Introduction
Vitamin D (VitD) is an important steroid hormone in bone and mineral physiology, mainly due to its effects on calcium and phosphorus metabolism (1). By binding to VitD receptors in the whole body, including endothelium, vascular smooth muscle cells, and cardiomyocytes of its active metabolite, it also affects many vital functions such as homeostasis, autoimmunity, synthesis of inflammatory interleukins, cell proliferation, and differentiation, and blood pressure regulation (2-8). The prevalence of VDD can be at 30-50% (9,10). The main risk factors are high altitude, winter season, low sun exposure, restricted dietary intake, and advanced age(especially in postmenopausal women) (10,11).
Although its pathophysiology is not fully known, VDD has been linked with various cardiovascular outcomes; hypertension, adverse cardiac events, acute myocardial infarction complications, arterial stiffness, and inverse cardiac remodeling processes cause myocardial fibrosis, systolic and diastolic dysfunction (1,12-15). Hyperstimulation of the renin-angiotensin-aldosteron system(RAAS) and sympathetic nervous system, consequently increasing systemic inflammation, fluid-electrolyte balance distortions, and continuing these conditions in a vicious circle, can be considered as the underlying mechanism (13, 15, 16). Sunbul M. et al. showed that basal VitD values ​​might adversely associated with left ventricular basal global longitudinal strain values. VitD therapy may have positive effects on myocardial deformation (17). But in Omidi F. et al study, the global longitudinal subendocardial deformations were not statistically significantly correlated with the presence or absence of VDD (18). In addition, it was stated in a letter to the editor that age and renal insufficiency may play a role in the background of myocardial deformation in VDD (19).
Secondary hyperparathyroidism can be seen at rates 18-25% in VDD, which increases with age (20). Secondary hyperparathyroidism may be associated with disease severity in congestive heart failure, especially in older, due to bone loss and osteoporosis (21). When the literature is reviewed, there may be a relationship between PTH levels and arterial stiffness, coronary atherosclerosis, abnormal left ventricular function (global longitudinal strain), LV asynchrony, brachial flow-mediated dilatation (bFMD) (adversely), especially in primary hyperparathyroidism; a regression in pulse wave velocity and improvement in global longitudinal strain with parathyroidectomy (22-25). Although this finding could not be reached with primary hyperparathyroidism in a different study, improvements in pulse wave velocity were also observed using cinacalcet; a calcimimetic agent that provides a decrease in PTH levels in chronic renal failure and secondary hyperparathyroidism, in literature (26,27).
The relationship between VDD and hyperparathyroidism with arterial stiffness has been shown separately, as mentioned above (12,15,22,23). Pirro et al. investigated independent associations between VitD, PTH levels, and arterial stiffness in the postmenopausal stage with normal kidney functions. In this study, an inverse relationship, albeit weak, was found between VitD levels and pulse wave velocity. This relation was significantly associated with PTH levels regardless of existing risk factors and factors involving bone formation (28).
The risk of cardiovascular disease increases in the postmenopausal period, especially hormonal changes (29). Menopause can be considered as a confounding factor in terms of cardiac risks. In the light of these pieces of information and taking into account the missing points, our study aims to reveal the differences that secondary hyperparathyroidism will create on endothelial and diastolic functions, if present, using echocardiography, carotid, and brachial tDi in premenopausal women with VDD independent of confounding risk factors.