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\begin{document}

\title{Vitamin D Deficiency in Premenopause: Endothelial and Diastolic
Functions With Hyperparathyroidism}



\author[1]{Onur Akhan}%
\author[2]{Mustafa Dogdus}%
\affil[1]{Affiliation not available}%
\affil[2]{Usak University Training and Research Hospital}%


\vspace{-1em}



  
  \date{May 29, 2024}


\begingroup
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\selectlanguage{english}
\begin{abstract}
Introduction: Vitamin D deficiency(VDD) is a common condition in all
ages worldwide, especially in winter, and causes several adverse
cardiovascular outcomes. Although there is conflicting information about
the causes of adverse cardiac events in VDD, the accepted leading cause
is a pathogenic relationship with hyperparathyroidism. Aim: We aim to
demonstrate hyperparathyroidism's effects, if present, on endothelial
and diastolic functions using echocardiography, carotid, and brachial
tissue Doppler imaging (tDi) in premenopausal women with VDD independent
from confounding risk factors. Methods: Our study is a cross-sectional,
observational study investigating premenopausal women aged 18-50 who
applied to internal medicine department. The patients are divided into
two groups according to parathyroid hormone(PTH) levels (Normal PTH 41
patients, abnormal PTH 27 patients). Study groups are analyzed for basal
characteristics, standard echocardiographic evaluation, carotid, and
brachial artery tDi features. Results: There were no significant
differences in age, height, weight, body mass index(BMI), and blood
pressures between the groups (all p values\textgreater{}0.05). The rate
of severe VDD was 76\%. In terms of diastolic parameters, prolongation
of A wave durations and decreased E/A ratio were observed in the
secondary hyperparathyroidism (p values 0.042 and 0.031, respectively).
Also, carotid IMT is significantly higher in secondary
hyperparathyroidism(p=0.034). Conclusion: Our study showed that high PTH
levels have adverse effects on diastolic(A wave, E/A ratio) and
endothelial functions(carotid IMT) in premenopausal women diagnosed with
VDD, even in the absence of other confounding risk factors. We can state
that our study's findings will contribute to the literature and are
predictive for future studies.%
\end{abstract}%



\sloppy


\textbf{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.

\textbf{Materials and Methods}

Our study is a cross-sectional, observational study, includes
premenopausal women aged 18-50 who applied to internal disease and were
diagnosed with VDD. Our study was carried out in Bilecik City in the
period November-December 2020. Bilecik, located at an approximate
altitude of 500 meters and a latitude of 40\selectlanguage{ngerman}°N, is a small city in
Turkey. During the study period, the average temperature in Bilecik city
was determined as 8.5 degrees Celsius (maximum 13°C, minimum 2°C).

The fasting routine blood samples (including PTH levels) were
investigated of these patients' internal medicine records. In evaluating
VitD, the serum circulating 25-hydroxyvitamin D {[}25(OH)D{]} level was
measured. VDD was defined as a serum 25-hydroxyvitamin D level of
\textless{}20 ng/ml, and severe VDD was also defined as a serum
25-hydroxyvitamin D level of \textless{}10 ng/ml (30). Patients
diagnosed with VDD who have not yet started replacement therapy were
evaluated using essential echocardiographic evaluation, brachial and
carotid tissue doppler, and flow-mediated dilatation. Local ethics
committee approval was obtained.

Patients diagnosed with diabetes mellitus, hypertension, hyperlipidemia,
coronary artery disease, congestive heart failure, peripheral artery
disease, moderate-severe heart valve disease, cardiomyopathies, thyroid
dysfunction, chronic obstructive pulmonary disease, malignancy,
rheumatological disease, active infection, kidney failure, liver
disease, hormonal diseases (affecting calcium level, including primary
hyperparathyroidism), obesity (BMI\textgreater{}30), drug usage
(including beta-blockers and medications affect calcium level),
menopause, pregnancy, and heavy alcohol users and smokers were excluded
from the study. A total of 68 patients were included in the survey by
excluding patients with low echogenicity.

Patients were divided into two groups according to their PTH levels.
While PTH levels were in the normal reference range (\textless{}65
pg/ml) in 41 patients, it was high in 27 patients. Groups were compared
in terms of basal demographic characteristics, standard
echocardiographic evaluation, carotid and brachial artery tDi features.

\textbf{Image Recordings and Analysis}

Standard echocardiographic measurements; left ventricular ejection
fraction(EF) with modified Simpson method, tissue Doppler measurements,
and cardiac valve evaluations performed with transthoracic
echocardiography (EPIQ 7 echocardiography device (Philips, Amsterdam,
Netherlands)) with reference of 2015 ASE (American Society of
Echocardiography) guideline (31). In echocardiographic tissue Doppler
evaluations, global systolic and diastolic ventricular function
indicator, the myocardial performance index(MPI), also known as Tei
Index, is also calculated. The formula '{[}Isovolumetric contraction
time(IVCT)+Isovolumetric relaxation time(IVRT){]}/Ejection Time(ET)' is
used for both left ventricle lateral and septal parts(32,33).

Carotid systolic and diastolic diameters, intima-media thickness (IMT),
and bFMD performed with duplex ultrasound (Toshiba Sonolayer SSA 270 A
equipped with a 7.5 Mhz linear array transducer, Toshiba Medical
Systems, Japan). The distal 1 cm of each common carotid artery's far
wall and plaque-free segments were used for carotid IMT measurements.
The mean carotid IMT value was derived from the measurements made in
both carotid arteries' locations (34).

All ultrasonic examinations were made with continuous
electrocardiography (ECG), in a semi-dark room. Brachial artery
measurements were made by keeping the patient's left arm steady in a
horizontal plane, approximately 2 cm above the elbow, in the
longitudinal plane at the diastolic phase. Basal measurements were taken
after 15 minutes of rest in the fasted state. The appropriate
sphygmomanometer cuff located in the patient's upper arm inflated to the
level of 200 mmHg and waited for 5 minutes, and recordings will be
continued until 2 minutes after cuff deflation. The maximum rate of
change, which is also named as peak bFMD was calculated in a
percentage(\%) with the formula '{[}(maximum diameter - basal
diameter)/basal diameter{]}*100' (35,36).

\textbf{Statistical Analysis}

Statistical analysis was performed by the SPSS version 20.0 (IBM,
Armonk, New York, United States). The normality of distribution was
examined by using both the Shapiro-Wilk W test. Descriptive statistical
methods, including percent and mean ± standard deviation(SD) or median
(interquartile range{[}IQR{]}), were used to provide the basic features
of the data. Mann-Whitney U test was used for non-normally distributed
continuous variables for normal PTH levels group and secondary
hyperparathyroidism group. A p-value less than 0.05 was accepted as
significant.

\textbf{Results}

There were no significant differences in age, height, weight, BMI, blood
pressures, and laboratory parameters between the groups \emph{(all p
values\textgreater{}0.05)} . Baseline characteristics and laboratory
results of the groups are shown in Table 1. Vitamin D and PTH levels are
demonstrated in Figure 1.

Vit D levels \selectlanguage{english}\selectlanguage{english}were relatively low in the secondary hyperparathyroidism
compared to the group with normal PTH levels \emph{(mean values 8.1+-4.1,
9.3+-7.8, respectively; p=0.369)} . The rate of severe VDD in our study's
total population was 76\%.

Echocardiographic and peripheral tDi findings are shown in Table 2. Some
significant differences related to diastolic parameters are observed,
which will explain in the discussion section in detail. Other
echocardiographic parameters were similar, including EF \emph{(p
values\textgreater{}0.05)} . Regarding carotid and brachial tDi, only a
significant difference was observed according to carotid IMT
(\emph{p=0.034)} .

\textbf{Discussion}

VDD is a common condition that can be seen in all age groups worldwide,
especially in winter, and causes several adverse outcomes, including
cardiovascular diseases (38). The removal of inhibitory effects on the
RAAS system and proinflammatory cytokines can be accepted as the primary
mechanism for cardiovascular involvement in VDD (13,15,16,37).
Hyperparathyroidism cases secondary to VDD are not uncommon and lead to
adverse cardiac outcomes (20,38).

Menopause may be considered a risk factor for VDD and, consequently,
secondary hyperparathyroidism (28,39). It is also known that
cardiovascular risk increases in menopause with hormonal changes
(29,39). Therefore regardless of the confounding factors, we aimed 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.

As stated before, the prevalence of secondary hyperparathyroidism is
approximately 18-25\% according to vitamin D levels, the prevalence of
secondary hyperparathyroidism in severe VDD (\textless{}10 ng/ml) was
shown as 33\%. In Gomez-Alonso C et al. study, the autumn-winter months
covered 60\% of the study period in 40degN latitude in a city 400 meters
above sea level (20). However, Islam MZ. et al. showed that this
prevalence could vary in the range of 16\% and 89\%, according to ethnic
differences (40). Secondary hyperparathyroidism was observed with a rate
of 39.7\% in our study. Ethnic differences, characteristics of the city,
and the time interval may have influenced these differences.

In the secondary hyperparathyroidism group, A wave durations were
longer, and E/A ratios were lower than the group with normal PTH
levels\emph{(p values are 0.042 and 0.031, respectively)} . It can be
accepted that the prolongation of the A wave duration is effective in
decreasing the E/A ratio. In Pandit A. et al. study investigating VDD
and left ventricular diastolic dysfunction in a population of 67\%
women, there was no significant relationship between vitamin D levels
and diastolic parameters (Deceleration time, e' wave, E/A, and E/e'
ratios) (41). In Pilz S. et al. study, which evaluated approximately 600
patients over 65 years of age, the prevalence of diastolic dysfunction
might increase seasonally in VDD. Even in the seasons with high risk,
VDD lost its significance when adjusted for age and cardiovascular risks
(42).

In 'the fifth Tromso study,' myocardial systolic contraction rates were
significantly lower in the secondary hyperparathyroidism group
(approximately 100 patients), even after adjustments for
covariables\emph{(for lateral s' and septal e ', s' waves; p
\textless{}0.05)} . In the follow-up of these patients 6-12 months
later, in case of persistently elevated PTH, a similar trend was
observed in myocardial systolic contraction velocities, but the
significance is lost. This study's difference from our study was that
the mean VitD values after the relevant unit conversions\selectlanguage{english}\selectlanguage{english}(nmol/l to
ng/ml) were 17.2+-5.0 in the high PTH group and 18.7+-5.4 ng/ml in the
normal PTH group\emph{(p\textgreater{}0.05) (In our study VitD levels
8.1+-4.1 and 9.3+-7.8 ng/ml; respectively)} . Also, no significant
difference was found in diastolic parameters (E, A waves, IVRT,
pulmonary vein atrial reversal flow) in 'the fifth Tromso study.' (43).

The study's design differences, the population, the city where the study
was conducted, and some other factors may have been influential in these
differences. Suppose we interpret the findings of diastolic parameters
in our study; there may be additional impairment in diastolic functions
due to PTH levels in vitamin D deficiency, even if there is no
confounding factor.

Lim S. et al. showed VDD is associated with endothelial dysfunction and
coronary atherosclerosis (44). In diabetic nephropathy patients, VDD is
significantly linked with increase in carotid IMT, but no significant
relation was found in chronic renal failure patients (45,46). Studies
conducted with chronic renal failure and secondary hyperparathyroidism
found a significant relationship between carotid thickness and PTH
levels (47). In Yankouskaya L. et al. study, which investigates women
with arterial hypertension, the effects on endothelial dysfunction were
explained by the pathogenic relationship between VDD and PTH levels, not
a single factor (48).

Our study carotid IMT mean values are 0.6+-0.1 mm in secondary
hyperparathyroidism and 0.5+-0.1 mm in the group with normal PTH
levels\emph{(p=0.034)} , no other significant difference related to
carotid and brachial artery. We can say that hyperparathyroidism may
cause an increase in carotid intima thickness independent of other risk
factors in VDD.

As a result, we observed a significant relationship between PTH levels
and endothelial (carotid IMT) and diastolic functions (A wave duration,
E/A ratio) in premenopausal women with VDD, independent of all other
confounding factors. Therefore, patients should be evaluated in terms of
possible future cardiac risks by paying attention to PTH levels in
diagnosing VDD.

\textbf{Limitations}

A limited number of patients could be included in our study. Our study
population may not fully reflect the target population due to the
pandemic process, the inclusion of patients in a limited time frame (it
may have helped clarify the findings.), and the recruitment of only
patients referred to cardiology.

\textbf{Conclusion} Our study showed that PTH might adversely affect
diastolic functions (A wave, E/A ratio) and endothelial functions
(carotid IMT) in premenopausal women with VDD, independent of other
confounding risk factors. We can state that our results will contribute
to the literature since conflicting information in the literature and
confounding factors are included in these studies. The recent literature
is insufficient, and there is a need for further, multicentric studies
with advanced subgroup analyses and longer follow\selectlanguage{english}-up periods also with
other multi-modality imaging methods.

As a result of our study's findings, an awareness should also be created
regarding possible cardiac risks in high parathyroid hormone in VDD.

\textbf{Declarations}

\textbf{Conflict Of Interest and Funding}

There is no conflict of interest and no financial support in our study.
We want to thank our hospital's internal diseases departments for their
helpfulness in conducting our study.

\textbf{Availability Data and Material}

The data that support the findings of this study are available on
request from the corresponding author (Onur Akhan, akhanonur@gmail.com).
The data are not publicly available due to privacy or ethical
restrictions.

\textbf{Author contributions}

Concept/design: Onur Akhan, Data collection: Onur Akhan, Data
analysis/interpretation: Onur Akhan, Mustafa Dogdus, Drafting article:
Onur Akhan, Critical revision of article: Onur Akhan, Mustafa Dogdus:
Approval of article: Onur Akhan, Mustafa Dogdus

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\end{enumerate}

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