Abstract

Background. Premature ventricular contractions (PVCs) are not mentioned in the list of risk factors of stroke. Methods. In our investigation, we included 440 patients with PVCs more than 700 per 24 hours. In control group, there were 88 patients with PVCs less than 700 per 24 hours. Within instrumental methods we performed echocardiography (transthoracic or transesophageal), Doppler ultrasound of brachiocephalic arteries, 24-hours electrocardiography (ECG) monitoring, digital sphygmography of common carotid arteries (SG); computer tomography or magnetic resonance imaging of the brain. Laboratory tests were used to identify lipids level, hemoglobin A1c. The patients of the main group were divided into two subgroups up to the characteristics of the revealed PVCs. The 1st subgroup comprised 120 patients with PVCs whose ventricular systole occurred in the phase before the peak of transmitral blood flow in the cardiac cycle, regardless of the location of ectopic foci. In 320 patients with PVCs of the 2nd subgroup the systole of ventricular contraction occurred in the phase after the peak of transmitral blood flow in the cardiac cycle. We observed the patients during 1 year from the onset of the investigation and analyzed the appearance of stroke or transient ischemic attack (TIA). Results. In most instrumental and laboratory parameters subgroups 1, 2 and control group were identical. The most important differences were in hemodynamic and kinetic parameters in accordance to the quantity of PVCs per 24 hours (700 and more in the main subgroups 1,2) and the moment of the ventricular contraction appearance of the PVCs (before or after the transmitral blood flow peak in cardiac cycle). We revealed the following tendency: the earlier PVCs appeared in cardiac cycle the more an increase in hemodynamic and kinetic parameters was observed. All patients were on the common standard therapy. Despite of that, during 1 year from the beginning of the investigation we remarked the statistically significant different appearance of the stroke and TIA within the groups which was more frequent in the 1 subgroup. Conclusion. PVCs are an additional risk factor of stroke. The most dangerous type is when the ventricular contraction (PVC) appears before the transmitral blood flow peak in cardiac cycle. Increased hemodynamical parameters during the spread of the 1st post-extrasystolic wave cause an additional mechanical trauma of arterial intima and can be the key moment in atherosclerotic plaques non-stability with further defragmentation, embolism and onset of stroke. In patients with PVCs more than 700 per 24 hours the promising research can be using novel oral anticoagulants to prevent the cardiovascular events in the dosages as it is indicated in atrial fibrillation.

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