A Prospective Randomized Controlled Trial of the Effects of Vitamin D Supplementation on Cardiovascular Disease Risk

Vitamin D (VitD) supplementation has been advocated for cardiovascular risk reduction; however, supporting data are sparse. The objective of this study was to determine whether VitD supplementation reduces cardiovascular risk. Subjects in this prospective, randomized, double-blind, placebo-controlled trial of post-menopausal women with serum 25-hydroxyvitamin D concentrations >10 and <60 ng/mL were randomized to Vitamin D3 2500 IU or placebo, daily for 4 months. Primary endpoints were changes in brachial artery flow-mediated vasodilation (FMD), carotid-femoral pulse wave velocity (PWV), and aortic augmentation index (AIx). The 114 subjects were mean (standard deviation) 63.9 (3.0) years old with a 25-hydroxyvitamin D level of 31.3 (10.6) ng/mL. Low VitD (<30 ng/mL) was present in 47% and was associated with higher body-mass index, systolic blood pressure, glucose, CRP, and lower FMD (all p<0.05). After 4 months, 25-hydroxyvitamin D levels increased by 15.7 (9.3) ng/mL on vitamin D3 vs. −0.2 (6.1) ng/mL on placebo (p<0.001). There were no significant differences between groups in changes in FMD (0.3 [3.4] vs. 0.3 [2.6] %, p = 0.77), PWV (0.00 [1.06] vs. 0.05 [0.92] m/s, p = 0.65), AIx (2.7 [6.3] vs. 0.9 [5.6] %, p = 0.10), or CRP (0.3 [1.9] vs. 0.3 [4.2] mg/L, p = 0.97). Multivariable models showed no significant interactions between treatment group and low VitD status (<30 ng/mL) for changes in FMD (p = 0.65), PWV (p = 0.93), AIx (p = 0.97), or CRP (p = 0.26).In conclusion, VitD supplementation did not improve endothelial function, arterial stiffness, or inflammation. These observations do not support use of VitD supplementation to reduce cardiovascular disease risk

Analysis of aortic remodeling and stiffness in patients with obstructive sleep apnea syndrome: Preliminary results

Obstructive sleep apnea (OSA) is a well-known risk factor for cardiovascular diseases. Several studies have shown that OSA is associated with vessel remodeling, but few studies have examined aorta. Aim: to analyse aortic remodelling in OSA. Methods: Thirty consecutive OSA patients (22 males and 8 females, aged 58.5 ± 13.2&nbsp;years) were studied. All patients underwent a morning blood gas analysis, a full cardiorespiratory evaluation, including nocturnal polygraphy and echocardiography, that assessed aortic root diameter (ARD) and aortic stiffness index (ASI). Patients were grouped as follows: Group 1, non-severe OSA (Apnea-Hypopnea Index; AHI &lt;30, 14 patients); Group 2, severe OSA (AHI ≥30, 16 patients). Results: No difference was found between the groups in ARD as absolute value (Group 1, 33.64 ± 0.91&nbsp;mm; Group 2, 33.64 ± 1.02, p = ns) and as normalized value for the body surface area&nbsp;– ARDi (Group 1, 16.72 ± 0.63&nbsp;mm/m2; Group 2, 16.09 ± 0.44, p = ns). Moreover, no difference was found in the ASI (Group 1, 14.04 ± 2.26; Group 2, 13.41 ± 2.22, p&nbsp;=&nbsp;ns). Considering all OSA patients, AHI showed an inverse correlation with ARDi (p&nbsp;=&nbsp;0.018) and ASI (p&nbsp;=&nbsp;0.0449). Moreover, the ASI showed a direct correlation with ARDi (p&nbsp;=&nbsp;0.01) and morning PaO2 (p&nbsp;=&nbsp;0.0349) as well as an inverse correlation with the oxygen desaturation index (ODI, p&nbsp;=&nbsp;0.031) and total time with apnea and hypopnea (p&nbsp;=&nbsp;0.039). Conclusion: No difference was found between severe and non-severe OSA in ARD. Surprisingly, the data show that the severity of OSA correlates inversely with the ASI and ARDi. The relation between PaO2 and stiffness might be explained by a feedback mechanism that tries to overcome the reduction of aortic elasticity due to night desaturation. These findings need to be investigated in further studies with a larger study population

Atherosclerosis screening by noninvasive imaging for cardiovascular prevention: a systematic review.

BACKGROUND: Noninvasive imaging of atherosclerosis is being increasingly used in clinical practice, with some experts recommending to screen all healthy adults for atherosclerosis and some jurisdictions mandating insurance coverage for atherosclerosis screening. Data on the impact of such screening have not been systematically synthesized. OBJECTIVES: We aimed to assess whether atherosclerosis screening improves cardiovascular risk factors (CVRF) and clinical outcomes. DESIGN: This study is a systematic review. DATA SOURCES: We searched MEDLINE and the Cochrane Clinical Trial Register without language restrictions. STUDY ELIGIBILITY CRITERIA: We included studies examining the impact of atherosclerosis screening with noninvasive imaging (e.g., carotid ultrasound, coronary calcification) on CVRF, cardiovascular events, or mortality in adults without cardiovascular disease. RESULTS: We identified four randomized controlled trials (RCT, n=709) and eight non-randomized studies comparing participants with evidence of atherosclerosis on screening to those without (n=2,994). In RCTs, atherosclerosis screening did not improve CVRF, but smoking cessation rates increased (18% vs. 6%, p=0.03) in one RCT. Non-randomized studies found improvements in several intermediate outcomes, such as increased motivation to change lifestyle and increased perception of cardiovascular risk. However, such data were conflicting and limited by the lack of a randomized control group. No studies examined the impact of screening on cardiovascular events or mortality. Heterogeneity in screening methods and studied outcomes did not permit pooling of results. CONCLUSION: Available evidence about atherosclerosis screening is limited, with mixed results on CVRF control, increased smoking cessation in one RCT, and no data on cardiovascular events. Such screening should be validated by large clinical trials before widespread use