From Cardiology Today:
In a study of over 500 patients, low levels of the vitamin D marker 25-hydroxyvitamin D significantly increased the likelihood of arterial stiffness and endothelial dysfunction in the conductance and resistance blood vessels.
“Our findings … provide mechanistic explanation of how depressed vitamin D status, by precipitating vascular dysfunction, might predispose individuals to a higher risk for the development of CVD and adverse events,” the researchers wrote.
n the study, a group of researchers from Georgia and the United Kingdom measured 25-hydroxyvitamin D (25-OH D) in 554 subjects between the ages of 20 and 79. They then determined arterial stiffness as well as endothelial and microvascular function.
Overall, mean 25-OH D among the population was 31.8 ± 14 ng/ml. Following adjustment for several variables, including age, sex, race, BMI, medication use, total cholesterol, LDL, triglycerides and CRP, 25-OH D was associated with reactive hyperemia index (P<.001), subendocardial viability ratio (P=.001), flow-mediated vasodilation (P=.03), augmentation index (P=.03) and pulse wave velocity (P=.04).
Among those with vitamin D deficiency (n=42), 25-OH D normalization by 6 months resulted in increases in both reactive hyperemia index (P=.009) and subendocardial viability ratio (P=.04), and a decrease in mean arterial pressure (P=.02).
As a result of these findings, the researchers called for larger trials to assess the effect of vitamin D therapy on prevention of CVD in individuals with vitamin D insufficiency.