The article concerns on the problems of vascular comorbidity epidemiology and pathophysiological aspects of heart disease, which became a leading etiopathologic factor of cerebral infarctions and hemorrhages. The relationship between coronary artery disease (CAD), atrial fibrillation, hypertension and cerebral infarction types is emphasized.Aim. To analyze the role of comorbidity, attributable to cardio-vascular pathology in the initiation, course, clinical features and outcomes of cerebral infarction.Material and methods. We performed a prospective study, including 1072 patients with stroke, attributable to various cardiovascular pathology, evaluated the influence of vascular comorbidity of variable degree on the course and outcomes at an inpatient stage and at follow-up.Results. We demonstrated a negative influence of CAD, atrial fibrillation and postinfarction cardiosclerosis on the incidence of cerebral infarction, unfavorable course of the disease and functional outcomes at inpatient stage. The combination of vascular comorbidity resulted in an increased mortality in post-stroke period during 6 years of follow-up.Conclusion. Epidemiology of vascular comorbidity, its role in cerebrovascular accidents in patients with cardiac pathology justifies the need of active realization of contemporary multidisciplinary prevention programs, prolonged instrumental monitoring and implementation of energy deficiency correction therapy in comprehensive treatment programs.

The first paper of the series on the treatment of patients with vascular comorbidity (VC) is focused on the role and therapeutic potential of the correction of free radical processes (FRP) as pathogenetic factors of multifocal vascular pathology. Aim. To analyse the effects of VC on the incidence and outcomes of cerebral stroke (S), in order to create therapeutic algorithms of FRP correction. Material and methods. This prospective study included 634 S patients. The following factors were analysed: pre-stroke disability due to various VC variants; VC effects on the clinical course, as well as in-hospital and post-discharge outcomes; and FRP specifics in various VC variants. Results. VC was registered in 97% of S patients; in 45,3%, it resulted in pre-stroke disability. FRP parameters, reflecting the progression of tissue energy deficiency, differed significantly in patients with coronary heart disease, myocardial infarction, atrial fibrillation, and diabetes mellitus. Based on these findings, the therapeutic algorithms for effective energy deficiency correction have been created. Conclusion. The analysis of pre- and post-stroke disability and prevention of repeat events in cardiovascular patients has demonstrated the need for a more active implementation of modern multidisciplinary preventive programs.

No abstract

Актуальность работы обусловлена поиском путей улучшения результатов лечения больных инсультом. Цель исследования: выявить критерии прогноза риска развития венозных тромбозов, а также ключевые звенья патогенеза тромбоэмболических осложнений у пациентов с острым инсультом. Материалы и методы: в проспективное исследование включено 145 больных с инсультом (104 с ишемическим (ИИ) и 41 с геморрагическим (ГИ)), госпитализированных в отделение нейрореанимации в период 3,5-24 часа от начала заболевания и имеющих на момент включения в исследование различную степень депрессии сознания (тяжелая степень инсульта). Пациентам проводилась терапия в соответствии со стандартами оказания медицинской помощи, согласно которым всем пациентам назначали антикоагулянтную терапию (АКТ). Выполняемый в динамике стандартный клинико-диагностический и лабораторный мониторинг был дополнен тестом «Тромбодинамика». Результаты: у 95% пациентов с инсультом зарегистрированы различные факторы риска венозных тромбоэмболических осложнений (ВТЭО). Тромбоэмболия легочной артерии (ТЭЛА) развилась в 24% случаев, преимущественно на 2-3 неделе, в среднем через 6 дней после отмены АКТ. Описана динамика и признаки дисбаланса в системе гемостаза у больных инсультом, нараставшие после отмены АКТ. Показано, что стандартные методы исследования системы гемостаза по сравнению с прямым методом менее информативны для выявления ВТЭО и оценки эффективности АКТ. Вероятность развития ВТЭО прямо пропорциональна скорости смены состояния гиперкоагуляции состоянием гипокоагуляции. При этом состояние фоновой гиперкоагуляции не коррелирует с развитием ВТЭО. Корреляционный анализ изменений в системе гемостаза с динамикой клинико-лабораторных маркеров у больных с тяжелым инсультом выявил закономерные изменения показателей коагуляционного гемостаза в условиях реализации разных схем стандартной АКТ. Эти схемы были сопоставимы по содержанию при развитии как ВТЭО и ТЭЛА, так и геморрагических осложнений. Вывод: К больным инсультом необходим персонализированный подход при динамическом мониторировании гемостаза и назначении антикоагулянтной терапии. This work was warranted by the need to improve results in the treatment of stroke. The aim of this study was to identify criteria for predicting the risk of venous thrombosis and to elucidate the pathogenesis of thromboembolic complications in patients with acute stroke. Materials and methods. This prospective study included 145 patients (104 patients with ischemic stroke and 41 patients (28.3%) with hemorrhagic stroke). All patients were hospitalized to the neuroresuscitation unit within 3.5 to 24 hours of the disease onset at different stages of consciousness impairment. The patients received anticoagulant therapy (ACT) according to current healthcare standards. Standard clinical diagnostic and laboratory monitoring was supplemented with a Thrombodynamics test. Results. Risk factors for venous thromboembolic events (VTE) were observed in 95% of patients. Pulmonary embolism developed in 24% of cases mostly during weeks 2-3, generally at 6 days of ACT withdrawal. Hemostatic changes and disbalance progressed after the ACT withdrawal. Standard methods of studying hemostasis were shown to be less informative in detecting VTE and evaluating ACT efficacy than the thermodynamics method. The probability of VTE was directly proportional to the velocity of hypercoagulation transformation into hypocoagulation. In this process, the background hypocoagulation was not correlated with the development of VTE. Analysis of correlations of hemostasis changes with changes in clinical-laboratory markers identified relationships of changes in coagulation hemostasis with different standard ACT programs. VTE, pulmonary embolism, and hemorrhagic complications developed in association with administration of comparable ACT programs to patients with severe stroke.

No abstract