Tthe efficacy and safety of drug therapy divaza in patients with chronic cerebral ischemia

Fateeva, V V; Шумахер, Г. И.; Воробьева, Е. Н.; Khoreva, M. A.; Voskanyan, L R

doi:10.17116/jnevro20171172132-37

Cited by 6 publications

(2 citation statements)

References 15 publications

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“…In the study of the combination of RAF Abs to S100 and RAF Abs to eNOS in patients with CBVD, the 1.9-fold decrease ineNOS (927.5±11.2 to 478.6±13.4 pg/mL, P <0.05 compared to baseline [reference value 450 pg/mL]) and the 1.5–fold decrease in number of circulating (desquamated) endothelial cells (6.98±0.52 to 4.62±0.75 cells/100 μL, P <0.05 compared to baseline [reference value two to four cells/100 μL]) were shown after 12 weeks of therapy. These results indicated that the preparation exerts endothelioprotective action 190…”

Section: Treatment Of Vci and Perspectives Of A Novel Preparationmentioning

confidence: 64%

<p>Vascular cognitive impairment: pathophysiological mechanisms, insights into structural basis, and perspectives in specific treatments</p>

Parfenov¹,

Остроумова²,

Остроумова³

et al. 2019

NDT

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Vascular cognitive impairment (VCI) and vascular dementia are the most common forms of cognitive disorder associated with cerebrovascular disease and related to increased morbidity and mortality among the older population. Growing evidence suggests the contribution of blood-pressure variability, cardiac arrhythmia, hyperactivation of the renin–angiotensin–aldosterone system, endothelial dysfunction, vascular remodeling and stiffness, different angiopathies, neural tissue homeostasis, and systemic metabolic disorders to the pathophysiology of VCI. In this review, we focus on factors contributing to cerebrovascular disease, neurovascular unit alterations, and novel approaches to cognitive improvement in patients with cognitive decline. One of the important factors associated with the neuronal causes of VCI is the S100B protein, which can affect the expression of cytokines in the brain, support homeostasis, and regulate processes of differentiation, repair, and apoptosis of the nervous tissue. Since the pathological basis of VCI is complex and diverse, treatment affecting the mechanisms of cognitive disorders should be developed. The prospective role of a novel complex drug consisting of released–active antibodies to S100 and to endothelial NO synthase in VCI treatment is highlighted.

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Section: Treatment Of Vci and Perspectives Of A Novel Preparationmentioning

confidence: 64%

<p>Vascular cognitive impairment: pathophysiological mechanisms, insights into structural basis, and perspectives in specific treatments</p>

Parfenov¹,

Остроумова²,

Остроумова³

et al. 2019

NDT

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“…В состав препарата Диваза входят релиз-активные антитела к мозгоспецифическому белку S100 и eNOS. На экспериментальных моделях показано, что один из активных компонентов препарата улучшает метаболизм эндотелия сосудов, снижает содержание [19]. Эффективность влияния препарата на параметры ЭД и их потенциальную прогностическую значимость у пациентов с ФП в течение года после перенесенного КЭИ требует изучения.…”

Section: îáñóAeäåíèåunclassified

Endothelial dysfunction a significant marker of adverse clinical outcome in patients with atrial fibrillation after cardioembolic stroke

Zolotovskaya

Александровна²,

Давыдкин

et al. 2019

Terapevticheskii arkhiv

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Aim. To study the prognostic significance of endothelial dysfunction (ED) markers in the development of adverse clinical outcome (death) in patients with atrial fibrillation (AF) within a year after cardioembolic stroke. Materials and methods. 260 patients with newly diagnosed (nAF), paroxysmal, persistent and permanent forms of AF who underwent stroke were included. Duration of observation-12 months. V1 - the beginning of the study: V2 - 180 (±5) days and V3 - 360 (±5) evaluated the level of von Willebrand factor (fW), antithrombin III (AT III) and plasminogen. Results and discussion. During the year of follow-up, patients with AF who underwent and had a high mortality rate. During the whole period 38 (14.6%) patients died, 15 (23.0%) - in the group with nAF, 6 (9.2%) - in the group with paroxysmal AF, 7 (10.8%) - in the group with persistent AF and 10 (15.4%) - in the group with permanent AF. After a year of follow-up, the level of fW in patients with nAF was higher than in patients of all groups, and statistically significant in patients with paroxysmal and persistent forms of AF. At III was important in the group of patients with nAF and with a constant form of AF, in the same groups there was no statistically significant increase in a year of follow-up. It was found that in survivors with nAF at III (73.54±8.67%) higher (p=0.002) compared with the dead (65.77±6.01%). In the group of patients with paroxysmal AF in survivors of III (77.75±10.15%) higher (p=0.031) compared with the dead (69.25±5.80%). In patients with persistent AF, the survivors of III (76.57±9.09%) were higher (p=0.002) compared to the dead (65.60±2.21%). Taking into account the results of the analysis of the dynamics of ed markers, it can be assumed that AT III is the most accurate prognostic marker for the studied cohort of patients. Conclusion. Detection and correction of ED in AF in patients within a year after stroke can optimize the tactics of management of patients and improve the prognosis of the diseas.

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Nitric oxide: from the mechanism of action to pharmacological effects in cerebrovascular diseases

Fateeva

Vorobyova

2017

Z. nevrol. psikhiatr. im. S.S. Korsakova

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The article presents the data of studies of nitric oxide (NO) in the pathogenesis of cerebrovascular diseases. It is emphasized that endothelial dysfunction contributes to the formation of cerebrovascular diseases. Generalized data on preparations with endothelioprotective effect, as well as own data on the use of the preparation 'Divaza' in patients of middle and advanced age with chronic cerebrovascular disease are given.

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Tthe efficacy and safety of drug therapy divaza in patients with chronic cerebral ischemia

Abstract: The use of divazа resulted in clinical improvement and normalization of markers of endothelial dysfunction as well.

Cited by 6 publications

References 15 publications

<p>Vascular cognitive impairment: pathophysiological mechanisms, insights into structural basis, and perspectives in specific treatments</p>

<p>Vascular cognitive impairment: pathophysiological mechanisms, insights into structural basis, and perspectives in specific treatments</p>

Endothelial dysfunction a significant marker of adverse clinical outcome in patients with atrial fibrillation after cardioembolic stroke

Nitric oxide: from the mechanism of action to pharmacological effects in cerebrovascular diseases

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