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.