Тип публикации: статья из журнала
Год издания: 2026
Идентификатор DOI: 10.52667/2712-9179-2026-6-3-28-54
Ключевые слова: acute myocardial infarction, cardiogenic cognitive disorder, experimental model, pharmacotherapy, efficacy, rosuvastatin, brain-specific protein S-100, Prospekta, epigenetic biomarker, microRNA
Аннотация: The definition of cardiogenic cognitive disorders (CCD) was first proposed in the mid-20th century, but in subsequent years it was unjustifiably omitted from current clinical guidelines. Preclinical and clinical studies using modern methods of laboratory, functional, and radiological diagnostics confirm the significance and specifiПоказать полностьюc features of CCD development compared with those in cerebrovascular pathology. The pathophysiological mechanisms of CCD associated with acute myocardial infarction (AMI) include vascular dysregulation, atherosclerosis, platelet activation, microinfarctions, perivascular inflammation, impaired hemostasis, and a dysfunctional neurohumoral response. These mechanisms may lead to the occurrence of clinically silent microinfarctions, as well as impaired functionality of the white matter in the cerebral cortex. Such pathologies can cause cerebral hypoperfusion and microvascular ischemia, which in turn contributes to the enlargement of periventricular spaces and the development of cerebral amyloid angiopathy, and also leads to hippocampal sclerosis. Objective: To study the role of circulating microRNAs as epigenetic biomarkers of cognitive disorder associated with acute myocardial infarction in an animal model. Materials and Methods: At the first part of this experimental study, the dynamics of cognitive deficit and neurological status were studied in sexually mature Wistar rats. The total sample of experimental animals was divided into three groups, including the study group AMI without therapy (n1 = 10), the comparison group AMI with CCD therapy (n2 = 15), and the control group without AMI and without therapy (n3 = 10). The observation groups were divided in equal numbers for the study of miR-19b-3p and miR-134-5p. The experimental model of AMI according to the method of N. Elmali was used. Blood sampling from the tail vein and assessment of cognitive functioning (the Morris test) and neurological deficit (neuropsychological test NSS) were performed before the experiment and 10 days later. Three strategies were used for the treatment of early CCD: monotherapy with rosuvastatin, monotherapy with Prospekta Vet, and combination therapy with rosuvastatin and Prospekta Vet. To exclude the error of multiple comparisons before pairwise comparison using the Mann Whitney test, all groups compared with each other were preliminarily compared using the Kruskal Wallis test. Results: Baseline indicators of locomotor activity and cognitive functions according to the Morris test, as well as neurological status according to the NSS scale, were comparable in all groups (p-value > 0.05). On day 10 after AMI modeling, no statistically significant changes in the parameters of the Morris test (speed, time in the target sector, distance, platform search time) were detected in any of the groups (p-value > 0.05). At the same time, significant intergroup differences were found according to the NSS test (p-value = 0.018, the Kruskal Wallis test), due to an increase in neurological deficit in the subgroup receiving Prospekta Vet monotherapy compared with the control group (p-value = 0.003) and the AMI group without therapy (p-value = 0.005). Analysis of the dynamics of neurological symptoms (difference in NSS test scores) confirmed a trend toward its increase in the Prospekta Vet monotherapy group, which was significantly higher than in the combination therapy group (p-value < 0.05). In 40% of animals in the AMI group without therapy and the Prospekta Vet monotherapy group, moderate neurological deficit developed, whereas in the subgroups receiving rosuvastatin and combination therapy with rosuvastatin and Prospekta Vet, this indicator was significantly lower. Conclusions: The present study successfully tested the AMI model according to the method of N. Elmali for studying CCD associated with AMI, revealing reproducible neurological deficit in the absence of gross cognitive deficit in experimental animals in the acute period. The most promising therapeutic strategy for the correction of early CCD associated with AMI is the combined administration of rosuvastatin and Prospekta Vet at moderate therapeutic doses. To translate the obtained results into real clinical practice, a further "bridging" clinical study involving middle-aged adults with AMI is required.
Журнал: Personalized Psychiatry and Neurology
Выпуск журнала: Т. 6, № 3
Номера страниц: 28-54
ISSN журнала: 27129179
Место издания: St. Petersburg
Издатель: Национальный медицинский исследовательский центр психиатрии и неврологии им. В.М. Бехтерева