Vitamin D deficiency may increase the risk of cardiovascular disease in adults, especially in people who also have hypertension, based on data from the Framingham Offspring Study.
More studies are needed to show whether correcting vitamin D deficiency could prevent or reduce the risk of cardiovascular disease, but the clinical implication of the finding is that correcting the deficiency, which is prevalent worldwide, could have a significant effect on public health, according to the study's authors.
Previous clinical studies have shown associations between lower levels of vitamin D and an increased risk of problems including prevalent cardiovascular disease, coronary artery calcification, and plasma renin activity (an indicator of high blood pressure). These associations may occur in part because vitamin D receptors are found in a range of tissues including vascular smooth muscle tissue, the lining of the interior surface of blood vessels, and heart muscle tissue.
But more data are needed to show whether vitamin D deficiency is a result of cardiovascular disease or a contributing factor. To determine the relationship between vitamin D status and the incidence of cardiovascular events in a population with no history of cardiovascular disease, Dr. Thomas J. Wang of Harvard Medical School, Boston, and his colleagues followed 1,739 participants in the Framingham Offspring Study for at least 5 years. The average age of the participants was 59 years, 55% were women, and all were white. The study consists of the children of participants in the original Framingham Heart Study that began in 1948.
In this study, a 25-hydroxyvitamin D (25-OH D) level lower than 15 ng/mL was used to define vitamin D deficiency. This value was chosen for consistency with other cross-sectional studies of the Framingham data and with hospital-based samples, although 25-OH D levels greater than 30 ng/mL are considered preferable for promoting bone metabolism, the researchers noted.
At the start of the study, 28% of the participants had 25-OH D levels lower than 15 ng/mL, and 9% had levels lower than 10 ng/mL (Circulation 2008 Jan. 29 [Epub doi:10.1161/circulationaha.107.706127]).
A total of 120 participants had a cardiovascular event after an average of 5.4 years of follow-up (approximately 8,069 person-years). Overall, those with 25-OH D levels lower than 15 ng/mL were significantly more likely to have had a cardiovascular event than were those whose 25-OH D levels were 15 ng/mL or higher. After adjusting for age and sex, the 5-year incidence rate was more than twice as high in those with 25-OH D levels lower than 15 ng/mL than in those with higher levels (4.4 vs. 8.9).
In particular, the highest rates of cardiovascular event risk were observed in subjects with hypertension as well as vitamin D deficiency. The 5-year rate of cardiovascular disease was more than twice as high in the subjects with hypertension and vitamin D deficiency, compared with the hypertensive subjects who were not vitamin D deficient (5.8 vs. 14.2).
Furthermore, the higher cardiovascular risk appeared to increase as vitamin D decreased in the hypertensive patients. When vitamin D levels were divided into three categories, the hazard ratios were 1.00, 1.93, and 2.51 for those with 25-OH D levels of 15 ng/mL or higher, 10-15 ng/mL, and lower than 10 ng/mL, respectively. But no similar progressions across categories of 25-OH D deficiency were noted among nonhypertensive subjects.
The cardiovascular events included 65 fatal or nonfatal coronary heart disease events, 28 fatal or nonfatal cerebrovascular events, 19 cases of heart failure, and 8 instances of claudication.
The study was limited because not all variables that affect vitamin D were measured. But using an objective measure of vitamin D (25-OH D) rather than relying on subjects' self-reports of vitamin D intake makes the findings stronger.
Although the findings suggest that treating vitamin D deficiency could reduce the risk of heart disease, the findings are not enough to advise a treatment plan, and more clinical and experimental research is needed. The study was supported in part by grants from the American Heart Association, the U.S. Department of Agriculture, and the National Institutes of Health. Dr. Wang, the lead author, had no financial conflicts to disclose.