Adverse cardiac remodeling leads to impaired ventricular function and heart failure, remaining a major cause of mortality and morbidity in patients with acute myocardial infarction. It have been shown that, even if all the recommended therapies for ST-segment elevation myocardial infarction are performed, one third of patients undergoes progressive cardiac remodeling that represents morphological basis for following heart failure. The need to extend our knowledge about factors leading to different clinical scenarios of myocardial infarction and following complications has resulted in a research of immuno-inflammatory pathways and molecular activities as the basis for post-infarction remodeling. Recently, macrophages (cells of the innate immune system) have become a subject of scientific interest under both normal and pathological conditions. Macrophages, besides their role in host protection and tissue homeostasis, play an important role in pathophysiological processes induced by myocardial infarction. In this article we summarize data about the function of monocytes and macrophages plasticity in myocardial infarction and outline potential role of these cells as effective targets to control processes of inflammation, cardiac remodeling and healing following acute coronary event.

The hospital mortality in patients with ST-segment elevation myocardial infarction (STEMI) is about 6% and has not decreased in recent years. The leading cause of death of these patients is ischemia/reperfusion (I/R) cardiac injury. It is quite obvious that there is an urgent need to create new drugs for the treatment of STEMI based on knowledge about the pathogenesis of I/R cardiac injury, in particular, based on knowledge about the molecular mechanism of ferroptosis. In this study, it was demonstrated that ferroptosis is involved in the development of I/R cardiac injury, antitumor drug-induced cardiomyopathy, diabetic cardiomyopathy, septic cardiomyopathy, and inflammation. There is indirect evidence that ferroptosis participates in stress-induced cardiac injury. The activation of AMPK, PKC, ERK1/2, PI3K, and Akt prevents myocardial ferroptosis. The inhibition of HO-1 alleviates myocardial ferroptosis. The roles of GSK-3β and NOS in the regulation of ferroptosis require further study. The stimulation of Nrf2, STAT3 prevents ferroptosis. The activation of TLR4 and NF-κB promotes ferroptosis of cardiomyocytes. MiR-450b-5p and miR-210-3p can increase the tolerance of cardiomyocytes to hypoxia/reoxygenation through the inhibition of ferroptosis. Circ_0091761 RNA, miR-214-3p, miR-199a-5p, miR-208a/b, miR-375-3p, miR-26b-5p and miR-15a-5p can aggravate myocardial ferroptosis.

Aim. To describe profile of a modern portrait with non-ST-segment elevation myocardial infarction (non-STEMI) through a comprehensive analysis of the Emergency Cardiology Unit (ECU) practice, which discharge a function of a regional vascular centre.Material and methods. To describe the non-STEMI trends of the last decade, we analysed the annual reports on ECU work. The main analysis included patients with a documented non-STEMI treated in 2019 (n=221). We used information from the department database. A Microsoft Excel software was used to create the database. The base has been filled in by the ECU head in real time since 2009. Statistical data processing was performed using the Statistica 10,0 software package. The methods of descriptive statistics and Yates-corrected chi-square test were used.Results. The following clinical and demographic trends of the last decade were revealed: an increase in the number of patients with non-STEMI, proportion of male patients, mean age of patients, proportion of patients with MI with non-obstructive coronary artery disease; no decrease in in-hospital mortality, despite the introduction of modern guidelines, pharmacological and invasive treatment of non-STEMI. In 2019, the proportion of male patients and patients 75 years and older was 62,4% and 32%, respectively. The mean age of patients was 64,6±13,0 years. Clopidogrel was the predominant P2Y12 receptor blockers (56,1%). A total of 176 patients (79,6%) underwent the invasive procedures. Endovascular myocardial revascularization was performed in 97 patients (43,9%), while in the group over 75 years old — in 16 (7%) patients. The leading causes for absence of myocardial revascularization were chronic kidney disease (4,6%), severe coronary artery disease (6,3%), “borderline” (50-60%) coronary artery stenosis. The overall in-hospital mortality rate was 9,0%, while in the group of patients over 75 years old — 19,7%. Mortality rates did not differ in patients with and without myocardial revascularization (p=0,2). However, the incidence of pulmonary oedema was higher in the conservative treatment group (p=0,04).Conclusion. Treatment of patients 75 years and older remains the main barrier in management of patients with non-STEMI. We observe the treatment-risk paradox, which consists in choosing a less aggressive treatment strategy in the group of the most high-risk patients. Other relevant aspects in the management of non-STEMI patients are the selection of a method for myocardial revascularization in multivessel coronary artery disease, assessment of the hemodynamic significance of coronary artery stenosis, and patients with non-obstructive coronary artery disease.

Microvascular obstruction (MVO) of coronary arteries increases the mortality rate and major adverse cardiac events in patients with acute myocardial infarction (AMI) and percutaneous coronary intervention (PCI). According to preliminary data platelets, inflammation, Ca2+ overload, neuropeptide Y, and endothelin-1 could be involved in the pathogenesis of MVO. Many questions related to the pathogenesis of MVO remain unanswered. The role of endothelial cell damage in the formation of MVO in patients with AMI and PCI is unknown. It is unclear whether nitric oxide (NO) production reduces or decreases sensitivity of smooth muscle cells of coronary arteries to NO in patients with MVO. It was obtained only indirect evidence on the involvement of inflammation in the development of MVO. The role of ROS in the pathogenesis of MVO is not studied. The role of necroptosis and pyroptosis in the pathogenesis of MVO in patients with AMI and PCI is also not studied.The significance of thromboxane A, vasopressin, angiotensin II, and prostacyclin in the formation of MVO is unknown before. It was not obtained conclusive evidence on the involvement of coronary artery spasm in the development of MVO. Correlation analysis of the neuropeptide Y, endothelin-1 levels and the MVO size in patients with AMI and PCI was not performed. It is not clear whether endogenous adrenaline exacerbates MVO or, conversely, prevents MVO.

Changes in the macrophage infiltration of kidneys in rodents under ischemic conditions may affect cardiac macrophages and lead to development of adaptive cardiac remodeling. The aim of our study was to translate experimental findings into clinically relevant applications and assess the features of macrophage infiltration of the kidney and its correlations with changes in macrophage infiltration of the myocardium and with clinical data in patients who experienced a fatal myocardial infarction (MI). We examined fragments of both organs taken from patients (n = 30) who suffered from fatal MI. Macrophage infiltration was assessed by immunohistochemistry. Macrophage infiltration of the kidneys in patients with fatal MI is heterogeneous. The early period of MI was shown to be characterized by the prevalence of CD163+ and CD68+ cells, and in the long-term period by only CD163+ cells. However, only the level of CD206+ cells in the kidneys showed the dynamics representing the late MI period. Its decrease accompanied increase in the numbers of cardiac CD68+, CD163+, CD206+, and stabilin-1+ cells in the infarct area. Kidney CD206+ cells had more correlations with cardiac macrophages than other cells, and the presence of these cells also correlated with impairment of renal function and early death.