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STUDY OF PATHOLOGICAL CHANGES IN THE CARDIOVASCULAR SYSTEM IN
PULMONARY TUBERCULOSIS
Ergashov Behruzjon Komilovich
https://doi.org/10.5281/zenodo.15292159
Abstract. Study of pathological changes in the cardiovascular system in pulmonary
tuberculosis and development of modern therapeutic solutions.
Keywords: pulmonary tuberculosis, ventricular diastolic dysfunction, stress, smoking,
anticholinergic drugs, b2-agonists.
ИЗУЧЕНИЕ ПАТОЛОГИЧЕСКИХ ИЗМЕНЕНИЙ СЕРДЕЧНО-СОСУДИСТОЙ
СИСТЕМЫ ПРИ ТУБЕРКУЛЕЗЕ ЛЕГКИХ
Аннотация. Изучение патологических изменений сердечно-сосудистой системы
при туберкулезе легких и разработка современных терапевтических решений.
Ключевые слова: туберкулез легких, желудочковая диастолическая дисфункция,
стресс, курение, антихолинергические препараты, b2-агонисты.
Relevance. It is known that in tuberculosis and other chronic inflammatory processes in
the lungs, inflammatory epithelial growth, squamous metaplasia and cancer in situ are not
uncommon, which is considered a conditio sine qua non of malignant neoplasm. At the same
time, inflammatory and cancerous epithelial growth are different entities. Although they may be
“pre-neoplastic” from the point of view of histological differentiation, they do not necessarily
become cancerous; rather, they are “conditionally precancerous” changes. They are
interconnected, as the inflammatory growth of the epithelium, in no way capable of
autonomously growing cancer cells, is 308diameter. On the other hand, the phenotypic diversity
of lung cancer in patients with tuberculosis (their localization in the central and even peripheral
departments, histological features, etc.), as well as the significant time interval between the
development of both, do not allow Tuberculosis remains the leading cause of morbidity and
mortality worldwide. Every year, 8.8 million cases of tuberculosis are recorded worldwide. At
the same time, 1.61 million people are diagnosed with lung cancer worldwide. In some countries,
the number of patients with malignant lung diseases admitted to tuberculosis hospitals is
increasing, which makes it difficult to accurately diagnose tuberculosis and malignant
neoplasms. There are many similarities between these two diseases, both are widespread, affect
the lung parenchyma, and are primarily characterized by similar symptoms. However, there are
many differences between these two nosologies: the consequences of different etiologies and the
management of patients in general are different.
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Currently, special attention is paid to the study of risk factors for pulmonary tuberculosis,
including urban air pollution, increased industrial dust, age, tobacco smoking, respiratory tract
infections, their frequent exacerbations, and exacerbation of obstructive pulmonary disease.
Thus, tobacco smoking is associated not only with the occurrence of pathological
processes in the lungs, but also with the development of systemic inflammatory reactions,
oxidative stress, vascular endothelial dysfunction, increased activity of procoagulant factors,
increased expression of oncogenes, and other systemic effects [1-7].
Left ventricular dysfunction and the occurrence of ventricular arrhythmias in patients
with pulmonary tuberculosis have been relatively poorly studied. Researchers Incalzi RA, Pistelli
R et al. There is a correlation between left ventricular function and cardiac rhythm disturbances
in patients with pulmonary tuberculosis. Ventricular arrhythmias were monitored for 24 hours
and the study was repeated because the clinical manifestations of respiratory failure improved.
Left ventricular diastolic dysfunction is one of the factors contributing to the
development of ventricular arrhythmias. The authors found a direct relationship between the
degree of respiratory failure and the manifestation of left ventricular diastolic dysfunction, while
blood gas parameters did not correlate with the clinical manifestations of arrhythmic episodes. In
clinical practice, a detailed diagnostic assessment of episodes of ventricular arrhythmia that
occurred against the background of left ventricular diastolic dysfunction is recommended, since
this clinic can be hidden myocardial ischemia, painless forms of angina pectoris, and right
ventricular overload during the formation of cor pulmonale [1].
It is worth noting that with the development of arrhythmia, the clinical manifestations of
respiratory failure also worsen, i.e., a syndrome of mutual overload is formed. Thus, the main
morphological sign of ventricular tachycardia, the discreteness of the "P" wave with different P-
P, P-R, RR intervals in leads I, II, III of the ECG, is mainly associated with the development and
occurrence of respiratory failure. The prognosis for pulmonary tuberculosis with the
development of this type of cardiac arrhythmia is considered unfavorable [10-12]. Studies of
arrhythmia in patients with pulmonary tuberculosis are clearly insufficient - there are many
unresolved problems, in particular, the role of secondary pulmonary hypertension has been
practically not studied [14,17]. The role of drugs is also poorly studied. This is no less important
among other problems.
Extrapulmonary systemic effects of pulmonary tuberculosis include weight loss,
functional impairment, malnutrition and skeletal muscle atrophy, mental disorders, i.e., the
clinical syndrome of secondary trophic deficiency. This problem is of increasing interest to
researchers in patients with a therapeutic profile, including pulmonary tuberculosis [15, 16].
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It is known that secondary immunological deficiency exists in patients with chronic
obstructive pulmonary disease. Violation of the differentiation of highly organized tissues can
lead to a decrease in the immune system due to tissue hypoxia in patients with broncho-
obstructive syndrome, as well as to a deficiency of immunity against infection and a violation of
immunological dependence.
There is a clear correlation between a decrease in myocardial contractility and increased
autosensitization. With an increase in the inflammatory process in the lungs in patients,
sensitivity to cardiac antigens is determined. In patients with reduced myocardial contractility,
sensitivity to cardiac antigens is preserved during remission of chronic obstructive pulmonary
disease, which indicates that autoimmune mechanisms are activated in the development of
myocardial lesions in them. Autoimmune damage to the myocardium inevitably changes its
bioelectrical properties, which leads to the development of rhythm disturbances in the heart [18,
19]. In recent years, anticholinergic drugs (ipratropium bromide, tiotropium bromide), β2-
agonists (short-acting - isoprenaline, salbutamol, fenoterol, long-acting - salmeterol, formoterol)
and methylxanthines have been used as bronchodilators for pulmonary tuberculosis. M-
anticholinergics do not change the heart rate (HR) and blood pressure, but in some cases, i.e.,
when used irregularly, they can cause arrhythmias.
Ipratropium bromide causes a short-term increase in heart rate. Tachycardia occurs in
0.01% to 1% of patients with tiotropium bromide. In isolated cases, supraventricular tachycardia
and ventricular fibrillation have been observed.
According to most researchers, the selectivity of β2-agonists is dose-dependent [1, 3].
The appointment of β2-adrenergic agonists is associated with adverse effects on the heart,
which is mainly associated with the development of sinus tachycardia [3]. Potentially, this group
of drugs is less effective in the following diseases: sinus tachycardia, when ischemic changes in
the myocardium are observed, in acute and chronic heart failure, in cardiac arrhythmias that can
lead to sudden death [6].
Another mechanism that can lead to cardiac arrhythmias when using β2-agonists may be
hypokalemia. β2-agonists, with the correct dosage regimen, do not cause arrhythmogenic effects
and do not aggravate existing cardiac arrhythmias. However, uncontrolled use of β2-agonists is
observed, especially in severe forms of pulmonary tuberculosis complicated by hypoxemia,
which increases their cardiotoxic effect [1, 5].
When prescribing theophyllines, the process of controlling therapeutic doses is
complicated, which, if exceeded, can lead to cardiotoxic
effects, sinus tachycardia, premature ventricular contractions, supraventricular
tachycardia, ventricular fibrillation and other arrhythmias may develop.
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