2015
Ioana Mozos and Otilia Marginean

 

Abstract

The aim of the present paper was to review the most important mechanisms explaining the possible association of vitamin D deficiency and cardiovascular diseases, focusing on recent experimental and clinical data. Low vitamin D levels favor atherosclerosis enabling vascular inflammation, endothelial dysfunction, formation of foam cells, and proliferation of smooth muscle cells.

The antihypertensive properties of vitamin D include suppression of the renin-angiotensin-aldosterone system, renoprotective effects, direct effects on endothelial cells and calcium metabolism, inhibition of growth of vascular smooth muscle cells, prevention of secondary hyperparathyroidism, and beneficial effects on cardiovascular risk factors.

Vitamin D is also involved in glycemic control, lipid metabolism, insulin secretion, and sensitivity, explaining the association between vitamin D deficiency and metabolic syndrome. Vitamin D deficit was associated in some studies with the number of affected coronary arteries, postinfarction complications, inflammatory cytokines and cardiac remodeling in patients with myocardial infarction, direct electromechanical effects and inflammation in atrial fibrillation, and neuroprotective effects in stroke.

In peripheral arterial disease, vitamin D status was related to the decline of the functional performance, severity, atherosclerosis and inflammatory markers, arterial stiffness, vascular calcifications, and arterial aging. Vitamin D supplementation should further consider additional factors, such as phosphates, parathormone, renin, and fibroblast growth factor 23 levels.

 

Conclusions

Maintaining an optimal vitamin D serum level seems important not only for calcium homeostasis but also for cardiovascular risk, blood pressure control, prevalence of stroke, metabolic syndrome, and peripheral artery disease. Observational data support the link between vitamin D status and cardiovascular diseases, and vitamin D deficiency can be considered a cardiovascular risk marker.

Vitamin D exerts its cardiovascular effects by reducing the activity of the renin-angiotensin-aldosterone system, lowering blood pressure values, and having an anti-inflammatory, antiproliferative, antihypertrophic, antifibrotic, antidiabetic, and antithrombotic effect and beneficial modulation of classical cardiovascular risk factors.

The mentioned effects might be very important for public health, considering the high prevalence of vitamin D deficiency, the aging population, and the indoor oriented lifestyle.

Vitamin D deficiency is treatable and supplementation is inexpensive. Vitamin D could be combined with antihypertensive agents in order to control blood pressure, as a simple, inexpensive, and important prophylactic method in order to prevent cardiovascular morbidity, especially in the elderly.

Even small gains in prevention are important from a public health perspective. Further proteomics and basic research studies are needed in order to identify the missing pieces in the vitamin D-cardiovascular disease puzzle. Large randomized controlled trials could confirm the promising findings of observational studies, considering endothelial function, arterial stiffness, and patients undergoing percutaneous coronary interventions.

Guidelines are needed in order to establish optimal vitamin D level and intake, to maintain a healthy vitamin D status in patients with cardiovascular diseases, and to include vitamin D blood tests, genotyping for vitamin D receptor variants, and serum calcium and phosphates level and bone mineral density as mandatory in evaluating patients with cardiovascular disease.

The benefits of screening and treating vitamin D deficiency would be, probably, reflected by reduced cardiovascular morbidity and mortality. Vitamin D supplementation should further consider additional factors, such as phosphates, PTH, RAA, and fibroblast growth factor 23.