Extrasystoles: relationship with arterial thromboembolic complications

Abstract

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.