The use of computer-based virtual reality (VR) technologies in the educational process is continuously increasing for a variety of professional activities. Medical education is one of the examples, where such efforts are particularly visible. Today’s VR products provide the maximum immersion into a virtual environment and active interaction with their components. These VR products are becoming increasingly more popular, even in comparison with pseudo-3D simulators. VR facilitates the development of the abilities for precision work as much as mechanical skills. In emergency medical care, it is particularly important to practice the skills requiring specialized knowledge and abilities. In this work, we discuss VR-simulators built to practice the algorithm of emergency medical assistance in a maximally realistic environment.
Heart failure is an important medical, social and economic problem around the world. In recent years, a number of diagnostic and prognostic biological markers of blood in cardiovascular diseases have been studied. Identification of new biological markers, analysis of their pathophysiological aspects and changes in concentration under the influence of various treatment options, allow us to understand many pathogenetic features of the development and course of heart failure. In recent decades, natriuretic peptides have been introduced into clinical practice, which are widely used as reliable markers for diagnostic and prognostic assessment. Growth differentiation factor-15 is a cytokine belonging to the family of transforming growth factors, the activity of which is significantly increased under stress and inflammation. In patients with chronic heart failure, the concentration of this marker is associated with an increased risk of overall mortality and adverse cardiovascular events; in patients with heart failure with preserved left ventricular ejection fraction, the use of the marker showed prognostic and diagnostic significance. Data from the Framingham Heart Study showed that growth differentiation factor-15 was the only marker in multivariate analysis that showed a statistically significant association with all adverse cardiovascular events. Eight studies showed that overexpression of growth differentiation factor-15 was associated with an increased risk of mortality in patients with heart failure. It was shown that growth differentiation factor-15 as a prognostic marker in patients with acute heart failure is not inferior to the brain natriuretic peptide precursor. To confirm the value of this marker in blood in patients with heart failure, it is necessary to conduct extensive prospective randomized clinical trials.
This clinical case report describes the simultaneous development of an acute myocardial infarction, stroke, and a massive pulmonary thromboembolism in a 44-year-old patienta carrier of the thrombophilia gene polymorphisms: MTHFR C677T, A1298C, PAI-1 4G/5G, ITGA2 C807T. Multifocal thrombosis was probably due to the initial congenital deficiency of anticoagulants, accompanied by a decrease in antithrombin III and protein C, against the background of their critical consumption in cascade thrombosis, in combination with the carrier of polymorphisms of moderate and low thrombogenic risk. This case is unique in that there is usually a tendency toward clinical thrombosis when the level of antithrombin III is less than 70%. Such patients develop thrombosis at a younger age, and by the age of 35-40 years usually have a verified diagnosis of extremely high-risk hereditary thrombophilia. In this case, multifocal thrombosis was accompanied by critically low values of anticoagulants: antithrombin III -3.4%, and protein C -36.8%. The patient had suffered from epilepsy since childhood and took anticonvulsant drugs that increase the deficit of active folic acid and can lead to hyperhomocysteinemia, which in this case, against the background of an innate decrease in the activity of methyltetrahydrofolate reductase, could have aggravated the situation.
Myocardial infarction (MI) is an acute myocardial injury (confirmed by increasing|decreasing of cardiac troponin T and/or I) in conditions of proven acute myocardial ischemia, manifested by clinical symptoms of acute ischemia and/or ischemic changes on the ECG. Type 2 MI is a form of MI that is not associated with coronary atherothrombosis, secondary to a condition that results in an imbalance between myocardial oxygen intake and oxygen consumption. Type 2 MI can be caused by coronary artery spasm, coronary microvascular dysfunction, embolism, dissection of coronary arteries, aorta, bradyarrhythmia, tachyarrhythmia, respiratory failure with severe hypoxemia, anemia, blood loss, hypotension/shock of other etiology, severe hypertension, surgical interventions. Type 2 MI accounts for 270% of all cases of MI. More often type 2 MI occurs in women, elderly, severe, comorbid patients. Type 2 MI is ST segment elevation MI in 324% of patients and non-ST elevation MI in others. Coronary angiography (and autopsy) in type 2 MI reveals coronary atherosclerosis in 2590%, but there is no coronary artery thrombosis. Mortality in patients with type 2 MI is generally higher than in patients with type 1 MI. This article is devoted to the problem of diagnosis and management of patients with type 2 myocardial infarction.
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