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Several studies have shown that vitamin D may play a role in many biochemical mechanisms in addition to bone and calcium metabolism. Recently, vitamin D has sparked widespread interest because of its involvement in the homeostasis of the cardiovascular system. Hypovitaminosis D has been associated with obesity, related to trapping in adipose tissue due to its lipophilic structure. In addition, vitamin D deficiency is associated with increased risk of cardiovascular disease (CVD) and this may be due to the relationship between low vitamin D levels and obesity, diabetes mellitus, dyslipidaemia, endothelial dysfunction and hypertension. However, although vitamin D has been identified as a potentially important marker of CVD, the mechanisms through which it might modulate cardiovascular risk are not fully understood. Given this background, in this work we summarise clinical retrospective and prospective observational studies linking vitamin D levels with cardio-metabolic risk factors and vascular outcome. Moreover, we review various randomised controlled trials (RCTs) investigating the effects of vitamin D supplementation on surrogate markers of cardiovascular risk. Considering the high prevalence of hypovitaminosis D among patients with high cardiovascular risk, vitamin D replacement therapy in this population may be warranted; however, further RCTs are urgently needed to establish when to begin vitamin D therapy, as well as to determine the dose and route and duration of administration. © 2011 Elsevier B.V.

The aetiology of aortic aneurysms (AAs) is the subject of intense clinical investigation. One of the critical points in their pathogenesis is the disruption of the balance between vascular extracellular matrix deposition and degradation. AAs are common features in some genetically determined diseases of the connective tissue, such as Marfan and Loeys-Dietz Syndromes. Acquired factors determining an enhanced inflammatory state of the arterial wall also play a key role. Previous studies have determined the role of TGF-beta as the principal mediator of the pathogenesis of the alterations of the arterial wall homeostasis in aneurysms. The current medical management of any AA is mainly focused on the use of pharmacological agents that reduce hemodynamic stress of aortic wall, since hypertension is the major risk factor for the enlargement and rupture of the AAs. Thus, this approach is useful to reduce the risk of aneurysm rupture but is far from being a comprehensive pathophysiology-based therapeutic approach. Drugs with the potential of reducing the action of TGF-beta, which activation and expression has been reported to have a major role in the molecular pathogenesis of the aneurysms, improving matrix repair, decreasing the proteolytic pattern and inhibition of angiotensin converting enzyme as well as preventing angiotensin II-induced AT1R (angiotensin type 1 receptor) activation, can represent new options in the medical therapy of AAs. We propose that a combination of statins and PPAR-gamma agonist could be a useful adjunctive therapy in this condition. The new pathophysiology-based therapeutic approach, involving the pathological patterns and mechanisms leading to the rupture of the AAs, could represent an interesting additional tool in combination with the current established anti-hypertensive therapy.