The aim of the study was to investigate whether visual stimuli have the same potency to increase electroencephalography (EEG) delta wave power density during non-rapid eye movement (NREM) sleep as do auditory stimuli that may be practical in the treatment of some sleep disturbances. Nine healthy subjects underwent two polysomnography sessions—adaptation and experimental—with EEG electrodes positioned at Fz–Cz. Individually adjusted auditory (pink noise) and visual (light-emitting diode (LED) red light) paired 50-ms signals were automatically presented via headphones/eye mask during NREM sleep, shortly (0.75–0.90 s) after the EEG wave descended below a preset amplitude threshold (closed-loop in-phase stimulation). The alternately repeated 30-s epochs with stimuli of a given modality (light, sound, or light and sound simultaneously) were preceded and followed by 30-s epochs without stimulation. The number of artifact-free 1.5-min cycles taken in the analysis was such that the cycles with stimuli of different modalities were matched by number of stimuli presented. Acoustic stimuli caused an increase (p < 0.01) of EEG power density in the frequency band 0.5–3.0 Hz (slow waves); the values reverted to baseline at post-stimuli epochs. Light stimuli did not influence EEG slow wave power density (p > 0.01) and did not add to the acoustic stimuli effects. Thus, dim red light presented in a closed-loop in-phase fashion did not influence EEG power density during nocturnal sleep.
Coronavirus disease 2019 (COVID-19) is a poorly understood and dangerous medical problem. COVID-19-related pulmonary vessels involvement is a complex set of interrelated pathophysiological processes associated with vascular endothelial dysfunction and accompanied by thrombosis of various localization, vasomotor disorders, severe respiratory failure, as well as pulmonary embolism (PE) resulting in chronic thromboembolic pulmonary hypertension (CTEPH). According to computed tomographic pulmonary angiography, the incidence of PE in patients with COVID-19 ranges from 23 to 30%. The aim of this work was to focus the doctors' attention on the risk of pulmonary hypertension in patients after COVID-19.Despite the ability of severe acute respiratory syndrome-related coronavirus 2 (SARS-CoV-2) to infect various organs and systems, the main and most serious complications are pulmonary infiltration, acute respiratory distress syndrome, acute respiratory failure and PE, which in some cases becomes the triggering mechanism for CTEPH development. The literature review presents data on main pathological abnormalities developing in target organs during COVID-19 and playing an important role in increasing the CTEPH risk. The paper describes the main methods of instrumental investigations of CTEPH and an algorithm for its use in COVID-19 survivors.The revealed data demonstrated that the absence of obvious signs of pulmonary hypertension/CTEPH, the cardiopulmonary system abnormalities cannot be ruled out. Therefore, it seems appropriate to actively follow up COVID-19 survivors. A thoroughly, purposefully collected anamnesis, pulmonary function tests and stress echocardiography in an ambiguous clinical situation will play a leading role as they identify cardiopulmonary disorders and provide the doctor with basic information for further planning of patient management.
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