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Aim. To evaluate the information value of a complex of clinical and biochemical parameters of myocardial damage in predicting the development of transmural myocardial damage according to magnetic resonance imaging (MRI) in patients with acute myocardial infarction (AMI).Material and methods. The study included patients admitted to the emergency cardiology department with acute coronary syndrome. All patients underwent invasive coronary angiography, laboratory tests, and dynamic determination of cardiac biomarkers. In the interval of 6,1±4 days from admission to the hospital, patients underwent contrast-enhanced cardiac MRI. According to the pattern of delayed contrast enhancement, patients were divided into two groups: with a transmural and subendocardial pattern.Results. The mean age of patients was 62,5±10,5 years, while 27 (71,1%) had ST-segment elevation AMI. Among the risk factors for coronary artery disease, dyslipidemia (89,5%), hypertension (68,4%), and smoking (57,9%) were the most common. Creatine phosphokinase-MB (CPK-MB), serum high-sensitivity cardiac troponin I (cTnI) and C-reactive protein (CRP) values after 24 h were significantly higher in patients with transmural hyperenhancement. Moderate positive relationship was found between the global size of left ventricular (LV) damage according to MRI data and the levels of CPK-MB after 24 h and 4 days, as well as with CRP after 24 h, 4 and 7 days, and cTnI level after 24 h and 4 days. In the group of patients with transmural pattern, the global size of LV damage was significantly higher. Patients of this group were characterized by higher prevalence of microvascular obstruction. In a univariate regression analysis, there were following significant predictors of transmural myocardial damage: CPK-MB after 4 days (p=0,023) and ST segment elevation (p=0,029). Multivariate regression analysis showed that the only independent predictor of transmural myocardial damage was an increase in CPKMB after 4 days (p=0,023).Conclusion. An independent predictor of LV transmural damage in AMI was an elevated level of CPK-MB after 4 days. However, this laboratory marker had unsatisfactory information completeness and predictive quality. In this regard, cardiac MRI in patients with AMI, compared with the standard clinical assessment, can be considered preferable for assessing the depth of myocardial damage, risk stratification, and prognosis.

Data of metabolic scintigraphy may be useful for the integrated prediction of CRT efficacy.

: The purpose of the review is the analysis of clinical and experimental data on the etiology and pathogenesis of takotsubo syndrome (TS). TS is characterized by contractile dysfunction, which usually affects the apical region of the heart, lack of coronary artery obstruction, moderate increase in myocardial necrosis markers, prolonged QTc interval (in 50% of patients), sometimes elevation of ST segment (in 19% of patients), increase N-Terminal Pro-B-Type Natriuretic Peptide level, microvascular dysfunction, sometimes spasm of the epicardial coronary arteries (in 10% of patients), myocardial edema, and life-threatening ventricular arrhythmias (in 11% of patients). Stress cardiomyopathy is a rare disease, it is observed in 0.6 - 2.5% of patients with acute coronary syndrome. The occurrence of takotsubo syndrome is 9 times higher in women, who are aged 60-70 years old , than in men. The hospital mortality among patients with TS corresponds to 3.5% - 12%. In many patients with TS, but not in all, physical or emotional stress precedes the disease. Many patients with TS, but not all, have neurological or mental illnesses. The level of catecholamines is increased in patients with TS, therefore, the occurrence of TS is associated with the excessive activation of the adrenergic system. The negative inotropic effect of catecholamines is associated with the activation of β2 adrenergic receptors. An important role of the adrenergic system in the pathogenesis of TS is confirmed by studies which were performed using 125I-metaiodobenzylguanidine (125I –MIBG). TS causes edema and inflammation of the myocardium. The inflammatory response in TS is systemic. TS causes impaired coronary microcirculation and reduces coronary reserve. There is reason to believe that an increase in blood viscosity may play an important role in the pathogenesis of microcirculatory dysfunction in patients with TS. Epicardial coronary artery spasm is not obligatory for the occurrence of TS. Cortisol, endothelin-1 and microRNAs are challengers for the role of TS triggers. A decrease in estrogen levels is a factor contributing to the onset of TS. The central nervous system appears to play an important role in the pathogenesis of TS.