Journal
EUROPEAN HEART JOURNAL
Volume 34, Issue 48, Pages 3691-3698Publisher
OXFORD UNIV PRESS
DOI: 10.1093/eurheartj/eht166
Keywords
Vitamin D; Vascular risk factors; Cardiovascular disease
Categories
Funding
- National Institute for Health Research [CL-2011-11-003] Funding Source: researchfish
- NHLBI NIH HHS [P20 HL113451] Funding Source: Medline
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Vitamin D deficiency, prevalent in 3050 of adults in developed countries, is largely due to inadequate cutaneous production that results from decreased exposure to sunlight, and to a lesser degree from low dietary intake of vitamin D. Serum levels of 25-hydroxyvitamin D (25-OH D) 20 ng/mL indicate vitamin D deficiency and levels 30 ng/mL are considered optimal. While the endocrine functions of vitamin D related to bone metabolism and mineral ion homoeostasis have been extensively studied, robust epidemiological evidence also suggests a close association between vitamin D deficiency and cardiovascular morbidity and mortality. Experimental studies have demonstrated novel actions of vitamin D metabolites on cardiomyocytes, and endothelial and vascular smooth muscle cells. Low 25-OH D levels are associated with left ventricular hypertrophy, vascular dysfunction, and reninangiotensin system activation. Despite a large body of experimental, cross-sectional, and prospective evidence implicating vitamin D deficiency in the pathogenesis of cardiovascular disease, a causal relationship remains to be established. Moreover, the cardiovascular benefits of normalizing 25-OH D levels in those without renal disease or hyperparathyroidism have not been established, and questions of an epiphenomenon where vitamin D status merely reflects a classic risk burden have been raised. Randomized trials of vitamin D replacement employing cardiovascular endpoints will provide much needed evidence for determining its role in cardiovascular protection.
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