American Journal of Medicine and Medical Sciences 2020, 10(6): 363-369 DOI:
10.5923/j.ajmms.20201006.03
Cardiovascular Diseases and Vitamin D
Akhmedova Nilufar
1
*, A
KHMEDOVA
D
ILOROM
2
1
PhD, Doctoral Student of the Department of Hospital Pediatrics №2, Tashkent Pediatric Medical Institute, Tashkent, Uzbekistan
2
Professor, Director,
Republican Specialized Scientific and Practical Medical Center of Pediatrics, Tashkent, Uzbekistan
Abstract
The article provides a review of the literature on the role of vitamin D in the development and course of various diseases of
the cardiovascular system. An analysis of the literature showed that the studies performed are often experimental in nature, while clinical
trial data are scarce and contradictory. In children, data on the role of vitamin D in the occurrence and progression of cardiovascular
diseases are sporadic, which indicates the need for further scientific research in this direction.
Keywords
Vitamin D, Cardiovascular disease
Vitamin D belongs to the group of secosteroid molecules,
enters the div with food, and is contained in a very limited
amount of food, and is able to be synthesized in the skin under the
influence of ultraviolet rays of sunlight [9].
In recent years, in the process of a thorough study of the broad
activity of vitamin D in the div, it has rightly been called the
hormone D. Obtained with ultraviolet or oral, vitamin D is
metabolized by hepatic hydroxylase to 25-hydroxyvitamin D
(25(OH) D), which is converted by the kidney 1b-hydroxylase to
the active form 1,25-dihydroxyvitamin D (1,25(OH) 2D -
calcitriol) and directly depends on the level of circulating 25(OH)
D. The main indicator in determining the status of vitamin D is
25(OH) D, as it circulates for longer periods (3-4 weeks) in the
blood. The optimal level of 25(OH) D is recognized as 75-150
NMOL
/L,
THE
DEFICIENCY
IS
CONSIDERED
TO
BE
50-75
NMOL
/L,
THE
DEFICIT
IS
LESS
THAN
50 nmol/L [59].
It exerts diverse biological effects when interacting with
specific receptors that are located in more than 40 target tissues
(osteoblasts, muscle cells, cardiomyocytes, pancreatic I-cells,
endothelium, cells of the nervous system, intestines, immune cells,
etc.) [20,43,54,78].
Vitamin D affects the biological reactions of the div through
the genomic mechanism (synthesis of Ca-binding protein,
osteocalcin, etc.) and rapid reactions of extragenomic origin
(synthesis
of
secondary
messengers:
cyclic
adenosine
monophosphate, inositol triphosphate, arachidonic acid). Each
tissue controls the activity of processes independently, but
depends on an adequate level of circulating 25(OH) D
[43,54,77,78].
* Corresponding author:
http://journal.sapub.org/ajmms
Copyright © 2020 The Author(s). Published by Scientific & Academic Publishing This work is
licensed under the Creative Commons Attribution International License (CC BY).
http://creativecommons.org/licenses/by/4.0/
Vitamin D deficiency is widespread throughout the world and
occurs in approximately 30-50% of the population. In most cases,
this problem is associated with pathology of the musculoskeletal
system: rickets in children and osteomalacia or osteoporosis.
According to some researchers, the functions of vitamin D are not
limited only to the control of calcium-phosphorus metabolism, it
also affects other physiological processes in the div, including
modulation of cell growth, neuromuscular conduction, immunity
and inflammation [54].
In recent years, convincing data have been obtained on the
relationship of vitamin D deficiency with pathology of the
cardiovascular system. A low level of vitamin D in humans is
associated with unfavorable risk factors for cardiovascular disease,
such as arterial hypertension, diabetes mellitus, dyslipidemia,
which are predictors of cardiovascular catastrophes, including
strokes and heart attacks. Vitamin D has been shown to have a
vasoprotective effect by improving endothelial dysfunction,
interferes with vascular and myocardial remodeling, improves
blood pressure parameters, helps to reduce the risk of left
ventricular hypertrophy, slows down fibrosis, reduces the risk of
developing atherosclerosis, reduces insulin resistance, and also
affects inflammation and immunity. According to studies, the
effect of vitamin D deficiency on the development of
atherosclerosis, arterial hypertension, cardiac arrhythmias and the
progression of chronic heart failure has been demonstrated
[10,32,46,55, 73].
Several of studies have shown that vitamin D deficiency
increases the risk of developing cardiovascular disease. Thus, in
the study, a low level of vitamin D compared with the optimal one
increased the risk of coronary heart disease by 40%, the risk of
developing myocardial infarction by 64%, the risk of early death
by 57%, and at least 81% the increased risk of death from heart
disease. Similar data were obtained after a survey of 27,686 people
[40], where it was found that
364
Akhmedova Nilufar and Akhmedova Dilorom: Cardiovascular Diseases and Vitamin D
people with vitamin D deficiency had a 77% higher risk of early
death, a 78% higher risk of developing a stroke, and 45% more
likely to develop coronary heart disease than those with a normal
level of 25(OH) D. It was also found that participants with vitamin
D deficiency are twice as likely to suffer from chronic heart
failure. Available data show that in most patients with chronic
heart failure, levels of 25(OH) D are in the insufficiency range,
which can be explained by the insufficient reception of ultraviolet
radiation, since diseases of the cardiovascular system accompanied
by chronic heart failure significantly reduce the mobility of
patients. Patients unable to move have a high risk of developing
severe vitamin D deficiency, which is known to lead to
osteomalacia [25,37,58].
A number of clinical and epidemiological studies have also
proved the relationship between calcitriol deficiency and
cardiovascular diseases such as congestive heart failure, coronary
heart disease, hypertension, valvular calcification, cerebrovascular
accident [1,33,52]. Vitamin D deficiency leads to a change in
smooth muscle cells of the vascular wall and its calcification,
endothelial dysfunction, an increase in lipid peroxidation and
inflammation factors. Vitamin D receptors are found in all cells of
the
cardiovascular
system.
Moreover,
endothelial
cells,
cardiomyocytes and vascular smooth muscle cells are capable of
producing the enzyme a1-hydroxylase, which converts calcium
idiol into active calcitriol [17 65,71,72].
The effect of calcitriol on the course of hypertension has been
established. When vitamin D is added to antihypertensive therapy
in patients with arterial hypertension, a more significant decrease
in systolic blood pressure occurs [59]. According to the results of
the NHANES population study in the USA (National Health and
Nutrition Examination.
Survey), when evaluating the data of 27153 patients, a
relationship was found between vitamin D deficiency (the level of
the examined was less than 20 ng /ml) and an increase in heart rate
and systolic blood pressure compared with patients with normal
calcitriol levels [30].
Low levels of vitamin D are a predictor of cardiovascular
disease, including strokes and heart attacks. Vitamin D has been
shown to have a vasoprotective effect by improving endothelial
dysfunction, interferes with vascular and myocardial remodeling,
improves blood pressure parameters, helps to reduce the risk of
left ventricular hypertrophy, slows down fibrosis, reduces the risk
of atherosclerosis, reduces insulin resistance, and also affects
inflammation and immunity [5,8,22,27,71,72].
However, patients with heart failure and vitamin D deficiency
have an extremely high risk of death by reason of sudden death
due to cardiovascular disease. Vitamin D affects genetic
expression associated with all types of cardiovascular cells,
thereby contributing to the regulation of cell differentiation,
apoptosis, hormone production and oxidative stress [10,15,69,73].
Vitamin D supplementation may be effective in hypocalcemic
cardiomyopathy, as shown in studies of the
pediatric population with cardiomyopathy and heart failure
associated with rickets [54,68].
The first publications on the relationship of vitamin D
deficiency with the development of hypertension appeared in the
70s of the last century. So, in 1979 S.G. Rostand reports that
people living in higher latitudes around the world have an
increased risk of developing atrial hypertension. The author
suggested that the cause of this phenomenon is a tendency to
develop vitamin D deficiency in people living farther from the
equator [58].
The number of studies that confirm the role of vitamin D in the
development of arterial hypertension is growing every year. The
study proved the inverse relationship between the level of 25(OH)
D and an increase in blood pressure [39,71,72]. Other studies have
shown an increase in the risk of hypertension by 3.03 times in men
and 1.42 times in women with vitamin D deficiency compared
with the general population [18,19,28]. It was also found that the
initial level of 25(OH) D in blood serum below 30 ng/ml is
associated with an increase in the risk of arterial hypertension by
1.47 times [18,28,48,71].
Experimental and clinical data indicate that vitamin D
deficiency directly contributes to the development of hypertension
[26,29]. Moreover, vitamin D deficiency is an independent
predictor of hypertension, which does not depend on age, div
mass index, physical activity, race, and the presence of menopause
[19].
The renin-angiotensin-aldosterone system occupies a very
important place in the control of blood pressure, vascular tone and
water-salt metabolism. There are potential mechanisms that may
explain the association of vitamin 1.25(OH) 2D deficiency and
increased blood pressure. According to recent studies, 1,25(OH)
2D is involved in the regulation of the renin-angiotensin-
aldosterone system by suppressing the expression of the renin
gene. An experiment was conducted on laboratory mice that
inhibited vitamin D receptors by pharmacological preparations,
while a sharp increase in the level of renin and angiotensin II was
recorded, which in turn stimulated the development of arterial
hypertension and left ventricular myocardial hypertrophy
[12,42,71].
Carriage of certain polymorphisms of the vitamin D receptor
gene may be accompanied by a decrease in the expression of
endothelial nitric oxide (NO) synthetase, which will inevitably
lead to a decrease in the bioavailability of NO, the manifestation
of which will be an increase in vascular stiffness and the
development of endothelial dysfunction [2,28]. It has been
experimentally shown that 1,25(OH) 2D can increase NO
production in endothelial cells [2].
Vitamin D, affecting various pathophysiological processes,
such as fibrosis, inflammation and repair, provides structural and
functional safety of the kidney and myocardium, is able to slow
the progression of cardiorenal syndrome and allograft nephropathy
by 38%, which is confirmed in clinical studies of Russian
scientists [29]. With an increase in the expression of the nuclear
vitamin D
American Journal of Medicine and Medical Sciences 2020, 10(6): 363-369
365
receptor in the glomerulus and proximal nephron, fast non-
genomic mechanisms are launched, which are realized in the
multilevel defense of the nephron, preventing inflammation,
fibrosis and apoptosis, stimulating its natural regeneration and
repair. And with the expression of the nuclear vitamin D receptor
in the distal nephron, "slow" genomic effects are realized -
maintaining the repair and functional activity of the tubules. The
renoprotective effect of vitamin D is also realized due to a certain
decrease in blood pressure. In the work of A.N. Kharlamova et al.
Vitamin D has been shown to be able to reduce systolic blood
pressure by at least 8% [29].
In patients with arterial hypertension who were exposed to
ultraviolet rays for 3 months more than 3 times a week, the level
of calcitriol increased by about 180%, and blood pressure, both
systolic and diastolic, decreased by 6
MM
H
G
. A
RT
. A
PROVEN
CONTRIBUTION
TO
THE
NORMALIZATION
OF
BLOOD
PRESSURE
IS
THE
SUPPRESSION
OF
VITAMIN
D
SYNTHESIS
OF
RENIN
IN
THE
JUXTAGLOMERULAR
APPARATUS
OF
THE
KIDNEY
BY
VITAMIN
D
[13,58,63,74]. It has been shown that vitamin D reduces the
expression of the renin gene through a receptor-dependent
mechanism, thus reducing the concentrations of renin and
angiotensin II, which ultimately leads to a decrease in aldosterone
production and an improvement in the course of arterial
hypertension [3,67]. However, according to some authors, there
was no association between a decrease in blood pressure and the
use of vitamin D in various groups of patients [27,66,68].
The data on the antihypertensive effects of vitamin D need to
be clarified in further studies. The correlation between vitamin D
deficiency and subsequent serious adverse vascular disorders has
been confirmed in the study. Levels of 25(OH) D were measured
at the start of the study and after 5.4 years. The frequency of fatal
and non-fatal cases (ischemia, stroke, or heart failure) was 53 and
80%, respectively, and it was higher in subjects with low levels of
vitamin D. A correlation was found between vitamin D deficiency
and arterial hypertension
[70].
According to the results of another no less large study, it was
found that patients with a low level of 25(OH) D (<37.5
NMOL
/L)
COMPARED
WITH
SUBJECTS
WITH
A
SUFFICIENT
LEVEL
OF
25(OH)
D (>75 nmol/L) are at risk of developing myocardial infarction
more than doubled [20].
A cohort study in Germany, which included 3258 patients with
cardiovascular disease lasting 7.7 years, confirmed that patients
with a low level of 25(OH) D double the risk of death of
cardiovascular origin, in contrast to patients with a normal level of
25(OH) D [11].
Analyzing the numerous data obtained on the prognostically
adverse effects of vitamin D deficiency, the medical community
came to the conclusion that it is necessary to correct this
hypovitaminosis. This idea was clearly demonstrated by a
prospective study conducted in the UK. According to the authors,
a two-fold increase in the concentration of 25(OH) D in blood
plasma compared with the low initial level was associated with a
20% reduction in mortality from cardiovascular diseases and a
23% decrease
in total mortality [66].
Any damage to the endothelial layer of the vascular wall can
lead to endothelial dysfunction, which ultimately plays a key role
in the development of atherosclerosis. Moreover, the protective
role of vitamin D in reducing the risk of developing
atherosclerosis is to increase the production of endothelial NO
[44]. Decrease the adhesion and aggregation of platelets, reduce
oxidative stress, regulate muscle tone of blood vessels, decrease
the release of vasoconstrictive metabolites, and suppress the
release of pro-inflammatory cytokines, modulating the immune
response and inhibiting the proliferation and migration of smooth
muscle cells.
In experimental studies, it was proved that the active metabolite
of vitamin D - 1.25 (OH) 2D reduces the deposition of mineral
deposits in the inner shell of arteries, and regulates the content of
calcium and phosphorus in the blood serum [25,43,50]. An
increase in stiffness of the vascular wall is an important factor in
the development of atherosclerosis. Studies have shown that
vitamin D deficiency affects arterial stiffness. It was shown that in
patients with a level of 25(OH) D less than 20 ng/ml, the pulse
wave velocity in the aorta was more than 9 m/s (at a rate of 4-6
m/s). An increase in pulse wave velocity is directly correlated with
an increased risk of developing atherosclerosis. The authors
concluded that the lower the level of vitamin D, the greater the
stiffness of the arteries, and regular maintenance of a normal level
of vitamin D contributes to a twofold reduction in the risk of
developing atherosclerosis [40]. An increase in the concentration
of 25(OH) D to 30-60 ng/ml reduces the risk of obliterating
atherosclerosis of the vessels of the lower extremities by 80%
[24].
Inflammation plays an important role in the development of
atherosclerosis. The highly sensitive C-reactive protein (CRP) is
one of the most widely studied biomarkers of cardiovascular
inflammation, with a proven pro-inflammatory effect. Numerous
studies have confirmed that serum vitamin D levels are inversely
related to CRP concentrations [35,49,78].
The anti-inflammatory effect of vitamin D is multifactorial; it
also lies in the fact that a high blood concentration of 25(OH) D is
reliably associated with a high concentration of interleukin (IL) -
10 [76].
The cardioprotective effect of IL-10 is to suppress the
production of pro-inflammatory cytokines. It is proved that a low
concentration of IL-10 leads to severe atherosclerosis. Vitamin D
is able to eliminate this deficiency and, therefore, slow the
progression of atherosclerosis [38,59].
The role of vitamin D in inflammation is also undeniable
because its ability to suppress the release of tumor necrosis factor-
a (TNF-a) [7,23].
It should be noted that a deficiency of vitamin D leads to an
increase in cholesterol synthesis, which undoubtedly provokes the
development of atherosclerosis. An important enzyme in the
pathogenesis of atherosclerosis is HMG-CoA reductase - 3-
hydroxy-3-methylglutaryl-coenzyme A reductase, vitamin D is
able to inhibit it, exerting a
366
Akhmedova Nilufar and Akhmedova Dilorom: Cardiovascular Diseases and Vitamin D
synergistic
effect
with
statins.
There
are
publications
recommending the combined use of statins with vitamin D to
potentiate their effects [37].
Some authors recommend the use of high doses of vitamin D
(more than 800 IU
PER
DAY
)
TO
PREVENT
THE
DEVELOPMENT
OF
ATHEROSCLEROSIS
[26].
More evidence is being provided showing that vitamin D is
associated with many diseases and their complications, including
heart failure. Vitamin D deficiency has been found to play a
significant role in the pathogenesis of chronic heart failure.
However, patients with heart failure and vitamin D deficiency
have an extremely high risk of death. Vitamin D3 affects the
genetic expression associated with all types of cardiovascular
cells, thereby contributing to the regulation of cell differentiation,
apoptosis, hormone production and oxidative stress [45,61,68].
Vitamin D supplementation may be effective in hypocalcemic
cardiomyopathy, as shown in studies of the pediatric population
with cardiomyopathy and heart failure associated with rickets
[4,64,68].
Therefore, it is important to evaluate whether taking vitamin D
affects the hormonal and inflammatory markers, as well as the
health-related quality of life among patients with heart failure, to
achieve adequate circulating blood levels [6,20,34, 36,45].
A study conducted in 30 patients on predialysis with chronic
kidney disease and with secondary hyperparathyroidism to
determine the effect of regular vitamin D intake on left ventricular
diastole showed that regular intake of 1.25(OH) 2D increases left
ventricular diastole time, which contributes to reduce heart load
and the risk of developing chronic heart failure
[14,63].
In vitro studies have shown that vitamin D affects
cardiomyocyte contractility by altering the distribution of myosin
chains and modulating calcium intake in cardiomyocytes. Vitamin
D also affects growth, hypertrophy, collagen deposition and
cardiomyocyte differentiation, providing a key role for activation
of the nuclear vitamin D receptor in heart physiology [3,29].
The need to maintain a normal concentration of vitamin D
becomes quite obvious, since its deficiency makes a significant
contribution to the onset and progression of chronic heart failure.
A clinical study of the effect of vitamin D in 80 children with
heart failure revealed its positive effect on the myocardium and
pumping function of the heart [22].
In addition, treatment with calcitriol leads to a decrease in
plasma renin activity, a decrease in angiotensin II levels, a
decrease in blood pressure and a decrease in myocardial
hypertrophy [28,37].
Prospective observations show that low concentrations of
vitamin D are associated with an increased risk of developing
cardiovascular diseases, mortality from them and mortality from
all causes [44,51,67,69].
These data are important for health care, as vitamin D
deficiency is widespread among children and adults. It is
necessary to take into account the fact that patients suffering from
hypertension, coronary heart disease, chronic heart
failure, as a rule, people are not always mobile, forced to lead a
sedentary lifestyle, are less likely to leave the house, are few in
the sun, so they Vitamin D deficiency may well develop.
The medical community is inclined to believe that the
correction of vitamin D deficiency is of great prognostic value.
Vitamin D treatment has a low cost, ease of use, and prevention
additionally contributes to the formation of a healthy lifestyle
[5,47,53,56,64,69].
However, further clinical and experimental studies are needed
to study in more detail the mechanisms of the negative effects of
vitamin D deficiency on the cardiovascular system. Currently, the
effect of vitamin D therapy on such indicators of patients with
chronic heart failure as the cardiac output fraction, muscle
strength, concentration of pro-inflammatory cytokines and
cerebral natriuretic peptide, general clinical condition and quality
of life has not been studied much. More research is needed to
determine the role of vitamin D deficiency in the development and
progression of chronic heart failure in children with
cardiomyopathies, as well as to determine the role of vitamin D in
the treatment of this disease.
Thus, an analysis of the available data suggests that vitamin D
plays an important role in the functioning of the cardiovascular
system. Conducted studies are often experimental in nature, while
clinical trial data are scarce and contradictory. In children, data on
the role of vitamin D in the occurrence and progression of
cardiovascular diseases are sporadic, which indicates the need for
further scientific research in this direction.
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