[Characteristics of Inferior Myocardial Infarction With a Special Electrocardiographic Pattern (Aslanger) in Metabolic Syndrome].

AIM: To evaluate the features of ST-segment elevation myocardial infarction with the Aslanger pattern in comparison with traditional forms of inferior myocardial infarction in metabolic syndrome. MATERIAL AND METHODS: This study included 30 patients with inferior myocardial infarction in the presence of metabolic syndrome: 9 patients with the Aslanger electrocardiographic pattern (group 1, age 59.7 [58.4; 63.1] years) and the rest with one of the traditional forms (control group, 59.9 [57.2; 63.8] years, matched by all criteria of metabolic syndrome). All patients underwent primary percutaneous intervention with assessment of the angiographic picture. The magnitude of ST-segment elevation was measured in lead III at the J point and following 0.06 seconds, and the optimal threshold value of this indicator was determined for a new picture of myocardial infarction. RESULTS: The infarct-related artery in the Aslanger pattern was more often the circumflex artery (p=0.0099), and coronary thrombosis was characterized by a lower TIMI thrombus grade (p=0.014). SYNTAX values for the Aslanger pattern and for the traditional picture of inferior infarction with ST elevation in lead II≥III were higher than for a similar picture with ST elevation in lead III>II. The level of cTnI at admission (p=0.013) and after 24 hours (p=0.0017), the platelet count (p=0.0011) and mean volume (p=0.0047) in group 1 had smaller values than with traditional inferior infarction. The ST elevation at J point and at J+0.06 s point for lead III with the Aslanger pattern was significantly lower than values of such shift in lead III>II and lead II≥III with traditional inferior infarction (p<0.001). An elevation value ≤1.5 mm at J point +0.06 s was a predictor of infarction with the Aslanger pattern. Constructing the ROC curve made it possible to determine that with the Aslanger pattern, the best cutoff value for this index is 2 mm. CONCLUSION: Myocardial infarction with the Aslanger pattern as compared with traditional lower infarction in metabolic syndrome is characterized by specific individual angiographic signs, lower ST segment elevation, cTnI level, and thrombotic disorders.

Meta-Analysis of Non-Alcoholic Fatty Liver Disease and Electromechanical Reconstruction of Myocardium.

In developed countries, non-alcoholic fatty liver disease (NAFLD), which results from obesity, has become endemic and kills many adults annually. Health research centers in most countries are looking to examine the relationship between metabolic syndrome (MetS) and metabolic biomarkers. A bleeding-prone standard liver biopsy or costly magnetic resonance imaging scan is used to diagnose NAFLD. The present study aimed to analyze medical databases using various scientific articles; moreover, this experiment analyzed medical databases using published scientific articles related to NAFLD, endovascular treatment, cardiac arrhythmias and conduction disorders, changes in the geometry of atria and ventricles, changes in myocardial mass volume as well as diastolic flow left and right ventricular systolic functions, coronary blood flow, analysis of the dependence of epicardial fat tissue (EFT) thickness, and the presence of chronic heart failure (CHF). It is demonstrated that the index of EFT in NAFLD positively correlated with the criteria of cardiovascular health, values of the carotid intima-media thickness, and calcification of the coronary arteries on the coronary artery calcium scale (P<0.0001). The index of per EFT significantly correlated with the factor of the age of the NAFLD patients (P=0.04), hemoglobin A1C level (P<0.001), systemic inflammatory index (P=0.02), the index of impaired glucose tolerance (P=0.03), and especially, the patient's diabetes factor (P<0.001). In addition, adiponectin levels were significantly lower in individuals with NAFLD (P=0.001) and patients with MetS (P=0.02). NAFLD in association with an increase in epicardial adipose tissue (EAT) is an independent risk factor for atherosclerosis, coronary heart disease, CHF, as well as structural and electrophysiological myocardial remodeling. The study of pathogenetic mechanisms in the context of the role of EAT and clinical monitoring of its condition are urgent problems of modern medicine.