Cardiovascular Diseases and Vitamin D

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Ахмедова, Н., & Халикова, Д. (2023). Cardiovascular Diseases and Vitamin D. in Library, 20(2), 363–369. извлечено от https://inlibrary.uz/index.php/archive/article/view/24532
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Аннотация

В статье представлен обзор литературы о роли витамина D в развитии и течении различных заболеваний сердечно-сосудистой системы. Анализ литературы показал, что проводимые исследования зачастую носят экспериментальный характер, а данные клинических исследований скудны и противоречивы. У детей данные о роли витамина D в возникновении и прогрессировании сердечно-сосудистых заболеваний единичны, что указывает на необходимость дальнейших научных исследований в этом направлении.

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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:

anilufar74@mail.ru

(Akhmedova

Nilufar) Published online at

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


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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


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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


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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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participation of vitamin D in the pathogenesis of diseases of the
cardiovascular system. Russian Bulletin of Perinatology and
Pediatrics. - 2018; 63: (5): 43-50. DOI: 10.21508 / 1027-4065-2018-
63-5-43-50.

[33] Larina VN, Raspopova TN. Mineral bone density and bone

metabolism in chronic heart failure. Kardiologiia. 2016; 56 (7): 33-
45 (In Russ.).

[34] Lavie CJ, Dinicolantonio JJ, Milani RV. Vitamin D and

cardiovascular health. Circulation. 2013; 128: 2404-6.

[35] Liefaard MC, Ligthart S, Vitezova A, Hofman A, Uitterlinden AG,

Kiefte-de Jong JC, et al. Vitamin D and C-Reactive


background image

368

Akhmedova Nilufar and Akhmedova Dilorom: Cardiovascular Diseases and Vitamin D

Protein: A Mendelian Randomization Study. PLOS ONE. 2015; 10
(7): e0131740.

[36] Liu LC, Voors AA, van Veldhuisen DJ van der Veer E., Belonje AM,

Szymanski MK et al. Vitamin D status and outcomes in heart failure
patients. Eur J Heart Fail 2011; 13: 619-625. DOI: 10.1093 / eurjhf /

HFR

032.

[37] Lynn Kane, Kelly Moore, Dieter Lutjohann, et al. Vitamin D3 Effects

on Lipids Differ in Statin and NonStatin- Treated Humans:
Superiority of Free 25-OH D Levels in Detecting Relationships. J
Clin Endocrinol Metab. 2013 Nov; 98 (11): 4400-9.

[38] Mallat Z, Besnard S, Duriez M, et al. Protective role of interleukin-10

in atherosclerosis. Circ Res. 1999; 85: E17-24.

[39] Martins D, Wolf M, Pan D, et al. Prevalence of cardiovascular risk

factors and the serum levels of 25-hydroxyvitamin D in the United
States: data from the Third National Health and Nutrition
Examination Survey. Arch Intern Med. 2007; 167: 1159 -116524.

[40] Mayer OJr, Filipovsky J, Seidlerova J, Vanek J, Dolejsova M,

Vrzalova J, Cifkova R. The association between low 25-
hydroxyvitamin D and increased aortic stiffness. J Hum Hypertens.
2012 Nov; 26(11): 650-5.

[41] McNally JD, Nama N., O'Hearn K., Sampson M., Amrein K., Iliriani

K. et al. Vitamin D deficiency in critically ill children: a systematic
review and meta-analysis. Critical Care 2017; 21(1): 287. DOI:
10.1186 / s13054-017-1875-y.

[42] Mehta V, Agarwal S. Does Vitamin D Deficiency Lead to

Hypertension? Cureus. 2017 Feb; 17; 9(2): e1038.

[43] Melaku L, Mossie A. Molecular mediators and controlling mechanism

of vascular calcification. Int J Clin Exp Physiol. 2017; 4: 3-14.

https://doi.org/10.4103/ijcep.ijcep_3_1

.

[44] Menezes AR, Lamb MC, Lavie CJ, DiNicolantonio JJ. Vitamin D and

atherosclerosis. Curr Opin Cardiol. 2014; 29 (6): 571-7.

[45] Moretti HD, Colucci VJ, Berry BD Vitamin D3 repletion versus

placebo as adjunctive treatment of heart failure patient quality of life
and

hormonal

indices:

a

randomized,

double-blind,

placebocontrolled trial. BMC Cardiovasc. Disord., 2017: 17(1): 274.

[46] Motiwalaa SR, Wang TJ Vitamin D and cardiovascular risk. Current

Hypertens Rep 2012; 14 (3): 209-218.
DOI: 10.1007/s11906-012-0262-y.

[47] Murphy NF, Stewart S, MacIntyre K, et al. Seasonal variation in

morbidity and mortality related to atrial fibrillation. Int J Cardiol.
2004; 97: 283 -8.

[48] Nadir MA, Szwejkowski BR, Witham MD. Vitamin D and

cardiovascular prevention. Cardiovasc Ther. 2010; 28 (4): 5-12.

[49] Nathan Carlson, Robert Mah, Maria Aburto, Mark Jason Peters,

Meagan V Dupper, Lie Hong Chen. Hypovitaminosis D. Correction
and High-Sensitivity C-Reactive Protein Levels in Hypertensive
Adults. Perm J. 2013 Fall; 17 (4): 19-21.

[50] Norman PE, Powell JT. Vitamin D and Cardiovascular Disease.

Circulation Research. 2014; 114: 379 -93.

[51] Pigarova EA, Rozhinskaya LYa, Belaya JE, Dzeranova LK, Karonova

TL, Ilyin AV, Melnichenko GA, Dedov II. Russian Association of
Endocrinologists recommendations for diagnosis, treatment and
prevention of vitamin D deficiency in adults. Problems of
Endocrinology. 2016; 4: 60 -84 (In Russ.).

[52] Pilz S, Marz W, Wellnitz B, Seelhorst U, Fahrleitner-Pammer A, Di-

mai H, Boehm B, Dobnig H. Association of vitamin D deficiency
with heart failure and sudden cardiac death in a large cross-sectional
study of patients referred for coronary angiography. J Clin
Endocrinol Metab. 2008; 93 (10): 3927-35.

[53] Pittas AG, Chung M., Trikalinos T. Systematic review: Vitamin D and

cardiometabolic outcomes. Ann Intern Med 2010; 152: 307-314.
DOI: 10.7326/0003-4819-152-5-201003020-00009.

[54] Podzolkov VI, Pokrovskaya AE, Panasenko OI Vitamin D deficiency

and cardiovascular pathology. Therapeutic Archive. 2018; 09: 144-
150.

[55] Pourdjabbar A., Dwivedi G., Haddad H. The role of vitamin D in

chronic heart failure. Curr Opin Cardiol 2013; 28: 216-222. DOI:
10.1097/ HCO.0b013e32835bd480.

[56] Povoroznyuk VV, Snezhitsky VA, Yankovskaya LV, Mailian EA,

Reznichenko NA, Maylyan DE The importance of vitamin D in the
pathogenesis of cardiovascular diseases. Zurnal Grodnenskogo
gosudarstvennogo meditsinskogo universiteta (Journal of Grodno
State Medical University) 2015; 2 (50): 6-14. (in Russ).

[57] Robert K. Scragg, Carlos A. Camargo, Jr. and Robert U. Simpson.

Relation of Serum 25-Hydroxyvitamin D to Heart Rate and Cardiac
Work (from the National Health and Nutrition). Am J Cardiol. 2010;
105: 122 -8.

[58] Rostand SG. Ultraviolet light may contribute to geographic and racial

blood pressure differences. Hypertension 1979; 30: 150 -6.

[59] Schleithoff SS, Zittermann A, Tenderich G, Berthold HK, Stehle P,

Koerfer R. Vitamin D supplementation improves cytokine profiles
in patients with congestive heart failure: a double-blind, randomized,
placebo-controlled trial. Am J Clin Nutr. 2006; 83: 754 -9.

[60] Scragg RK, Camargo CAJr., Simpson R. Relation of serum 25-

hydroxyvitamin D to heart rate and cardiac work (from the National
Health and Nutrition Examination Surveys). Am J Cardiol 2010;
105: 122-128.
DOI: 10.1016/j.amjcard.2009.08.6.6.

[61] Shedeed, SA. Vitamin D supplementation in infants with chronic

congestive heart failure / Shedeed SA. // Pediatr cardiol. 2012; 33
(5): 713-719.

[62] Shoben AB, Kestenbaum B, Levin G, et al. Seasonal variation in 25-

hydroxyvitamin D concentrations in the cardiovascular health study.
Am J Epidemiol. 2011; 174: 1363 -72.

[63] Singh NP, Sahni V, Garg D, Nair M. Effect of pharmacological

suppression of secondary hyperparathyroidism on cardiovascular
hemodynamics in predialysis CKD patients: a preliminary
observation. Hemodial Int. 2007; 11: 417-23.

[64] Smirnova, GE The role of vitamin D in the development of


background image

American Journal of Medicine and Medical Sciences 2020, 10(6): 363-369

369

the child's div and the correction of its deficiency. Sonsilium
physician. / Smirnova GE, Vitebskaja AV, Shmakov NA//
Prilozhenie Pediatrija. - 2010; 34:7-12.

[65] Snezhickij, VA Correlation of Calcium and Lipid Metabolism in

Coronary

Heart

Disease.

/

Snezhickij

VA,

Jankovskaja

LV//Klinicheskaja gerontologija. 2012; 3-4:33-38.

[66] Tomson J, Emberson J, Hill M, et al. Vitamin D and risk of death

from vascular and non-vascular causes in the Whitehall study and
meta-analyses of 12,000 deaths. Eur Heart J. 2013; 34(18): 1365-74.

[67] Verdoia M, Schaffer A, Sartori C, et al. Vitamin D deficiency is

independently associated with the extent of coronary artery disease.
Eur J Clin Invest. 2014; 44: 634-42.

[68] Wang L., Manson JE, Song Y., Sesso HD Systematic review: vitamin

D and calcium supplementation in prevention of cardiovascular
events. Ann Intern Med 2010; 152: 315-323. DOI: 10.7326/0003-
4819-152-5-201003020-00010.

[69] Wang TJ, Pencina MJ, Booth SL, Jacques PF, Ingelsson E., Lanier K.

et al. Vitamin D deficiency and risk of cardiovascular disease.
Circulation

2008;

117:

503-511.

DOI:

10.1161/

CIRCULATIONAHA. 107.706127.

[70] Wang TJ, Pencina MJ, Booth SL, et al. Vitamin D deficiency and risk

of cardiovascular disease. Circulation. 2008; 117: 503-51.

[71] Witham MD, Nadir MA, Struthers AD Effect of vitamin D on blood

pressure: a systematic review and metaanalysis. J Hypertens 2009;
27: " 1948-1954. DOI: 10.1097/ HJH. 0b013e32832f075b.

[72] Wu SH, Ho SC, Zhong L. Effects of vitamin D supplementation on

blood pressure. South Med J 2010; 103: 729-737. DOI: 10.1097/
SMJ.0b013e3181e6d389.

[73] Zhiwei Zhang, Yajuan Yang, Chee Yuan Ng, Dandan Wang,

JianlongWang, Guangping Li, Tong Liu, PhD. Analysis-of the Meta
Vitamin D De fi ciencyand Risk of Atrial Fibrillation. Clin. Cardiol.
2016; 39(9): 537-43.

[74] Zhou C., Lu F., Cao K., Xu D., Goltzman D., Miao D. Calciumin

dependent and 1,2 (OH) 2D3-dependent regulation of the renin-
angiotensin system in 1-alpha-hydroxylase knockout nice. Kidney
Int 2008; 74: 170-179. DOI: 10.1038 / ki.2008.101.

[75] Zitterman A., Frisch S., Berthold HK Vitamin D supplementation

enhances the beneficial effects of weight loss on cardiovascular
disease risk markers. Am J Clin Nutr 2009; 89: 1321-1327. DOI:
10.3945 / ajcn.2008.27004.

[76] Zittermann A, Dembinski J, Stehle P. Low vitamin D status is

associated with low cord blood levels of the immunosuppressive
cytokine interleukin-10. Pediatr Allergy Immunol. 2004; 15: 242-6.

[77] Zittermann A, Schulze Schleithoff S, Tenderich G, Berthold HK,

Korfer T, et al. Low vitamin D status: a contributing factor in the
pathogenesis of congestive heart failure? J Am Coll Cardiol. 2003
Jan; 41: 105-12.

[78] Zittermann, A. Low Vitamin D status: a contributing factor in the

pathogenesis of congestive heart failure? / Zittermann A et al. // J.
Am Coll Cardiol. 2003; 41:105-112.

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Kharlamov AN, Perrish AN, Gabinsky YaI, Ronne Kh, Ivanova EYu. Vitamin D in the Treatment of Cardiorenal Syndrome in Patients With Chronic Nephropathy. Kardiologiia. 2012;3:33 -45. (In Russ.).

Kim DH, Sabour S., Sagar UN, Adams S., Whellan DJ Prevalence of hypovitaminosis D in cardiovascular diseases (from the National Health and Nutrition Examination Survey 2001 to 2004). Am J Cardiol 2008; 102: 1540-1544. DOI: 10.1016/j.amjcard.2008.06.0.067.

Kimie Ohkubo, Ichiro Watanabe, Yasuo Okumura, et al. Usefulness of High Sensitivity C-Reactive Protein in Predicting Recurrence of Atrial Fibrillation after Electrical Cardioversion. J Nihon Univ Med Ass. 2015; 74 (5): 233-7.

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Larina VN, Raspopova TN. Mineral bone density and bone metabolism in chronic heart failure. Kardiologiia. 2016; 56 (7): 33-45 (In Russ.).

Lavie CJ, Dinicolantonio JJ, Milani RV. Vitamin D and cardiovascular health. Circulation. 2013; 128: 2404-6.

Liefaard MC, Ligthart S, Vitezova A, Hofman A, Uitterlinden AG, Kiefte-de Jong JC, et al. Vitamin D and C-Reactive Protein: A Mendelian Randomization Study. PLOS ONE. 2015; 10 (7): e0131740.

Liu LC, Voors AA, van Veldhuisen DJ van der Veer E., Belonje AM, Szymanski MK et al. Vitamin D status and outcomes in heart failure patients. Eur J Heart Fail 2011; 13: 619-625. DOI: 10.1093 / eurjhf / HFR032.

Lynn Kane, Kelly Moore, Dieter Lutjohann, et al. Vitamin D3 Effects on Lipids Differ in Statin and NonStatin- Treated Humans: Superiority of Free 25-OH D Levels in Detecting Relationships. J Clin Endocrinol Metab. 2013 Nov; 98 (11): 4400-9.

Mallat Z, Besnard S, Duriez M, et al. Protective role of interleukin-10 in atherosclerosis. Circ Res. 1999; 85: E17-24.

Martins D, Wolf M, Pan D, et al. Prevalence of cardiovascular risk factors and the serum levels of 25 hydroxyvitamin D in the United States: data from the Third National Health and Nutrition Examination Survey. Arch Intern Med. 2007; 167: 1159 -116524.

Mayer OJr, Filipovsky J, Seidlerova J, Vanek J, Dolejsova M, Vrzalova J, Cifkova R. The association between low 25-

hydroxyvitamin D and increased aortic stiffness. J Hum Hypertens. 2012 Nov; 26(11): 650-5.

McNally JD, Nama N., O'Hearn K., Sampson M., Amrein K., Iliriani K. et al. Vitamin D deficiency in critically ill children:a systematic review and meta-analysis. Critical Care 2017; 21(1): 287. DOI: 10.1186 / s13054-017-1875-y.

Mehta V, Agarwal S. Does Vitamin D Deficiency Lead to Hypertension? Cureus. 2017 Feb; 17; 9(2): e1038.

Melaku L, Mossie A. Molecular mediators and controlling mechanism of vascular calcification. Int J Clin Exp Physiol. 2017; 4: 3-14. https://doi.org/10.4103/ijcep.ijcep_3_1.

Menezes AR, Lamb MC, Lavie CJ, DiNicolantonio JJ. Vitamin D and atherosclerosis. Curr Opin Cardiol. 2014; 29 (6): 571-7.

Moretti HD, Colucci VJ, Berry BD Vitamin D3 repletion versus placebo as adjunctive treatment of heart failure patient quality of life and hormonal indices: a randomized, double-blind, placebocontrolled trial. BMC Cardiovasc. Disord., 2017: 17(1): 274.

Motiwalaa SR, Wang TJ Vitamin D and cardiovascular risk. Current Hypertens Rep 2012; 14 (3): 209-218. DOI: 10.1007/s11906-012-0262-y.

Murphy NF, Stewart S, MacIntyre K, et al. Seasonal variation in morbidity and mortality related to atrial fibrillation. Int J Cardiol. 2004; 97: 283 -8.

Nadir MA, Szwejkowski BR, Witham MD. Vitamin D and cardiovascular prevention. Cardiovasc Ther. 2010; 28 (4): 5-12.

Nathan Carlson, Robert Mah, Maria Aburto, Mark Jason Peters, Meagan V Dupper, Lie Hong Chen. Hypovitaminosis D. Correction and High-Sensitivity C-Reactive Protein Levels in Hypertensive Adults. Perm J. 2013 Fall; 17 (4): 19-21.

Norman PE, Powell JT. Vitamin D and Cardiovascular Disease. Circulation Research. 2014; 114: 379 -93.

Pigarova EA, Rozhinskaya LYa, Belaya JE, Dzeranova LK, Karonova TL, Ilyin AV, Melnichenko GA, Dedov II. Russian Association of Endocrinologists recommendations for diagnosis, treatment and prevention of vitamin D deficiency in adults. Problems of Endocrinology. 2016; 4: 60 -84 (In Russ.).

Pilz S, Marz W, Wellnitz B, Seelhorst U, Fahrleitner-Pammer A, Di-mai H, Boehm B, Dobnig H. Association of vitamin D deficiency with heart failure and sudden cardiac death in a large cross-sectional study of patients referred for coronary angiography. J Clin Endocrinol Metab. 2008; 93 (10): 3927-35.

Pittas AG, Chung M., Trikalinos T. Systematic review: Vitamin D and cardiometabolic outcomes. Ann Intern Med 2010; 152: 307-314. DOI: 10.7326/0003-4819-152-5-201003020-00009.

Podzolkov VI, Pokrovskaya AE, Panasenko OI Vitamin D deficiency and cardiovascular pathology. Therapeutic Archive. 2018; 09: 144-150.

Pourdjabbar A., Dwivedi G., Haddad H. The role of vitamin D in chronic heart failure. Curr Opin Cardiol 2013; 28: 216-222. DOI: 10.1097/ HCO.0b013e32835bd480.

Povoroznyuk VV, Snezhitsky VA, Yankovskaya LV, Mailian EA, Reznichenko NA, Maylyan DE The importance of vitamin D in the pathogenesis of cardiovascular diseases. Zurnal Grodnenskogo gosudarstvennogo meditsinskogo universiteta (Journal of Grodno State Medical University) 2015; 2 (50): 6-14. (in Russ).

Robert K. Scragg, Carlos A. Camargo, Jr. and Robert U. Simpson. Relation of Serum 25-Hydroxyvitamin D to Heart Rate and Cardiac Work (from the National Health and Nutrition). Am J Cardiol. 2010; 105: 122 -8.

Rostand SG. Ultraviolet light may contribute to geographic and racial blood pressure differences. Hypertension 1979; 30: 150 -6.

Schleithoff SS, Zittermann A, Tenderich G, Berthold HK, Stehle P, Koerfer R. Vitamin D supplementation improves cytokine profiles in patients with congestive heart failure: a double-blind, randomized, placebo-controlled trial. Am J Clin Nutr. 2006; 83: 754 -9.

Scragg RK, Camargo CAJr., Simpson R. Relation of serum 25-hydroxyvitamin D to heart rate and cardiac work (from the National Health and Nutrition Examination Surveys). Am J Cardiol 2010; 105: 122-128. DOI: 10.1016/j.amjcard.2009.08.6.6.

Shedeed, SA. Vitamin D supplementation in infants with chronic congestive heart failure / Shedeed SA. // Pediatr cardiol. 2012; 33 (5): 713-719.

Shoben AB, Kestenbaum B, Levin G, et al. Seasonal variation in 25-hydroxyvitamin D concentrations in the cardiovascular health study. Am J Epidemiol. 2011; 174: 1363 -72.

Singh NP, Sahni V, Garg D, Nair M. Effect of pharmacological suppression of secondary hyperparathyroidism on cardiovascular hemodynamics in predialysis CKD patients: a preliminary observation. Hemodial Int. 2007; 11: 417-23.

Smirnova, GE The role of vitamin D in the development of the child's body and the correction of its deficiency. Sonsilium physician. / Smirnova GE, Vitebskaja AV, Shmakov NA// Prilozhenie Pediatrija. - 2010; 34:7-12.

Snezhickij, VA Correlation of Calcium and Lipid Metabolism in Coronary Heart Disease. / Snezhickij VA, Jankovskaja LV//Klinicheskaja gerontologija. 2012; 3-4:33-38.

Tomson J, Emberson J, Hill M, et al. Vitamin D and risk of death from vascular and non-vascular causes in the Whitehall study and meta-analyses of 12,000 deaths. Eur Heart J. 2013; 34(18): 1365-74.

Verdoia M, Schaffer A, Sartori C, et al. Vitamin D deficiency is independently associated with the extent of coronary artery disease. Eur J Clin Invest. 2014; 44: 634-42.

Wang L., Manson JE, Song Y., Sesso HD Systematic review: vitamin D and calcium supplementation in prevention of cardiovascular events. Ann Intern Med 2010; 152: 315-323. DOI: 10.7326/0003-4819-152-5-201003020-00010.

Wang TJ, Pencina MJ, Booth SL, Jacques PF, Ingelsson E., Lanier K. et al. Vitamin D deficiency and risk of cardiovascular disease. Circulation 2008; 117: 503-511. DOI: 10.1161/ CIRCULATIONAHA. 107.706127.

Wang TJ, Pencina MJ, Booth SL, et al. Vitamin D deficiency and risk of cardiovascular disease. Circulation. 2008; 117: 503-51.

Witham MD, Nadir MA, Struthers AD Effect of vitamin D on blood pressure: a systematic review and metaanalysis. J Hypertens 2009; 27: " 1948-1954. DOI: 10.1097/ HJH. 0b013e32832f075b.

Wu SH, Ho SC, Zhong L. Effects of vitamin D supplementation on blood pressure. South Med J 2010; 103: 729-737. DOI: 10.1097/ SMJ.0b013e3181e6d389.

Zhiwei Zhang, Yajuan Yang, Chee Yuan Ng, Dandan Wang, JianlongWang, Guangping Li, Tong Liu, PhD. Analysis-of the Meta Vitamin D De fi ciencyand Risk of Atrial Fibrillation. Clin. Cardiol. 2016; 39(9): 537-43.

Zhou C., Lu F., Cao K., Xu D., Goltzman D., Miao D. Calciumin dependent and 1,2 (OH) 2D3-dependent regulation of the renin-angiotensin system in 1-alpha-hydroxylase knockout nice. Kidney Int 2008; 74: 170-179. DOI: 10.1038 / ki.2008.101.

Zitterman A., Frisch S., Berthold HK Vitamin D supplementation enhances the beneficial effects of weight loss on cardiovascular disease risk markers. Am J Clin Nutr 2009; 89: 1321-1327. DOI: 10.3945 / ajcn.2008.27004.

Zittermann A, Dembinski J, Stehle P. Low vitamin D status is associated with low cord blood levels of the immunosuppressive cytokine interleukin-10. Pediatr Allergy Immunol. 2004; 15: 242-6.

Zittermann A, Schulze Schleithoff S, Tenderich G, Berthold HK, Korfer T, et al. Low vitamin D status: a contributing factor in the pathogenesis of congestive heart failure? J Am Coll Cardiol. 2003 Jan; 41: 105-12.

Zittermann, A. Low Vitamin D status: a contributing factor in the pathogenesis of congestive heart failure? / Zittermann A et al. // J. Am Coll Cardiol. 2003; 41:105-112.

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