Does Vitamin D Provide Added Benefit to Antihypertensive Therapy in Reducing Left Ventricular Hypertrophy Determined by Cardiac Magnetic Resonance?

Author:

Levy Phillip D12,Twiner Michael J12ORCID,Brody Aaron M12,Dawood Rachelle12,Reed Brian12,Mango LynnMarie12,Gowland Laura1,Grandits Greg3,Svendsen Kenneth3,Haacke Ewart Mark4,Li Tao5,Zhang Liying26,McNaughton Candace D7,Flack John M8

Affiliation:

1. Department of Emergency Medicine, Wayne State University , Detroit, Michigan , USA

2. Emergency Medicine, Integrative Biosciences Center, Wayne State University , Detroit, Michigan , USA

3. Division of Biostatistics, School of Public Health, University of Minnesota , Minneapolis, Minnesota , USA

4. Department of Radiology and College of Engineering, Wayne State University , Detroit, Michigan , USA

5. Department of Radiology, School of Medicine, University of Washington , Seattle, Washington , USA

6. Department of Family Medicine and Public Health Sciences, Wayne State University , Detroit, Michigan , USA

7. Department of Emergency Medicine, Vanderbilt University Medical Center and the Geriatric Research Education Clinical Center, Tennessee Valley Healthcare System VA Medical Center , Nashville, Tennessee , USA

8. Department of Internal Medicine, Southern Illinois University , Springfield, Illinois , USA

Abstract

Abstract 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.

Funder

NIH

National Institute on Minority Health and Health Disparities

Robert Wood Johnson Foundation Physician Faculty Scholars Program

NHLBI

American Heart Association Health Equity Research Network

MDHHS

MHEF

VA Office of Rural Health

Publisher

Oxford University Press (OUP)

Subject

Internal Medicine

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