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The evaluation of the clustering of magnetic resonance imaging (MRI) signs into MRI types and their relationship with circulating markers of vascular wall damage were performed in 96 patients with cerebral small vessel disease (cSVD) (31 men and 65 women; mean age, 60.91 ± 6.57 years). The serum concentrations of the tumor necrosis factor-α (TNF-α), transforming growth factor-β1 (TGF-β1), vascular endothelial growth factor-A (VEGF-A), and hypoxia-inducible factor 1-α (HIF-1α) were investigated in 70 patients with Fazekas stages 2 and 3 of white matter hyperintensities (WMH) and 21 age- and sex-matched volunteers with normal brain MRI using ELISA. The cluster analysis excluded two patients from the further analysis due to restrictions in their scanning protocol. MRI signs of 94 patients were distributed into two clusters. In the first group there were 18 patients with Fazekas 3 stage WMH. The second group consisted of 76 patients with WMH of different stages. The uneven distribution of patients between clusters limited the subsequent steps of statistical analysis; therefore, a cluster comparison was performed in patients with Fazekas stage 3 WMH, designated as MRI type 1 and type 2 of Fazekas 3 stage. There were no differences in age, sex, degree of hypertension, or other risk factors. MRI type 1 had significantly more widespread WMH, lacunes in many areas, microbleeds, atrophy, severe cognitive and gait impairments, and was associated with downregulation of VEGF-A compared with MRI type 2. MRI type 2 had more severe deep WMH, lacunes in the white matter, no microbleeds or atrophy, and less severe clinical manifestations and was associated with upregulation of TNF-α compared with MRI type 1. The established differences reflect the pathogenetic heterogeneity of cSVD and explain the variations in the clinical manifestations observed in Fazekas stage 3 of this disease.

The purpose of our study is to investigate the risk factors of in-hospital mortality among patients who were admitted in an emergency setting to a non-specialized tertiary center during the first peak of coronavirus disease in Moscow in 2020. The Federal Center of Brain and Neurotechnologies of the Federal Medical and Biological Agency of Russia was repurposed for medical care for COVID-19 patients from 6th of April to 16th of June 2020 and admitted the patients who were transported by an ambulance with severe disease. In our study, we analyzed the data of 635 hospitalized patients aged 59.1 ± 15.1 years. The data included epidemiologic and demographic characteristics, laboratory, echocardiographic and radiographic findings, comorbidities, and complications of the COVID-19, developed during the hospital stay. Results of our study support previous reports that risk factors of mortality among hospitalized patients are older age, male gender (OR 1.91, 95% CI 1.03–3.52), previous myocardial infarction (OR 3.15, 95% CI 1.47–6.73), previous acute cerebrovascular event (stroke, OR = 3.78, 95% CI 1.44–9.92), known oncological disease (ОR = 3.39, 95% CI 1.39–8.26), and alcohol abuse (ОR 6.98, 95% CI 1.62–30.13). According to the data collected, high body mass index and smoking did not influence the clinical outcome. Arterial hypertension was found to be protective against in-hospital mortality in patients with coronavirus pneumonia in the older age group. The neutrophil-to-lymphocyte ratio showed a significant increase in those patients who died during the hospitalization, and the borderline was found to be 2.5. CT pattern of “crazy paving” was more prevalent in those patients who died since their first CT scan, and it was a 4-fold increase in the risk of death in case of aortic and coronal calcinosis (4.22, 95% CI 2.13–8.40). Results largely support data from other studies and emphasize that some factors play a major role in patients’ stratification and medical care provided to them.

Cerebral small vessel disease (SVD) is one of the leading causes of cognitive impairment and stroke. The importance of endothelial dysfunction and high blood–brain barrier (BBB) permeability in pathogenesis, together with ischemia, is under discussion. The aim of this study was to clarify the relationship between tissue plasminogen activator (t-PA), plasminogen activator inhibitor (PAI-1), and magnetic resonance imaging (MRI) signs of SVD. We examined 71 patients (23 men and 48 women; mean age: 60.5 ± 6.9 years) with clinical and MRI signs of SVD, and 21 healthy volunteers with normal MRIs. All subjects underwent 3T MRI and measurements of t-PA and PAI-1 levels. An increase in t-PA level is correlated with the volume of white matter hyperintensities (WMH) (R = 0.289, p = 0.034), severity on the Fazekas scale (p = 0.000), and with the size of subcortical (p = 0.002) and semiovale (p = 0.008) perivascular spaces. The PAI-1 level is not correlated with the t-PA level or MRI signs of SVD. The correlation between t-PA and the degree of WMH and perivascular spaces’ enlargement, without a correlation with PAI-1 and lacunes, is consistent with the importance of t-PA in BBB disruption and its role in causing brain damage in SVD.

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