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MYOCARDIODYSTROPHY IN CHILDREN AND ADOLESCENTS
Toshboyeva Shaxlo Yusup qizi
Samarkand State Medical University, 1st year clinical residents
of the Department of Cardiology
Eshmurzayev Asror To'lqin o'g'li
Tashkent Medical Academy, 1st year master's student
in the field of Therapy
Annotatsiya:
"Miokardiodistrofiya" (MKD) yoki "miokard distrofiyasi"
tushunchasi miokarddagi metabolizmning biokimyoviy darajada buzilishini
anglatadi, ular ularni keltirib chiqargan sababni bartaraf etishda qisman yoki to‘liq
qaytariladi. Miokardning uzoq vaqt davom etib boradigan va zo‘rayib boradigan
distrofiyasi uning qisqarish funksiyasi susayib, yurak yetishmovchiligi boshlanishiga
olib keladi. O‘tkir MKD o‘tkir yurak yetishmovchiligiga olib kelishi mumkin. Har
qanday etiologiyali MKD rivojlanishining asosida, odatda, miokardning o‘tkir yoki
surunkali gipoksiyasi yotadi.
Abstract:
The concept of "myocardiodystrophy" (MCD) or "myocardial
dystrophy" refers to metabolic disorders in the myocardium at the biochemical level,
which are partially or completely reversible when the cause that caused them is
eliminated. Prolonged and progressive myocardial dystrophy leads to a decrease in its
contractile function and the development of heart failure. Acute MCD can cause acute
heart failure. The development of CVD of any etiology is usually based on acute or
chronic myocardial hypoxia.
Kalit so’z:
Miokardiodistrofiya, yurak, qon tomirlar, infarct, qon aylanishining
buzulishi, endokard.
Keywords:|
Myocardial dystrophy, heart, blood vessels, infarction, circulatory
disorders, endocardium.
Article content : Causes of MCD development
The development of myocardial dystrophy can be caused by myocardial
diseases (myocarditis, cardiomyopathy), extracardiac diseases (anemia, chronic
tonsillitis, various poisonings, thyrotoxicosis, hypothyroidism, chronic somatic
diseases), as well as physical overstrain in athletes (hyperfunctionogenic, contributing
to the development of "pathological sports heart"). These causes lead to disorders of
protein, energy, especially electrolyte metabolism in cardiomyocytes, as well as the
accumulation of pathological metabolites, which can cause corresponding clinical
symptoms: chest pain, various rhythm and conduction disorders, heart failure.
Myocardiodystrophy is always a secondary process, including vegetative,
dysmetabolic, enzymatic (congenital or acquired), electrolyte, and neurohumoral
disorders. As early as the last century, G.F. Lang (1960s) proposed classifying
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myocardiodystrophy according to the etiological principle. This approach is still
maintained today. Myocardial dystrophy can be observed in children of any age, even
in newborns. The causes can be previous intrauterine infections, perinatal
encephalopathy, and "deadaptation" syndromes of the CNS and cardiovascular
system, especially against the background of labor stress and hypoxia. In subsequent
periods of childhood, frequent colds, anemia of various origins, chronic
nasopharyngeal infection, blood diseases, endocrine pathology, past myocarditis,
hypodynamia, physical and sports overloads, obesity, accumulation of various
xenobiotics in the div, some medications (hormonal drugs, cytostatic
immunosuppressants, some antibiotics, tranquilizers, etc.) can lead to the
development of myocardiodystrophy.
Diagnosis of MCD
Complaints: pain in the heart area, shortness of breath during physical exertion,
palpitations, weakness, a feeling of "breaks" in the heart. However, many patients
may not have any complaints.
Anamnesis. Patients usually have diseases or pathological conditions in which
there is always tissue chronic hypoxic syndrome (anemia, thyroid diseases, other
endocrinopathies, chronic tonsillitis, significant physical overload and sports
overload, past myocarditis, various poisonings, etc.), which contributes to the
formation of myocardiodystrophy. Objective examination of the heart: irregular
pulse, tachycardia, bradycardia, extrasystole, muffled heart sounds, weakening of the
1st heart sound at the apex, appearance of a systolic murmur. Electrocardiographic
examination has special diagnostic value, but only in combination with medical
history and clinical findings. On the ECG, various arrhythmias of varying nature are
detected, which do not significantly affect systemic hemodynamics (moderate sinus
tachycardia or sinus bradycardia, rare, often supraventricular extrasystoles),
decreased voltage of the QRS complex, incomplete blocks of the bundle of Giss's
bundles. Diagnostically significant ECG signs of myocardial dystrophy are impaired
repolarization processes in the myocardium, which manifest as ST-T changes:
flattened or negative T wave, depression or elevation of the ST interval. These ECG
manifestations are a direct reflection of disorders in the electro-physiological
properties of conductive and contractile myocardial cells. In this case, the load and
pharmacological tests are generally negative.
Echocardiography, as a rule, does not reveal deviations from the age norm and
only in some patients, especially in the distal stages of myocardiodystrophy, slight
dilation of the heart chambers and a decrease in the contractile function of the
myocardium can be determined.
Nuclear magnetic resonance imaging is a highly promising method for
diagnosing myocardial dystrophy. This research method allows visualization of the
heart and, in combination with radioactive phosphorus spectroscopy, quantitative
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assessment of the content of high-energy phosphates in cardiomyocytes, allowing for
intracellular pH measurement. In broad practice, these studies are not yet being used.
Currently, one of the informative methods for diagnosing MCD in children is
scintigraphy with Tl-201. Thallium is incorporated into the K+-, Na+-ATPase cellular
pump, where it replaces the K+ ion and, without compromising the function of the
ionic cellular pump, is distributed throughout the myocardium, allowing for the
assessment of the functional integrity of cardiomyocytes, i.e., perfusion and
metabolism. Using scintigraphy, it was determined that in children with myocardial
dystrophy, metabolic processes predominantly suffer. Both diffuse and focal
accumulation defects were identified, indicating a decrease in the number of
functioning cardiomyocytes, but at the same time, sufficient myocardial contractility
persisted.
In recent years, numerous works have emerged discussing mitochondrial
dysfunctions in many diseases, particularly myocardiodystrophy. Mitochondrial
dysfunctions lead to cell energy deficiency, which plays an important pathogenetic
role in the development of MCD. Thus, a group of Russian authors conducted a study
to determine the activity of mitochondrial enzymes in peripheral blood lymphocytes
in children with myocardiodystrophy, revealing significant metabolic disorders.
Myocardial biopsy can be considered a crucial diagnostic method for MCD. However,
in MCD, there are usually no indications for it. In the initial stages of MCD, only
ultrastructural changes in cardiomyocytes are detected, and gistochemical
examination confirms enzymopathies.
We present the most common diseases and conditions in which there are always
signs of myocardial dystrophy to one degree or another.
MCD in thyrotoxicosis.
In thyrotoxicosis, two factors play a key role in
the pathogenesis of MCD development:
1. Under the influence of an increased amount of thyroid hormones in the
myocardium, oxidative phosphorylation is disrupted. This leads to a decrease in ATP
levels, energy deficiency, and subsequently, protein deficiency.
2. Under the influence of thyroid hormones and increased sympathetic nervous
system activity, significant hemodynamic disturbances occur - the minute volume
increases, mainly due to increased heart rate, blood flow rate and circulating blood
volume increase, peripheral resistance in the systemic circulation decreases and
increases in the pulmonary circulation.
Such changes in hemodynamics require increased energy supply, which is
absent. Eventually, myocardiodystrophy develops. The peculiarities of the clinical
manifestations of myocardial dystrophy in thyrotoxicosis are the predominance of
such arrhythmias as sinus tachycardia, extrasystole, paroxysmal tachycardia attacks,
and even paroxysmal and/or atrial fibrillation can develop. Against this background,
with prolonged thyrotoxicosis, chronic circulatory insufficiency develops, mainly of
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the right ventricular type (swelling, hepatomegaly). Pain in the heart area is relatively
rare.
In some patients, signs of myocardial dystrophy (for example, rhythm
disturbances) may dominate the clinical picture of thyrotoxicosis, for which children
are admitted, first of all, to a cardiologist, and then only to an endocrinologist.
Treatment of myocardial dystrophy in thyrotoxicosis necessarily involves the
use of thyrostatic agents. Due to concurrent sympathicotonia, beta-blockers are also
indicated for them.
We observed patients with thyroid hyperfunction, in whom various
tachyarrhythmias practically did not respond to antiarrhythmic therapy. The effect
occurred only with the prescription of complex therapy for thyrotoxicosis with the
mandatory inclusion of thyrostatic drugs prescribed by an endocrinologist after a
thorough examination of the patient.
MCD in hypothyroidism.
In hypothyroidism, the basis for the development
of MCD is the decrease in metabolic processes in the myocardium due to a decrease
in thyroid hormones. Oxygen absorption decreases, protein synthesis decreases. At
the same time, the permeability of vessels in the myocardium increases, the amount
of interstitial fluid increases, which, as if pushing out myofibrils, leads to dismetabolic
disorders in the cells and their swelling (sodium content increases, potassium content
decreases, fluid retention occurs).
Clinically, myocardiodystrophy in hypothyroidism manifests as constant and
aching pain in the heart area, arrhythmias in the form of sinus bradycardia, and various
blockades (atrioventricular, atrial, ventricular). Rhythm and conduction disturbances
are documented by corresponding changes in the ECG. Typical changes in the ECG,
in addition to the indicated manifestations, are also the low voltage of the ECG waves,
the presence of a flattened or negative T wave, especially in the chest leads.
The main method of treating MCD in hypothyroidism is the administration of
thyroid hormones. The patient should be observed by an endocrinologist.
MCD in anemia.
In anemia of any origin, the hemoglobin content and the
number of erythrocytes decrease. Hemic hypoxia develops, which leads to energy
deficiency in the myocardium. In the initial stages of anemia, moderate energy
deficiency causes adaptive stimulation of blood circulation and increased cardiac
function (its hyperfunction), which is aimed at preventing disorders of oxidation
processes in tissues, including the myocardium.
The clinical manifestation of these disorders is a circulatory-hypoxic
(hypoxemic) syndrome, characteristic of all types of anemia, manifested by shortness
of breath, tachycardia, loud heart sounds, and systolic murmurs above the heart and
blood vessels, which is due to increased blood flow velocity. With prolonged
persistence of anemia, and therefore tissue hypoxia, an intensifying energy deficit
leads to the development of dystrophic changes in the myocardium and the
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suppression of its functional capacity. Against the background of increasing
circulatory-hypoxic syndrome, patients develop changes in the ECG: flattened or
negative T wave, incomplete ventricular blocks, moderate decrease in the ST interval
in the chest leads, atrial or ventricular extrasystole, sometimes atrioventricular block
of I and even II degree. With prolonged pronounced anemia, insufficient treatment
can lead to heart failure.
The therapy of myocardial dystrophy against the background of anemia consists,
first of all, in the treatment of anemia depending on its genesis (preparations of iron,
vitamins, if indicated - glucocorticosteroids, etc.). Treatment of MCD directly has no
specificity and is carried out against the background of anemia therapy according to
the generally accepted schemes described above.
MCD in chronic tonsillitis.
The most frequent manifestation of tonsillagen
MCD is pain in the heart area, piercing, aching, prolonged, often very intense. Often,
various rhythm disturbances are detected: irregular sinus rhythm, migration of the
rhythm source, intraventricular and intraventricular blockades, extrasystole.
Etiotropic therapy is active complex treatment of chronic tonsillitis up to
tonsillectomy (upon indications).
MCD post-myocarditic.
After experiencing acute myocarditis, dystrophic
changes in the myocardium can persist for 6-12 months or more. At the same time,
changes are detected mainly on the ECG. Reduction of repolarization processes in the
left chest leads (smoothing or inversion of the T wave), concomitant atrioventricular
blocks of I-II degree, as well as various blocks of the bundle of Giss's feet, are more
common. Sufficiently persistent ectopic rhythm disturbances in the form of
extrasystole, parasystole, and less frequently, atrial fibrillation can be observed.
In the treatment of patients with post-myocarditic MCD, cardiotrophic and
vascular drugs (
panangin
, mildronate, riboxin, neoton, magne-B6, etc.) are used.
MCD of toxic origin.
This variant of MCD occurs in patients who have been
receiving immunosuppressants (cytostatics, glucocorticosteroids, nonsteroidal anti-
inflammatory drugs) for a long time.
MKD mainly manifests as changes in the ECG in the form of depression of the
T wave, ST segment, and elongation of the QT interval. Some rhythm disturbances
may be observed: sinus tachycardia or bradycardia, extrasystole, bundle branch
blockades. Treatment is similar to the therapy for other variants of MCD
(cardiotrophic, vascular drugs, vitamins, antioxidants).
Tactics and Methods of Treatment of MCD in Children
The success and effectiveness of MCD therapy in a child largely depends on the
treatment and elimination of the cause that caused MCD, its duration, severity, and
the clinical manifestations of metabolic disorders in the myocardium.
Pathogenetic therapy of MCD is carried out with cardiotrophic agents. These are
medications of various pharmacological groups capable of improving metabolic
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processes in the myocardium. The question of the effectiveness of these drugs has not
been definitively resolved, since for most of them, the effectiveness has not been
assessed in strictly controlled studies. In this regard, when prescribing cardiotrophic
drugs, it is advisable to avoid polypragmasia, based on the predominance of the
visible link in the pathogenesis of MCD.
To correct protein metabolism in the myocardium, vitamins and their coenzymes
(folic acid, vitamins B6 and C) can be recommended, and magnesium and potassium
preparations that activate protein synthesis can be used. The absorption of amino acids
is enhanced by the administration of drugs with anabolic effects (retabolil, potassium
orotate, riboxin, mildronate, etc.), therefore, their administration may be appropriate
in combination with other medications.
Electrolyte imbalances are most actively corrected by prescribing combined
medications containing potassium and magnesium salts (panangin, magnerot, etc.).
To correct energy metabolism, vitamins of the B group, cocarboxylase, ATP are
used, and riboxin, mildronate, and antioxidant complexes (vitamins A + E + C) can
also be used, which contribute to a decrease in lipid peroxidation and improve the
antioxidant defense of the cell. Treatment courses with the drug "Neoton" (creatinine
phosphate) intravenously are effective.
To eliminate the clinical manifestations of MKD, symptomatic agents are used
(according to indications). Sanitation of chronic infection foci, all comorbidities that
can cause or maintain MCD formation, is mandatory.
Cardialgia syndrome in MCD (often of a neurotic nature) in the patient is usually
managed to be suppressed by etiotropic and pathogenetic therapy, sometimes it is
necessary to prescribe multicomponent drugs such as validol, valokordin, corvalol,
and sedatives (novopassit, tinctures or decoctions of arsenic, valerian, etc.).
In the presence of persistent arrhythmias, treatment is carried out with
antiarrhythmic agents; in heart failure - with the appointment of cardiac glycosides,
diuretics; if indicated, treatment courses can be conducted with agents from the group
of angiotensin-converting enzyme inhibitors.
For extrasystole, antiarrhythmic drugs are used. It is advisable to conduct a drug
test before prescribing them.
The drug of choice for supraventricular extrasystoles is calcium channel
antagonists (verapamil) at 80-120 mg/day for 10-14 days. Sotalol or beta-blockers can
be used.
For ventricular extrasystoles, ethacizine or etmozine is used up to 300-400
mg/day for 7 days, then at half a dose for 1-2 months.
In cases of sinus tachycardia and a positive functional test with adrenergic
blockers, selective beta-blockers (atenolol, metoprolol, etc.) are indicated for 2-3
weeks at 50-100 mg/day. In cases of pronounced sinus bradycardia combined with
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vagus-dependent extrasystoles, drugs that reduce vagus activity (amizil, bellataminal)
are indicated. They are prescribed at 1.0 mg 3-4 times a day for 2-3 weeks.
In the complex treatment of patients with MCD, it is possible to recommend
treatment courses with the daytime tranquilizer adaptol, which has a multifaceted
effect (vegetotropic, has a positive effect on the cardiovascular system, relieves
anxiety, improves sleep, etc.).
A special role in the treatment of all forms of CVD is given to the use of complex
preparations of magnesium and potassium salts, which play an important role in the
activity of the cardiovascular system.
It has been established that there is an antagonism between the action of
magnesium and calcium in relation to the smooth muscles of the vessels and the
myocardium. Therefore, magnesium is especially active in combination with
potassium (calcium's active antagonist). Minimal disruptions in intracellular
magnesium levels, especially in combination with potassium, actively alter
myocardial cell function and vascular tone.
In stressful situations, the loss of magnesium by the div increases due to the
influence of catecholamines on the absorption of magnesium and the metabolic
processes associated with its participation. Firstly, the increased release of
catecholamines (adrenal hormones) into the blood leads to the loss of cellular
magnesium and its elimination with urine due to reduced reabsorption in the tubular
apparatus. Secondly, catecholamines intensify lipolysis, which causes an increase in
the content of free fatty acids that bind the ionized magnesium of the plasma. The
release of intracellular magnesium is activated.
A decrease in magnesium content (especially in combination with a decrease in
potassium) leads to a change in the magnesium/calcium ratio in the adrenal cortex
cells, which causes an increase in the secretion of mineralocorticoid hormones, which
further exacerbate the div's magnesium loss.
A possible role of magnesium deficiency in the pathogenesis of atherosclerosis
has been established, since this microelement plays an important role in lipid
metabolism and the development of hyperlipidemia with magnesium deficiency: in
hypomagnesemia, the content of low-density lipoproteins increases.
In the experiment, when examining the vessels of animals with magnesium
deficiency, changes characteristic of the early stages of atherosclerosis were
established: muscle cell hyperplasia, fibrinoid necrosis and chronic adventitial
inflammation, lipid infiltration of the endothelium, swelling and thickening of the
intima, cleavage and fragmentation of the inner elastic layer, and the appearance of
lipid spots.
The mechanism of the hypolipidemic effect of magnesium salts is complex and
is interpreted ambiguously. Firstly, magnesium reduces lipolysis by activating the
release of noradrenaline from the adrenal glands and the ends of sympathetic nerve
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fibers. Secondly, magnesium salts increase the level of cAMP, which increases the
activity of lipoproteins-splitting lipases.
Magnesium enhances the activity of an enzyme that increases cholesterol
esterification and is a cofactor of enzymes that regulate lipid metabolism.
In arterial hypertension, significant magnesium retention was established during
the load test, and a reverse correlation between systolic and diastolic blood pressure
and the magnitude of magnesium excretion with urine was revealed. An inverse
correlation has also been established between the concentration of magnesium in
erythrocytes and blood pressure levels.
For patients with arterial hypertension who respond to magnesium therapy,
higher renin activity in blood plasma is characteristic compared to those who do not
respond to treatment.
Magnesium is one of the active regulators of vascular tone. It has been
established that the frequency of arterial hypertension increases in biogeochemical
regions where the magnesium content in drinking water is reduced.
Adverse effects associated with magnesium deficiency, manifested by increased
tone, coronary artery spasm, increased sensitivity to vasoconstricting agents
(angiotensin, serotonin, noradrenaline, acetylcholine), decrease quite quickly and
actively when magnesium and potassium preparations are included in the complex
therapy.
Currently, panangin, a complex drug, is most actively used in clinical practice.
Panangin
is a combination of magnesium asparaginate and potassium
asparaginate. The drug normalizes the intracellular and extracellular ratio of
potassium, magnesium, calcium, and sodium ions, which contributes to the
improvement of myocardial contractility. Upon entering the cells, asparaginate is
incorporated into metabolic processes.
Endogenous asparaginate is a conductor of ions due to its high affinity for cells.
In addition, ions in the form of complex compounds penetrate the cell due to the
insignificant dissociation of its salts. Potassium and magnesium aspartates improve
myocardial metabolism, improve coronary blood circulation, and enhance the effects
of antiarrhythmic drugs.
Indications for panangin are:
MCD, heart rhythm disturbances (ventricular
extrasystole, atrial fibrillation, tachycardia), overdose and glycoside intoxication, and
other conditions accompanied by symptoms of hypokalemia and hypomagnesemia.
Contraindications for prescribing the drug: hyperkalemia and hypermagnesemia,
atrioventricular blockades of I-III degree, acute and chronic renal failure, increased
individual sensitivity to the drug's components.
When prescribing panangin to patients, it is necessary to remember its
interaction with other medications. Simultaneous administration with potassium-
saving diuretics, beta-blockers, angiotensin-converting enzyme inhibitors, heparin,
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and nonsteroidal anti-inflammatory drugs increases the risk of developing
hyperkalemia. Prescribing potassium and magnesium drugs in conjunction with
hormonal drugs (glucocorticosteroids) eliminates the hypokalemia developing during
steroid administration. Panangin reduces the adverse side effects of cardiac
glycosides, enhances the negative drono- and bathmotropic effects of antiarrhythmic
drugs. It should also be noted that calcium preparations reduce the effect of
magnesium and potassium preparations.
Panangin
is available in tablet form, coated with a film film. It is
recommended to prescribe 1 tablet 2-3 times a day after meals, depending on the
patient's age (8-9 years old - 1 tablet, from 10 to 14 years old - 2 tablets, older than
14 years old - 3 tablets per day). The duration of the treatment course is determined
individually, usually 3-4 weeks.
Dispensary observation of patients with CMD of various origins continues until
all clinical symptoms disappear, as well as until the ECG normalizes (at least 6-12
months). The physical load is regulated individually. Schoolchildren are assigned
physical therapy or a preparatory group for physical education (without cross-country
races or competitions). Sanitation of chronic infection and comorbidity foci is
mandatory. Complex cardiotrophic therapy courses are recommended 2-3 times a
year (1.0-1.5 months).
Sports doctors, as well as pediatric cardiologists, rheumatologists, and
pediatricians, should be engaged in the prevention of ICD development, especially in
young athletes. First of all, it is necessary to carefully select children for sports.
Sanitation of chronic infection sites, timely treatment of all diseases, adherence to a
daily routine, and proper nutrition play an important role in the prevention of MCD.
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