Abstract

Premature ventricular contractions (PVCs) are not included in the risk factors for arterial thromboembolism. Aim: To determine the relationship between PVCs and the development of arterial thromboembolic complications. Methods: The study included 440 patients with PVCs 700 or more per 24 hours, control group - 88 people with PVCs less than 700. All patients underwent laboratory and instrumental studies: 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 - 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 PVCs ventricular systole in the cardiac cycle, regardless of the ectopic center: subgroup A (120) - patients with PVCs 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, a statistically significantly higher development of arterial thromboembolic events was observed in subgroup A. When comparing 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: PVCs are an additional risk factor for arterial thromboembolic events. The main danger is not the PVC 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 in the arterial vessels.

Full Text
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