LAUSR

Type of funding sources: None. In the list of reasons of atherosclerosis, there are no premature ventricular contractions (PVCs). To study the main arteries hemodynamics in patients with PVCs and to determine their influence on the atherosclerotic process. We studied 286 patients with PVCs (group 1 (142) – patients with PVCs less 3000 per 24 hours, 2 (144) – more 3000 per 24 hours. Groups were similar in age, gender, comorbidities. By Doppler-ultrasound and shygmography we determined the parameters of heart biomechanics and main arteries kinetics (common carotid, posterior tibial artery): speed, acceleration, power, work in each phase of heart cycle in systole and diastole, the periods of dominance of outflow over inflow. We valued the contribute to the circulation of the PVs and first post-extrasystolic contraction. The volume of cardiac output and transmitral blood flow were measured by echocardiography. We identified the moment of extrasysyoles' appearance by apex-cardiography and ECG. We classified the PVCs up to the moment of their appearance in cardio cycle: before the mitral valve opening; in rapid ventricular filling phase before or after the transmitral blood flow peak; in slow ventricular filling phase; others (group, allorhythmia). We identified the following hemodynamic effects of PVCs. 1) The main role in hemodynamic and kinetics changes play the time of PVC’ appearance in cardio cycle and the ability of the first post-extrasystolic contraction to reestablish an adequate resulting blood flow. The maximums of parameters were in first post-extrasystolic contraction in PVCs before the mitral valve opening and before the transmitral peak flow. 2) The prevalence of atherosclerotic process was observed in group 2 (p<0,05). (Carotid bifurcation stenosis hemodynamically not significant in 42 patients in group 2 vs 26 in group 1, significant – 28 vs 8, lower extremities arteries stenoses 37 vs 17, coronary arteries stenoses 74 vs 35, renal arteries stenoses 6 vs 1). 3) Additional stretching of arteries in the first post-extrasystolic pressure wave. It makes conditions for acute and chronic arteries traumatism. 4) Mechanic damage of endothelium and as a result lipid deposition. The "weak places" – are the places of the main effect of the first post-extrasystolic hydraulic shock: aorta arch in large radius, carotid bifurcation, aorta bifurcation. 5) Appearing the stand waves, interferention and diffraction in the places of already existing atheromas. Atheroma is deforming, the integrity of atheroma’s cover is violated and there’re appearing the atheroma’s complications: dissections, wall thrombus of hemodynamically important stenosis. PVCs change intra-arterial hemodynamics and can cause the mechanical injury of intima, as well as the injury of existing atherosclerotic plaques that can lead to progressing of atherosclerosis. We suppose to include the PVCs in the list of risk factors of atherosclerosis.