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ABSTRACT
Cardiovascular diseases are one of the most significant predictors of mortality in patients with end-stage renal disease
treated with chronic hemodialysis, and cause at least a third of all hospitalizations [Eisner D. et al., 2001; Johnston N.
et al., 2008]. According to the US Renal Disease Registry, the five-year survival rate in the general population of
patients on hemodialysis is 33.4% [U. S. Renal Data System, 2009]. More than half of the deaths of patients on renal
replacement therapy are due to cardiovascular pathology, the mortality from which in patients on
hemodialysis is 30-35 times higher compared to the general population [Zavy A.S. et al., 1998; Herzog S.A., 2003; U.S.
Renal Data System, 2009]. A significant proportion of deaths in patients with end-stage renal disease receiving
Research Article
STRUCTURAL AND FUNCTIONAL FEATURES OF THE MYOCARDIUM
AGAINST THE BACKGROUND OF RENAL REPLACEMENT THERAPY
Submission Date:
October 25, 2022,
Accepted Date:
October 30, 2022,
Published Date:
November 05, 2022
Crossref doi:
https://doi.org/10.37547/ijmscr/Volume02Issue11-01
Salyamova Feruza Erkinovna
Tashkent state dental institute, department of internal medicine, Republican specialized scientific and practical
medical center for nephrology and kidney transplantation. Uzbekistan
Xusanxodjaeva Feruza Tulkunovna
Tashkent state dental institute, department of internal medicine, Republican specialized scientific and practical
medical center for nephrology and kidney transplantation. Uzbekistan
Muhiddinova Nasiba Zoxiriddinovna
Tashkent state dental institute, department of internal medicine, Republican specialized scientific and practical
medical center for nephrology and kidney transplantation. Uzbekistan
Mavlyanov Sarvar Iskandarovich
Tashkent state dental institute, department of internal medicine, Republican specialized scientific and practical
medical center for nephrology and kidney transplantation. Uzbekistan
Islamova Malika Sanjarovna
Tashkent state dental institute, department of internal medicine, Republican specialized scientific and practical
medical center for nephrology and kidney transplantation. Uzbekistan
Journal
Website:
https://theusajournals.
com/index.php/ijmscr
Copyright:
Original
content from this work
may be used under the
terms of the creative
commons
attributes
4.0 licence.
Volume 02 Issue 11-2022
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hemodialysis treatment are attributed to those associated with coronary heart disease [Foley R.N. et al., 1998a; Sarnak
M.J. et al., 2003; Cheung A.K. et al., 2004]. The theoretical method of research was used. Many articles and
dissertations by international scientists were analyzed, which were based on various books, dissertations, as well as
electronic journals.
KEYWORDS
Cardiovascular diseases, hemodynamic syndialysis stress, hemodialysis-induced myocardial ischemia, hyperhydration,
pulmonary hypertension, heart failure.
INTRODUCTION
The article presents up-to-date data on morbidity and
mortality from cardiovascular diseases (CVD) in
patients undergoing programmed hemodialysis (PGD).
According to literature data, by the end of the first year
of PGD, approximately one in five patients dies, CVD
and their complications occupy a leading place in the
structure of mortality. High cardiac mortality is a
consequence of a combination of traditional and non-
traditional risk factors for the development of CVD in
the dialysis population of patients. Non-traditional risk
factors are combination of toxic-metabolic and
hemodynamic effects on the myocardium caused by
both kidney damage and replacement therapy. From
the perspective of a cardiologist, PGD-associated risk
factors for CVD are of particular interest, among which
the following deserve the closest study: hemodynamic
syndialysis stress, hemodialysis-induced myocardial
ischemia, hyperhydration, pulmonary hypertension,
intra- and postdialysis hypotension, heart failure with
high cardiac output and dynamic intraventricular
obstruction. All of the above phenomena have a direct
damaging effect on the myocardium and lead to
aggravation of heart failure. The stated problems
dictate the need to develop a specific methodology for
assessing the initial cardiological status of patients on
PGD and heart diseases are the cause of 40-50% of
death in patients with stage 5 in chronic kidney disease
(CKD 5) [13, 18, 26, 21]. The results of long-term
population studies initiated in the early 70s of the last
century and continuing to this may indicate that
patients with CKD5 die mainly from cardiovascular
diseases catastrophes [27, 43, 45]. In absolute terms,
patients receiving renal replacement therapy (HRT) by
dialysis methods have a 10-50 fold rise of
cardiovascular death compared to the general
population [19, 21, 58, 59]. It is becoming increasingly
obvious that programmatic hemodialysis (HD) is
associated with a number of independent risk factors
for by the beginning of 2014, at least 2.25 million
people in the world suffering from CKD5 were
receiving PGD [24]. The number of patients receiving
this type of renal replacement therapy, in most
countries, including Central Asia is steadily increasing
[29, 23, 1]. Among the causes of death of PGD patients,
cardiovascular pathology occupies a leading place. It is
important to note that, despite the revolutionary
changes in hemodialysis technology and the
continuous improvement of approaches to the
treatment of patients with CKD 5, over the past 20
years, the share of cardiovascular pathology in the
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mortality structure of PGD patients has not changed
and is 40-45% [60,59, 23, 3, 2]. At the same time, special
attention is drawn to the increase in mortality in the
first year of PGD, which is now increasingly regarded as
a global phenomenon [16, 37, 44, 50]. It is particularly
impressive that more than a third of deaths (about 35%)
occur during the first three months of RRT [44], with
more than half of the cases being sudden cardiac death
[28]. The critical point of mortality of patients on PGD
reaches 120 days and is 27.5 deaths per 100 patients per
year, and the integral annual mortality is approaching
20% [14, 50, 55]. Thus, by the end of the first year of
PGD, about one in five dies a patient, which is an
undoubted challenge to the professional medical
community. Data from the UK renal registry indicate
that a patient who started HD at the age of 25 to 29 has
an average life expectancy of only 18.5 years,
i.e. 33 years less than this indicator in the same age
group in the general population without CKD5 [56]. In
patients aged 65-74 years (the most typical age group
for patients starting PGD in developed countries),
according to the European Renal Registry, the average
life expectancy is 5 years approximately 50% less than
in the same age group in the general population
without CKD5 [23]. Thus, as the dialysis population
expands, the issues of diagnosis, prevention and
treatment
become
more
and
more
urgent
cardiovascular diseases (CVD). It should be
emphasized that chronic kidney disease (CKD) is itself
a strong independent risk factor for the development
and progression of CVD and, as CKD progresses, the
incidence of CVD increases [13, 26, 27]. According to
experts, the reason for this dependence is a
combination of traditional and non-traditional risk
factors for the development of CVD [37]. Traditional
risk factors are well known, in the context of the
problems discussed, the most important are: arterial
hypertension (AH) with concomitant remodeling of
the left ventricular myocardium (LV), left ventricular
hypertrophy (LVH), hyperlipidemia, diabetes mellitus
and anemia. The peculiarity of a patient with CKD5 is
the presence of most or all of the traditional risk
factors for the development and progression of CVD.
Non-traditional risk factors are a combination of
metabolic, toxic and hemodynamic features caused by
both CKD and dialysis itself (CKD-dialysis-associated)
[34, 37, 42]. The group of toxic and metabolic factors
includes a significant increase in pro-inflammatory
cytokines, homocysteine, hyperphosphatemia, hyper-
and hypocalcemia, hyperparathyroidism, sodium,
potassium and magnesium imbalance, oxidative stress
and nitric oxide deficiency, insufficient water
purification, etc. [22, 46, 52, 1]. The result of their action
is both direct and indirect (through increased chronic
inflammation) cardiotoxic effect, the development of
micro- and macrovascular endothelial dysfunction,
acceleration of atherogenesis and myocardial fibrosis,
increased vascular stiffness and rapid calcification of
intracardiac structures [15, 37, 41]. In addition,
significant fluctuations in the levels of K+, Na+ and
Ca2+ play a key role in the formation of
electrophysiological
mechanisms
of
ventricular
tachycardia, ventricular fibrillation and complete
transverse heart block The toxic effect of azotemia on
the heart, leading to the formation of uremic fibrinous
pericarditis and specific myocardial damage (uremic
cardiomyopathy), should not be underestimated
[41].An important risk factor for the development and
progression of CVD is the presence of anemia, the
genesis of which at the final stage of CKD is primarily
associated with a decrease in erythropoietin
production [26]. During the first year of RRT, a
compensatory increase in cardiac output is noted
against the background of anemia [51]. This
compensation mechanism eventually leads to
depletion of LV contractile function, its dilatation,
cardiomegaly and ultimately, to the formation of
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severe congestive heart failure (HF) [36, 1]. Correction
of anemia with drugs that stimulate erythropoiesis
does not lead to a decrease in mortality from CVD,
since an increase in viscosity is observed in parallel with
the growth of hemoglobin blood and AG aggravation
[53]. From a practical point of view, it is important to
emphasize that in the dialysis population, complete
correction of anemia should be avoided [26, 51, 53]
–
so, for today . However, most experts believe that
hemoglobin targets should be in the range of 11-12 g/dl.
This will compensate for hemic hypoxia of the
myocardium and minimize the risks of CVD progression
against the background of erythropoietin replacement
therapy. It should be noted that the incidence of
infectious endocarditis (IE) is certainly higher than in
the general population [30]. Diagnosis of this
pathology remains difficult in patients with calcified
valvular heart defects, both due to the complexity of
visualization of vegetations and due to the "blurring"
of the clinical picture. A separate problem is the
development of right-sided IE in patients with central
venous catheters as a vascular access for RRT. From
the perspective of a cardiologist working in a
nephrological clinic, hemodialysis-associated CVD risk
factors are of particular interest. The peculiarity of
these factors is the inevitability and repeatability of the
effect of the procedure itself on the heart muscle and
the parameters of central hemodynamics (CGD) from
dialysis to dialysis. We are talking about the formation
of a kind of "hemodynamic swing", which ultimately
leads to a persistent destabilization of the main
compensatory mechanisms of the cardiovascular
system as a whole. From our point of view, the
following factors deserve the closest attention and
study:
1. Recurrent hemodynamic stress during the HD
procedure. The results of echocardiographic (Echo-KG)
studies and positron emission tomography obtained
during dialysis sessions indicate that during each HD
procedure, myocardial perfusion decreases to one
degree or another, causing its transient stun
("stunning"), which can eventually lead to fixed
violations of local contractility and the development of
myocardial fibrosis [12, 17, 5, 11]. The term hemodialysis-
induced damage to the heart muscle has become
legitimate. Moreover, transient hemodialysis-induced
myocardial ischemia is a predictor of an increase in
annual mortality in patients with PGD [12, 17].
Acute and/or chronic hyperhydration (volume
overload).
It is well known that hyperhydration is a significant risk
factor for further progression of hypertension, LVH
and LV remodeling [32, 36, 61, 4, 6]. However, in the
context of the discussed problems, it is extremely
important to study the role of hyperhydration in the
formation of congestive HF. Acute decompensation of
CHF on the background and due to hyperhydration
leads to the development of pulmonary edema and
severe myocardial ischemia, which negatively affects
the main determinants of prognosis. Of course,
conducting HD critically reduces the degree of
hyperhydration and its destructive effect on the CCC.
But hemodynamic stress during the RRT procedure,
especially in combination with excessive filtration
volume, on the one hand, and an increase in the
volume characteristics of the heart during the
interdialysis period, on the other, will lead to further
progression of LV myocardial remodeling processes,
the formation of diastolic dysfunction and, ultimately,
an increase in CHF phenomena.
3. Pulmonary hypertension (PH) in patients with PGD.
LH in patients with PGD is a well-known fact, which is
reflected in the modern classification. It is also known
that the treatment of this condition is very problematic
and expensive today. About 50% of patients on HD
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have signs of LH. It is believed that the development of
LH almost 4 times increases the annual mortality rates
in patients with CKD 5
[62]. The formation and/or progression of LV occurs
both as a result of systolic LV dysfunction caused by the
first two factors and as a result of a specific effect on
the central hemodynamics of a functioning, both
native arteriovenous fistula (AVF)
and AVF formed with the use of a vascular prosthesis
[48].
4. Instability of blood pressure figures under the
influence of the DG procedure.
The phenomenon of intradialysis and postdialysis
hypotension is well known, which, in turn, is the cause
of the development of repeated episodes of
myocardial ischemia, and also contributes to the
processes of LV remodeling [7, 8, 9, 20].
5. Heart failure with high cardiac output in patients
with functioning AVF.
This condition is an interesting hemodynamic paradox:
against the background of a detailed clinical picture of
CHF, instrumental high rates of cardiac output are
determined [38]. This naturally complicates the
interpretation of the clinical situation, since sufficient
LV ejection fraction (LVEF) is traditionally considered in
most cases to be an indicator of a stable state of the
cardiovascular system. It is not superfluous to recall
that the diagnosis of HF with high cardiac output
requires the exclusion of thyrotoxicosis and severe
uncompensated anemia.
6. Dynamic intraventricular obstruction during a
dialysis session, leading to arterial hypotension and
increased myocardial oxygen demand [49]. The
combined influence of traditional and non-traditional
risk factors, as CPN progresses, leads to a decrease in
global and regional LV contractility, i.e. to the
development
of CHF proper. In the situation of the development of
HF, the main compensation mechanism is the further
activation of the div's pressor systems (sympathetic
ner
vе system (SNS) and the renin
-angiotensin-
aldosterone system (RAAS), which allows you to
maintain a cardiac output adequate to the needs of the
div. However, maintaining the hemodynamic status
has its price. Efferent vasoconstriction, which develops
due to hyperactivation of SNS and RAAS, provides the
necessary level of glomerular filtration, but high
vascular resistance sooner or later leads to a decrease
in renal blood flow. From a certain moment, the
mechanisms of hypoxic damage to the tubules,
apoptosis of nephrons are triggered,
development of renal replacement fibrosis. These
processes lead to further progression of renal
insufficiency due to persistent renal ischemia, which, in
turn, activates SNS and RAAS, maintains a high blood
pressure level and leads to the closure of a vicious
circle of mutual aggravation of CKD and CVD. The
described mechanisms underlie the formation of the
cardiorenal continuum, which is a continuous series of
sequential processes of damage and dysfunction of the
heart and kidneys [34, 42]. Thus, in the predialysis
period, specific prerequisites have already been
formed for further exacerbation of HF
–
it is believed
that about 35-40% of patients with CKD 5 have signs of
CHF by the beginning of RRT [19, 30, 10]. After the start
of HD in less than 2 years, the number of such patients
increases by another 25%, i.e. every second will have
signs of CHF [30]. As already mentioned above, the
reason is more half of the cases of cardiovascular
deaths during the first year of PGD are sudden cardiac
death. In this contingent of patients, unlike the general
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population, acute coronary occlusion is not the leading
cause of sudden cardiac death. On the contrary,
sudden cardiac death is explained by the summation of
the negative effects of LVH, prolonged arterial
hypertension, hyperhydration, chronic inflammation,
hyperactivation of the SNS, as well as a tendency to
ventricular arrhythmias due to electrolyte disturbances
–
i.e. a fatal combination traditional and CKD/dialysis-
associated CVD risk factors [29, 47].
CONCLUSION
Cardiovascular diseases and the high mortality rate
caused by them remain one of the main problems of
dialysis therapy. At the same time, despite the
improvement of dialysis technologies, the share of
cardiovascular deaths in the overall mortality structure
of patients with CKD5 receiving RRT has remained
unchanged over the past decades. Obviously, to
change this situation, it is necessary to solve a number
of problems concerning the optimal management
tactics of patients comorbid for cardiovascular
diseases. The stated problems dictate the necessity of
developing a certain methodology for the initial
assessment and subsequent monitoring of the
cardiological status of nephrological patients, which
will allow both objectifying the effectiveness of
ongoing therapeutic measures and offering new ones
in the future approaches to therapy. The solution of
cardiac problems in nephrologia cannot be the
prerogative of a cardiologist alone. Without counter
–
proposals and ongoing discussion of the tasks set by
the nephrological community, it is impossible to
achieve a common goal - to reduce mortality from CVD
in the dialysis population of patients. None of the
authors has any conflicts of interest.
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