Ultrasonic indicators of the heart and carotid arteries in arterial hypertension development in patients with chronic obstructive pulmonary disease

Abstract

Aim. To specify the sequence of changes in the functional parameters of arterial hypertension in patients with chronic obstructive pulmonary disease and asthma according to the results of echocardiography, carotid arteries duplex scan and ambulatory blood pressure monitoring.Methods. Ambulatory blood pressure monitoring, tissue Doppler echocardiography and carotid artery duplex scan were performed in 160 patients with chronic obstructive pulmonary disease, arterial hypertension, asthma, and 33 apparently healthy volunteers of both sexes aged 39-70 years.Results. In patients with chronic obstructive pulmonary disease, an increase in hypertensive indices of time and area with the development of non-dipper or inverse-dipper 24-hour blood pressure profile disturbances is registered only at night hours. In chronic obstructive pulmonary disease, unlike asthma, carotid arteries thickening, combined hypertrophy and diastolic dysfunction of both ventricles develop. The prevalence of the thickening of «intima-media» complex and atherosclerotic plaques among patients with comorbid pathology (chronic obstructive pulmonary disease + arterial hypertension) occurs significantly more frequently than in the groups with hypertension or chronic obstructive pulmonary disease, confirming the synergistic effect of the considered nosologies on the atherosclerotic process.Conclusion. In patients with chronic obstructive pulmonary disease changes of the ultrasonic and functional indicators of the cardiovascular system, typical for arterial hypertension are registered starting with stage I and amplified with increase in the disease severity, leading to the need of diagnostic and therapeutic management correction.

Electrophysiological Cardiac Parameters and Results of Antiarrhythmic Treatment in Patients with Paroxysmal Atrial Fibrillation (Lone and Associated with Arterial Hypertension)

“…Полученные результаты указывают на различия в электрофизиологических параметрах сердца больных с идиопатической ФП и ФП в сочетании с ГБ, играющие важную роль для возникновения и поддержания аритмии. ГБ является заболеванием, приводящим к гипертрофии кардиомиоцитов, увеличению объема предсердий и формированию множественных интрамуральных очагов фиброза в миокарде как желудочков, так и предсердий [14][15][16]. Неоднородность измененной структуры миокарда предсердий создает условия для возникновения множества зон, в которых может происходить циркуляция импульса по механизму re-entry, что является дополнительным фактором, способствующим возникновению ФП в ответ на пусковые механизмы [17,18].…”