CORRESPONDENCE: LETTER TO THE EDITOR
Vitamin D Deficiency and Myocardial Dysfunction
Stefan Pilz, MD* and
Andreas Tomaschitz, MD
* Department of Internal Medicine, Division of Endocrinology and Nuclear Medicine, Medical University of Graz, Auenbruggerplatz 15, 8036 Graz, Austria (Email: stefan.pilz{at}chello.at).
In a recent review, Lee et al. (1) have outlined the role of vitamin D deficiency as a cardiovascular risk factor. In this letter, we want to point out that direct effects of vitamin D on the myocardium might partially explain the link between vitamin D deficiency and adverse cardiovascular outcome. This notion is supported by observations that human cardiomyocytes express enzymes for the metabolism of vitamin D as well as a functional vitamin D receptor, which is up-regulated in myocardial hypertrophy (2,3). In animal models of heart failure, active vitamin D treatment was shown to reduce cardiac hypertrophy and to attenuate myocardial dysfunction (4). Several genes that are up-regulated in the course of cardiac hypertrophy, involving those of natriuretic peptides and renin, are down-regulated by vitamin D (4). Importantly, there exists increasing molecular and clinical evidence that a sufficient vitamin D status is required for maintenance of diastolic function of the heart (3,4). Furthermore, there are several case reports of vitamin D–deficient children with dilated cardiomyopathy that could be successfully treated with vitamin D and calcium (5). In line with this are data from a cohort of over 3,000 patients referred for coronary angiography that showed a significant association of vitamin D deficiency with reduced left ventricular function (6). In the same study cohort, vitamin D deficiency was prospectively associated with deaths caused by heart failure and with sudden cardiac deaths (6). These results fit well with observations that active vitamin D treatment in hemodialysis patients was shown to regress cardiac hypertrophy and to reduce QT interval and dispersion (4,7). In conclusion, there exists compelling evidence that vitamin D supplementation might be useful for the prevention and treatment of myocardial diseases.
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1. Lee JH, O'Keefe JH, Bell D, Hensrud DD, Holick MF. Vitamin D deficiency: an important, common, and easily treatable cardiovascular risk factor? J Am Coll Cardiol 2008;52:1949-1956.[Abstract/Free Full Text]2. Chen S, Glenn DJ, Ni W, et al. Expression of the vitamin D receptor is increased in the hypertrophic heart Hypertension 2008;52:1106-1112.[Abstract/Free Full Text] 3. Tishkoff DX, Nibbelink KA, Holmberg KH, Dandu L, Simpson RU. Functional vitamin D receptor (VDR) in the t-tubules of cardiac myocytes: VDR knockout cardiomyocyte contractility Endocrinology 2008;149:558-564.[Abstract/Free Full Text] 4. Bodyak N, Ayus JC, Achinger S, et al. Activated vitamin D attenuates left ventricular abnormalities induced by dietary sodium in Dahl salt-sensitive animals Proc Natl Acad Sci 2007;104:16810-16815.[Abstract/Free Full Text] 5. Weber KT, Simpson RU, Carbone LD. Vitamin D and calcium dyshomeostasis-associated heart failure Heart 2008;94:540-541.[Free Full Text] 6. Pilz S, März W, Wellnitz B, et al. Association of vitamin D deficiency with heart failure and sudden cardiac death in a large cross-sectional study of patients referred for coronary angiography J Clin Endocrinol Metab 2008;93:3927-3935.[Abstract/Free Full Text] 7. Kim HW, Park CW, Shin YS, et al. Clacitriol regresses cardiac hypertrophy and QT dispersion in secondary hyperparathyroidism on hemodialysis Nephron Clin Pract 2006;102:21-29.[CrossRef]
Related Article
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Reply
- James H. O'Keefe, John H. Lee, David S.H. Bell, and Michael F. Holick
J. Am. Coll. Cardiol. 2009 53: 2012-2013.
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