The prevalence of sudden death from chronic heart failure and cardiac arrhythmias caused by myocardial infarction is a complex problem in cardiology. Post-infarction cardiac remodeling occurs after myocardial infarction. This compensatory-adaptive reaction, regulated by mechanical, neurohumoral and genetic factors, includes the structural and functional changes of cardiomyocytes, stromal elements and extracellular matrix, geometry and architectonics of the left ventricular cavity. Adverse left ventricular remodeling is associated with heart failure and increased mortality. The concept of post-infarction cardiac remodeling is an urgent problem, since the mechanisms of development and progression of adverse post-infarction changes in the myocardium are completely unexplored. In recent years, the scientist attention has been focused on neurotrophic factors involved in the sympathetic nervous system and the vascular system remodeling after myocardial infarction. Nerve growth factor (NGF) is a protein from the neurotrophin family that is essential for the survival and development of sympathetic and sensory neurons, which also plays an important role in vasculogenesis. Acute myocardial infarction and heart failure are characterized by changes in the expression and activity of neurotrophic factors and their receptors, affecting the innervation of the heart muscle, as well as having a direct effect on cardiomyocytes, endothelial and smooth muscle vascular cells. The identification of the molecular mechanisms involved in the interactions between cardiomyocytes and neurons, as well as the study of the effects of NGF in the cardiovascular system, will improve understanding of the cardiac remodeling mechanism. This review summarizes the available scientific information (2019–2021) about mechanisms of the link between post-infarction cardiac remodeling and NGF functions.

Introduction. Cardiovascular disease is the leading cause of morbidity, disability and mortality in modern society. Coronary artery disease (CAD) and chronic obstructive pulmonary disease (COPD) are the most common comorbid pathology that worsens the quality of life and prospective prognosis of patients.Aim. The literature review is focused on postoperative outcomes of patients with COPD undergoing coronary artery bypass grafting surgery (CABG).Results. The review presents national and international data the prevalence of COPD in patients having CABG. The issues of risk stratification of comorbid patients in cardiac surgery are considered. It is shown that patients with CAD in combination with COPD are more at risk of various complications after CABG. COPD increases the chances of a complicated course of the in-hospital period by 2.1 times and risk of death in the long-term period after CAPG by 1.8 times. Patients with COPD are at a higher risk of developing postoperative pneumonia, respiratory failure, stroke, kidney failure, and wound infection of the sternum. Long-term 5-year and 10-year survival after CABG is lower in patients with COPD. The longterm adverse prognosis depends on the severity of the bronchial obstruction. Achievements in the field of cardiac surgery have had a significant impact on the results of surgical interventions in the comorbid course of CAD and COPD. Intensive pulmonary rehabilitation after surgery and effective drug therapy can improve the outcomes after CABG in patients with COPD. Hybrid coronary revascularization and minimally invasive coronary surgery appear to be viable alternatives to conventional CABG, offering a less invasive approach to coronary revascularization, which may be especially beneficial to high-risk patients with COPD.

Background. Studies of the role of cytokines in the pathogenesis of coronary artery disease (CAD) are quite relevant. Significant cytokine imbalance is mostly observed in patients with acute coronary syndrome. However, there are limited reports of serum cytokine levels in patients with chronic stable CAD. The problem of relationship between cytokines to the severity of coronary atherosclerosis is still urgent.Aim: To investigate the relationship between serum levels of cytokines and the severity of CAD.Material and Methods. Serum levels of IL-2, IL-4, IL-6, IL-10, TNF-a was analyzed in 24 healthy control patients and 70 patients with stable CAD who underwent coronary angiography. Coronary atherosclerosis was assessed with Gensini scoring system. Depending on the median of GS (38.0), the patients were divided into moderate CAD group (GS = 8–37) and severe CAD group (GS ≥ 38). The data were analyzed using Statistical Package for the Social Sciences (SPSS) software 26.0.Results. Patients with obstructive CAD presented higher TNF-α levels and lower IL-4. Patients with severe CAD increased IL-6 and reduced IL-2 levels. Logistic regression analysis showed that the IL-6 was independently related to the presence of obstructive CAD (OR = 3.836; 95% CI= 1.8–8.177). ROC analysis of the IL-6 logistic regression model showed that a cut-off of 5.19 pg/mL had 75.0 % sensitivity and 70.0 % specificity to predict severe atherosclerosis.Conclusion. Pro-inflammatory TNF-α and IL-6 cytokines increased, while regulatory IL-2 and anti-inflammatory IL-4 decreased in patients with stable CAD. Cytokine imbalance contributes to CAD progression. Elevated IL-6 levels and the pro-inflammatory potential of the blood increases in case of severe coronary atherosclerosis. It has been shown that with an increase in IL-6 levels, the odds of detecting severe CAD increases 3.5-folds.

Coronary artery disease (CAD) is defined as myocardial damage developing as a result of its organic and functional changes, and leading to impaired blood flow through the coronary arteries. An important pathogenetic component of CAD is atherosclerosis. Currently, key aspects of the molecular relationship between inflammation and atherosclerosis are being actively studied, the immunometabolic theory of atherosclerosis is being discussed, along with an involvement of perivascular adipose tissue in the pathogenesis of this pathology, due to its ability to respond to atherogenic stimuli via developing inflammatory reactions. Evidence has been accumulated that in patients with CAD, both in their blood and perivascular adipose tissue, the level of neurotrophic factors (in particular, brain-derived neurotrophic factor, BDNF) changes, which may be a promising area of research from the standpoint of studying this factor as a therapeutic target for atherosclerosis in CAD. Neurotrophic growth factors control the functioning of both immune and nervous systems, and the balance of energy metabolism and innervation of adipose tissue. They affect vascular homeostasis, and are also involved in causing and stopping inflammation. Currently, there are data on the role of BDNF in the pathogenesis of cardiovascular, neurodegenerative and metabolic diseases, and on the effect of polyunsaturated fatty acids and eicosanoids on the level of BDNF and, accordingly, the development and progression of coronary artery atherosclerosis. Our review summarizes published data (2019-2021) on the pathophysiological and pathogenetic mechanisms of the relationship between BDNF and CAD (atherosclerosis).