Evaluation of the correlation between cerebral hemodynamics and blood pressure by comparative analysis of variation in cerebral blood flow in hypertensive versus normotensive individuals: A systematic review and meta-analysis.

Current understanding of the cerebral vascular response to variations in blood pressure (BP) among individuals with hypertension is limited. The aim of this meta-analysis was to determine the correlation between hypertension, risk of stroke, and cerebral blood flow (CBF). We reviewed studies published between 2000 and 2023 from PubMed, Google Scholar, and Science Direct that compared mean CBF in normotensive and hypertensive patients. A random effects model was used to construct the risk ratio (RR), 95% confidence interval (CI), forest plot, and inverse variance weighting. Additionally, a mixed-effects meta-regression was employed to examine the impact of study-specific patient variables. This meta-analysis included eight prospective cross-sectional studies published from 2002 to 2023. It revealed a significant average difference in the standard mean CBF of -0.45 (95% CI -0.60 to -0.30, I2 = 69%, P < 0.00001), distinguishing normotensive from hypertensive subjects. A RR of 0.90 (95% CI 0.63 to 1.30, I2 = 89%, P = 0.04) indicated a significant decrease in CBF among individuals with hypertension. We found a statistically significant relationship between changes in diastolic and systolic BPs and the mean CBF (R = -0.81, P = 0.001 and R = -0.90, P = 0.005, respectively). Our research demonstrates a strong relationship between elevated BP and reduced CBF, with hypertension reducing CBF compared to normotensive individuals, by increasing cerebrovascular resistance.

Endothelialization of PTFE-covered stents for aneurysms and arteriovenous fistulas created in canine carotid arteries.

To investigate the endothelialization of covered and bare stents deployed in the canine carotid arteries and subclavian arteries for treating experimental aneurysms and arteriovenous fistulas, twenty aneurysms were created in 10 dogs, and 20 fistulas in another 10 dogs. The Willis balloon-expandable covered stent and a self-expandable covered stent were used to treat these lesions, and a self-expandable bare stent was deployed in the subclavian artery for comparison. Followed up for up to 12 months, the gross observation, pathological staining, and scanning electronic microscopic data were analyzed. Two weeks after creation of animal model, thirty self-expandable covered stents and ten balloon-expandable covered stents were deployed. Fifteen bare stents were deployed within the left subclavian arteries. Twenty days after stenting, the aneurysm significantly shrank. At 6 months, the thrombi within the aneurysm cavity were organized. Three to 12 months later, most covered and bare stents were covered by a thin transparent or white layer of endothelial intima. Layers of intima or pseudomembrane were formed on the stent 20-40 days after stent deployment. Over three months, the pseudomembrane became organized, thinner, and merged into the vascular wall. Under scanning electronic microscopy, the surface of covered and bare stents had only deposition of collagen fibers and rare endothelial cells 20-40 days after stenting. From three to ten months, the endothelial cells on the internal surface of stent became mature, with spindle, stripe-like or quasi round morphology along the blood flow direction. Over time, the endothelial cells became mature. In conclusion, three months after deployment in canines' arteries, the self-expandable bare and covered stents have mostly been covered by endothelial cells which become maturer over time, whereas the balloon-expandable covered stents do not have complete coverage of endothelial cells at three months, especially for protruding stent struts and areas. Over time, the endothelialization will become mature.

Complications and long-term in-stent restenosis of endovascular treatment of severe symptomatic intracranial atherosclerotic stenosis and relevant risk factors.

To investigate the complications and in-stent restenosis of endovascular treatment of severe symptomatic intracranial atherosclerotic stenosis and relevant risk factors. Three hundred and fifty-four consecutive patients with intracranial atherosclerotic stenosis (70%-99%) were retrospectively enrolled. The clinical data, treatment outcomes, complications and in-stent restenosis at follow-up were analyzed. The endovascular treatment was composed of balloon dilatation only in 21 (5.93%) patients, and deployment of self-expandable stents in 232 (65.54%), balloon-expandable stents in 75 (21.19%), and both balloon- and self-expandable stents in 26 (7.34%), with a total of 359 stents being successfully deployed at the stenotic location. After treatment, the residual stenosis ranged 9.2%±1.5% (range 7%-19%), which was significantly (P < .05) smaller than that before treatment. Periprocedural complications occurred in 43 patients with a complication rate of 12.15% including arterial dissection in 4 (1.13%) patients, new cerebral infarction in 21 (5.93%), cerebral hemorrhage in 12 (3.3%), and subarachnoid hemorrhage in 6 (1.69%). Hyperlipidemia [odds ratio (OR) 10.35, 95% confidence interval (CI) 4.42-24.28, and P < .0001] and location at the middle cerebral artery (MCA) (OR 4.15, 95% CI 1.92-8.97, and P < .001) were significant (P < .05) risk factors for periprocedural complications, whereas hyperlipidemia (OR 11.28, 95% CI 4.65-30.60, and P < .0001), location at the MCA (or 5.26, 95% CI 2.03-15.08, and P < .001), and angulation (OR 1.02, 95% CI 1.00-1.04, and P = .02) were significant (P < .05) independent risk factors for periprocedural complications. Follow-up was performed in 287 (81.07%) patients at 6 to 36 (28 ± 6.7) months. In-stent restenosis was present in 36 (12.54%), and female sex (OR 2.53, and 95% CI 1.27-5.06) and periprocedural complications (OR 9.18, and 95% CI 3.52-23.96) were significant (P < .05) risk factors for in-stent restenosis, with periprocedural complication (OR 9.61, and 95% CI 3.48-27.23) as the only significant (P < .0001) independent risk factor for in-stent restenosis. A certain rate of periprocedural complications and in-stent stenosis may occur in endovascular treatment of severe intracranial stenosis, and the relevant risk factors may include hyperlipidemia, MCA location, angulation at the stenosis and female sex.

Circ VRK1/microRNA-17/PTEN axis modulates the angiogenesis of human brain microvascular endothelial cells to affect injury induced by oxygen-glucose deprivation/reperfusion.

BACKGROUND: Circular RNAs (circRNAs) can act as microRNA (miRNA) sponges, thus regulating gene expression. The role of circRNAs in the process of oxygen-glucose deprivation/reoxygenation (OGD/R) is unclear. Here, we explored the mechanism underlying Circ VRK1 in human brain microvascular endothelial cells (HBMVECs) injury induced by OGD/R. METHODS: The OGD/R cell model was established in HBMVECs. The microarray was applied to detect differentially expressed circRNAs, followed by subcellular fractionation assay. Colony formation assay, flow cytometry, ELISA, tube formation, Transwell and western blot assays were performed for loss-of-function assay. HE staining, TTC staining, immunohistochemistry and western blot were performed in an established mouse model. The relationships between Circ VRK1 and miR-17, and between miR-17 and PTEN were detected by bioinformatics and dual-luciferase assays. Rescue experiments were conducted in vitro and in vivo, and PI3K/AKT activity was detected by Western Blot. RESULTS: Circ VRK1, predominantly present in the cytoplasm of cells, was upregulated in the HBMVECs exposed to OGD/R. Circ VRK1 downregulation decreased proliferation, migration, tube formation, inflammatory factors and oxidative stress, while increased apoptosis in HBMVECs. Moreover, Circ VRK1 silencing reduced neurological damage, cerebral infarct size, CD34-positive cell counts and VEGF expression in mice. Circ VRK1 mediated PTEN expression and the PI3K/AKT pathway by targeting miR-17. Deletion of miR-17 inhibited the effects of Circ VRK1 siRNA, and silencing of PTEN suppressed the effects of miR-17 inhibitor. CONCLUSION: Circ VRK1 was upregulated during OGD/R. Circ VRK1 downregulation regulates PTEN expression by targeting miR-17, thereby promoting PI3K/AKT pathway activity to alleviate OGD/R injury.