhances LVMI regression remained unknown.
Does vitamin D3 supplementation improve regression of left ventricular mass index in African American patients with uncontrolled hypertension, LVH, and vitamin D deficiency?
RCT (n=113)
double-blind
randomized
No
Does vitamin D3 supplementation improve regression of left ventricular mass index in African American patients with uncontrolled hypertension, LVH, and vitamin D deficiency?
High-dose vitamin D supplementation added to antihypertensive therapy did not significantly improve LV mass index regression or systolic blood pressure reduction in a high-risk cohort of African Americans.
Answers are grounded in this paper and cite their sources.
No role for adjunctive high-dose vitamin D3 in LV mass regression; confirms neutral effect on cardiac remodeling in this RCT.
BACKGROUND: Left ventricular hypertrophy (LVH) and vitamin D deficiency have been linked to hypertension (HTN) and cardiovascular disease, particularly in African Americans (AAs). Our objective was to determine if the addition of vitamin D to antihypertensive therapy would lead to greater regression of LV mass index (LVMI) as determined by cardiac magnetic resonance (CMR) after 1 year in vitamin D deficient AA patients with uncontrolled HTN and LVH. METHODS: This study was a randomized, double-blind, placebo-controlled, single-center study. AA patients with HTN (systolic blood pressure [BP] >160 mm Hg), increased LVMI, and vitamin D deficiency (<20 ng/ml) were randomized. All patients received antihypertensive therapy combined with biweekly 50,000 IU vitamin D3 (vitamin D group, n = 55) or placebo (placebo group, n = 58). RESULTS: At 1 year, there were no statistical differences between the vitamin D and placebo groups in LVMI (-14.1 ± 14.6 vs. -16.9 ± 13.1 g/m2; P = 0.34) or systolic BP (-25.6 ± 32.1 vs. -25.7 ± 25.6 mm Hg; P = 0.99) reduction, respectively. Serum vitamin D levels increased significantly in the vitamin D group compared with placebo (12.7 ± 2.0 vs. 1.8 ± 8.2 ng/ml; P < 0.001). CONCLUSIONS: In this high-risk cohort of AAs we did not find an association between vitamin D supplementation and differential regression of LVMI or reduction in systolic BP. However, our study suffered from a small sample size with low statistical power precluding a definitive conclusion on the therapeutic benefit of vitamin D in such patients. CLINICAL TRIALS REGISTRATION: Trial Number NCT01360476. Full trial protocol is available from corresponding author.
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Levy et al. (2022) conducted an RCT in Hypertension, left ventricular hypertrophy, and vitamin D deficiency (n=113). Vitamin D3 vs. Placebo was evaluated on Regression of LV mass index (LVMI) determined by cardiac magnetic resonance (p=0.34). Addition of biweekly 50,000 IU vitamin D3 to antihypertensive therapy did not improve regression of LV mass index compared with placebo at 1 year.
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