Vitamin D is a hormone with pleiotropic effects; it controls calcium homeostasis, immune response, hemodynamic wall stress (by inhibiting Renin Angiotensin Aldosterone System, RAAS, and modulating the endothelial function) and inflammation. In the last decade, numerous studies have focused on the role of vitamin D levels in the setting of cardiovascular disease. In particular, it has been shown that insufficient Vitamin D levels are frequently observed among patients with cardiovascular disease.
Hypovitaminosis D activates the renin angiotensin system, causes endothelial dysfunction, reduces cardiomyocyte contractility and is associated with adverse left ventricular remodelling after myocardial infarction. Also, low Vitamin D levels are associated with worse outcome.
However, there is still no evidence in supporting an extended use of oral hormone supplementation. Two big epidemiological studies including patients from general practice suggested a U-shape correlation between Vitamin D levels and survival; furthermore, we observed similar results in survivors after myocardial infarction; the prognosis of patients with Vitamin D -i.e., 25-(OH) D- levels < 10 or > 30 ng/mL was markedly worse than the prognosis of patients with levels between 10 and 30 ng/mL. Probably, the new therapeutic strategy should consider the non-linear relationship that exists between Vitamin D levels and the prognosis and should provide careful measurements of the blood levels of this hormone.