Objectives to determine the hemodynamic changes within arterial vessels in different variants of extrasystole, to analyze whether extrasystole is an additional risk factor for the development of atherosclerosis. Material and methods. The study included 286 patients (175 men and 111 women) with extrasystole of more than 3000 per day and 88 patients with extrasystole of less than 3000 per day as a control group. When selecting eligible patients for the study, we tried to minimize the impact of traditional risk factors of atherosclerosis. The presence of cardiocerebral complications in medical history was also considered. The examination methods used in the study are electrocardiography, phonocardiography, 24-hour electrocardiography monitoring, Doppler ultrasound of the brachiocephalic vessels, lower extremities arteries, renal arteries, transthoracic or transesophageal echocardiography. Stress echocardiography was performed if indicated; as well as renal artery angiography, coronary angiography, computed tomography of the brain with angioprogram. When performing a biochemical blood test, the lipid spectrum and hemostasiogram were necessarily determined. All patients underwent left ventricular apexcardiography, as well as sphygmography, recorded on arteries of elastic type (a. Carotis communis) and muscular-elastic type (a. Tibialis posterior). The clinical examinations were confirmed and modeled using the original "Device for modeling of intra-arterial circulation", developed by us (RF patent No. 202780 dated 05.03.2021). Results. We determined an increase in the main parameters of the heart biomechanics and the kinetics of the main arteries in the 1st post-extrasystolic wave in patients with various types of extrasystole with the following pattern: the earlier extrasystole had appeared in the cardiocycle, the greater was the increase in the parameters under observation. A universal concept of hydraulic shock and possible cases of its formation were described. Conclusion. Extrasystole is an additional risk factor for the onset and progression of atherosclerosis. Hydraulic shock during the passage of the 1st post-extrasystolic wave is a powerful traumatic factor for the walls of the arteries, which can lead to the formation of an atherosclerotic process.
Objectives to study the mechanism of restenosis after the intra-arterial stenting using the original device for modeling of intra-arterial blood flow. Material and methods. To perform the experiment, we have created the original device simulating the intra-arterial blood flow. A glass tube of rotameter was the imitation of the arterial vessel. The closed system was filled with the liquid imitating blood, specifically the solution of glycerin the same viscosity as the human blood plasma. Using our original model of intra-artetial blood flow, we were able to study the intra-arterial hemodynamics under different conditions of cardiovascular system functioning, including arrhythmias. Results. In extrasystolic arrhythmia, during the spread of the first post-extrasystolic wave, we observed the intensive impact of pressure wave (the indicator was the silk thread) on the vessel walls with forming of reflected and standing waves. Putting the piezo crystal probe of pressure inside the tube, we verified our observations. The increase of pressure during the spread of the first post-extrasystolic wave in multiple measurements had a mean value of 160% in comparison with the pressure during the regular heart rhythm. Conclusion. The hydraulic shock appears during the spread of the first post-extrasystolic wave in the arterial vessel. Its effect on hemodynamics grows in case of the frequent extrasystoles and allorhythmia. The mechanical impact of hydraulic shock in extrasystoles can be the starting point of the restenosis onset and progressing in the intra-arterial stent.
Aim. To determine the changes of parameters of heart biomechanics and kinetics of arteries, to reveal the adverse events of first post-extrasystolic contraction.Materials and methods. In our investigation we included 286 patients. We excluded all the main traditional risk factors of the atherosclerosis. All the patients were branched into two main groups in accordance to the quantity of extrasystoles per 24 hours: I group – less than 3000, II group – more than 3000 extrasystoles per 24 hours. We took the data about complaints, anamnesis, made laboratory and instrumental investigations to reveal the character and severity of atherosclerotic process.Results. We determined that the atherosclerotic process was more advanced and more often in the group II. Also the atherosclerosis was more severe in patients with extrasystoles in the phase of cardiocycle before opening of the mitral valve and before the transmitral blood flow peak. The parameters (acceleration, speed, power, work) that were calculated by apexcardiography and sphygmography increased with the further tendency: if earlier extrasystole appears in cardiocycle, than more changes were observed.Conclusion. The first post-extrasystolic contraction causes the increase of all parameters of heart biomechanics and kinetics of vessels and can be an additional factor of progressing of atherosclerosis.
Dabigatran is highly effective oral anticoagulant used in patients with atrial fibrillation, venous thrombosis, pulmonary embolism, orthopedic surgery. The most important role in activation and transport of dabigatran play hepatic carboxylesterase-1 (CES-1) and P-glycoprotein. To date were studied different polymorphisms that affect the pharmacokinetics of dabigatran such as rs2244613 (C > A), rs8192935 (T > C) и rs71647871 (G > A), rs1128503 (1236 C > T), rs2032582 (2677 G > T), rs1045642 (3435 C > T) и rs4148738 (G > A) and others. At the same time, there is no need of dabigatran pharmacogenetics testing in routine care. On the other side, existing literature data is often controversial, that’s why future studies are needed to answer the above-mentioned question.
Aim to determine the relationship between extrasystoles (ES) and the development of arterial thromboembolic complications. Material and methods. The study included 440 patients with ES 700 or more per 24 hours, control group 88 people with ES less than 700. All patients underwent laboratory and instrumental examinations: lipid spectrum, hemostasis indicators; 24-hours ECG monitoring; echocardiography (EchoCG); Doppler ultrasound and digital sphygmography (SG) of the main arteries; ultrasound of the aorta branches, renal arteries. According to the indications, the patients were administered: stress EchoCG with physical exercises, coronary angiography, pancerebral angiography, renal arteries angiography, computed tomography, magnetic resonance imaging of the brain. All patients of the main group were divided into 2 subgroups, depending on the moment of occurrence of ES ventricular systole in the cardiocycle, regardless of the ectopic center: subgroup A (120) patients with ES before the peak of transmitral blood flow; subgroup B (320) after the peak of the transmitral blood flow. Patients were observed during 1 year and the development of arterial thromboembolic events was analyzed. Results. According to the main clinical, laboratory and instrumental data, patients of subgroups A, B and the control group were equivalent. Also, during 1 year follow-up, a significantly higher development of arterial thromboembolic events was observed in subgroup A. When comparing the linear blood flow velocity and volumetric blood flow, there was a significant increase in parameters during the spreading of the first post-extrasystolic contraction wave. A similar trend was observed in the parameters of the kinetics of the arterial vascular wall (velocity, acceleration, power, work). Conclusion. Extrasystoles are an additional risk factor for arterial thromboembolic events. The main danger is not the ES itself, but the wave of the first post-extrasystolic contraction, which can become the starting point for the instability of atherosclerotic plaques, leading to tears, parietal thrombosis, and embolism along the arterial vessel.
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