ISCHEMIC HEART DISEASE. MICROVASCULAR ANGINA

Аннотация

Microvascular angina is defined by the presence of anginal pain, a positive stress test, and intact coronary arteries, which is observed in approximately 20-30% of patients with angina who have undergone coronary angiography. The prevalence of this disease is significantly higher in women than in men. Microvascular angina is a heterogeneous form of coronary heart disease, bothclinically and pathophysiologically, encompassing various pathogenetic mechanisms. Kеywоrds:microvascular angina, method, cardiac syndrome X. INTRОDUСTIОN Microvascular angina (MVA) is one of the forms of chronic ischemic heart disease (IHD) (a variant of stable angina) [1]. Currently, a distinction is made between primary MVA (previously, the term "cardiac syndrome X" was often used for this pathology in the literature) and secondary MVA, which develops against the background of existing heart diseases, such as: hypertrophic cardiomyopathy, aortic stenosis, diabetes mellitus, vasculitis, etc. At the same time, in each specific case there is a specific mechanism leading to myocardial ischemia, but not associated with the primary pathology of the microvascular bed of the heart. Further, we will discuss the features of the clinical picture, diagnosis and treatment of primary MVA. The current definition of primary MCC includes the following characteristics: anginal pain, a positive exercise stress test, intact coronary arteries according to coronary angiography, microvascular dysfunction and impaired coronary reserve proven bymodern diagnosticmethods [2]. MАTЕRIАLSАNDMЕTHОDS According to the literature, annually 30-50% of women and 10-20% of men undergo diagnostic coronary angiography due to complaints of chest pain are found to have angiographically unchanged or slightly changed coronary arteries [3]. However, not all of these patients have primary MCC. In clinical practice, this disease is currently overdiagnosed due to difficulties in confirming microvascular dysfunction and impaired coronary reserve at the microcirculation level [4]. Given the lack ofepidemiological registers ofMCC, thequestion of the trueprevalence of this disease remains open. As a rule, patients with primary MCC are younger than patients with classic angina pectoris due to atherosclerosis of the coronary arteries, and their average age is 49 ± 9 years [2]. If we consider the gender composition, women, especially those in peri- and postmenopause, suffer from MCC significantly moreoften [3]. RЕSULTSАNDDISСUSSIОN Currently, two main theories of the pathogenesis of MCC can be distinguished: ischemic (myocardial ischemia due to endothelial dysfunction of microvessels) and non-ischemic (impaired pain sensitivity), but neither of them can fully explain the pathogenesis of the disease. Supporters of the ischemic theory call the leading cause of microvascular changes in MCC endothelial dysfunction of coronary microvessels (pre-arterioles and arterioles), which is characterized by a violation of the vasodilation process and a decrease, as a result, in the www.wordlyknowledge.uz ILMIYMETODIK JURNAL JOURNAL OFIQRO –ЖУРНАЛ ИҚРО –IQRO JURNALI –volume 15,issue01,2025 ISSN:2181-4341, IMPACT FACTOR( RESEARCH BIB )–7,245,SJIF–5,431 coronary reserve, which is confirmed by numerous studies that have revealed a reduced reserve of coronary blood flow in response to atrial stimulation, as well as intracoronary administration of dipyridamole, adenosine and acetylcholine [9, 10]. According to the literature, patients with MCC have generalized disorders of both endothelium-dependent [4] and endothelium- independent vasodilation of coronary microvessels [2]. The causes of endothelial dysfunction in patients with MCC are varied: dysfunction of endothelial cells and their apoptosis, chronic inflammatory process accompanied by an increase in inflammation markers (C-reactive protein, interleukin-6, tumor necrosis factor-alpha), increased free oxidation processes associated with antioxidant deficiency [3], increased aggregation of platelets and erythrocytes, changes in autonomic regulation of arterial tone, and others [1]. There is evidence that a decrease in coronary reserve in CVS occurs not only due to impaired vasodilation of the microvascular link, but also as a result of microspasms arising from increased sensitivity of prearterioles and arterioles to vasoconstrictor stimuli [2]. Impaired endothelium-dependent vasodilation is associated with an imbalance of vasoactive factors: a decrease in the level of nitric oxide (a vasodilator) and an increase in the level of endothelin-1 (a vasoconstrictor) [3]. Such factors frequently encountered in CVS as hypoestrogenemia [4], dyslipidemia [1], arterial hypertension, hyperhomocysteinemia, and hyperinsulinemia [3] can also play a role in the formation of endothelial dysfunction. Thus, the causes of endothelial dysfunction in MCC are varied, and their contribution to the development of the disease may be different in each specific clinical situation. S