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.

Cardiogenic shock (CS) is one of the most serious complications of myocardial infarction (MI) with a high mortality rate. The timely and effective prevention and early suppression of this adverse event may influence the prognosis and outcome in patients with MI complicated by CS (MI CS). Despite the use of existing pharmaco-invasive options for maintaining an optimal pumping function of the heart in patients with MI CS, its mortality remains high, prompting the search for new approaches to pathogenetic therapy. This review considers the role of the systemic inflammatory response in the pathogenesis of MI CS. The primary processes involved in its initiation are described, including the progression from the onset of MI to the generalization of the inflammatory response and the development of multiple organ dysfunction. The approaches to anti-inflammatory therapy in patients with CS are discussed, and further promising research directions are outlined. In this review, we updated and summarized information on the inflammatory component of MI CS pathogenesis with a particular focus on its foundational aspects. This will facilitate the identification of specific inflammatory phenotypes and endotypes in MI CS and the development of targeted therapeutic strategies for this MI complication.

Кардиогенный шок – что нового?

This article presents two clinical cases of patients with myocardial infarction and stage A (at risk) and B (beginning) cardiogenic shock who underwent intra-aortic balloon counterpulsation (IABP). In patients with a high risk of classic cardiogenic shock and/or the no-reflow phenomenon, stenting of the infarct-related coronary artery during this type of mechanical circulatory support was performed without complications. Theoretical and practical aspects of using IABP at different stages of cardiogenic shock are discussed.

Background and Objectives: In-hospital mortality associated with myocardial infarction complicated by cardiogenic shock (MI-CS) remains critically high. A particularly challenging form, mixed shock (MS), combines features of cardiogenic shock (CS) with distributive elements such as vasodilation and reduced vascular resistance. MS is associated with elevated mortality rates and presents unique diagnostic and therapeutic challenges. This study aimed to analyze the clinical, historical, instrumental, and laboratory characteristics of the primary phenotypes of MI-CS, stratified according to the Society for Cardiovascular Angiography and Interventions (SCAI) shock severity scale. Materials and Methods: In this single-center, retrospective observational study, we reviewed the medical records of 1289 patients admitted to the emergency cardiology department from 1 January to 12 December 2020. Among them, 117 patients were identified as having MI-CS and were divided into two groups: MS (n = 48) and isolated CS (n = 69). The data were analyzed using the SCAI shock classification. Logistic regression analysis was employed to identify predictors of mortality and improved survival outcomes. Results: Patients with MS were older (80 years [71.0; 83.0] vs. 73 years [64.0; 81.0], p = 0.035). The overall mortality rate was significantly higher in the MS group (68% vs. 53%, RR = 1.438, 95% CI: 1.041–1.986, p = 0.03). Logistic regression identified mechanical ventilation (OR = 8.33, 95% CI: 2.54–22.80, p = 0.012), elevated lactate levels (OR = 1.20, 95% CI: 1.02–1.41, p = 0.026), and cardiopulmonary resuscitation (CPR) (OR = 7.97, 95% CI: 2.51–24.40, p < 0.0001) as independent predictors of mortality. Conversely, the use of an intra-aortic balloon pump (IABP) (OR = 0.22, 95% CI: 0.06–0.80, p = 0.021) and a higher body mass index (BMI) (OR = 0.91, 95% CI: 0.84–0.99, p = 0.038) were associated with reduced mortality risk. Conclusions: MS in the context of MI-CS represents a distinct clinical phenotype with specific hemodynamic features and significantly worsened outcomes. The identification of mortality predictors, such as mechanical ventilation, elevated lactate levels, and CPR, alongside protective factors like IABP use and a higher BMI, underscores the importance of early and tailored therapeutic interventions. These findings highlight the need for further studies to refine treatment protocols and improve outcomes in this high-risk population.

Aim: To access the features of the course of myocardial infarction (MI) in patients with different stages of MI complicated by cardiogenic shock (MI CS) according to the SCAI scale. Methods: We retrospectively described the portrait of CS MI (n = 117) at different stages of SCAI from the hospital MI registry (n = 1253). Results: Hospital mortality increased from stage to stage (p ≤ 0.001). Significant differences in biochemical parameters were found both for indicators characterizing intensive care measures, such as the presence of mechanical lung ventilation or an intra-aortic balloon pump, and for indicators of organ hypoperfusion such as lactate level, pHv (7.39 (7.36; 7.44) at stage A–B; 7.14 (7.06; 7.18) at stage E), creatinine, and glomerular filtration rate. Parameters related to MI characteristics, such as instrumental and laboratory data, anamnesis of ischemia, and performed treatment, did not differ between groups. Polynomial logistic regression showed that lactate level, mechanical ventilation, and monocyte count upon admission (1.15 (0.96; 1.23) at stage A–B; 0.78 (0.49; 0.94) at stage E, p = 0.005) correlated with CS severity. Conclusion: The characteristics of MI at different stages of SCAI do not have differences and do not determine the severity of shock. We revealed a high discriminatory potential of the pH level in predicting refractory shock. The value of monocytes at admission may be a promising predictor of the severity of MI CS. The question of the causes of heterogeneity of MI CS, taking into account the homogeneity of MI characteristics, remains open and promising.