Middle cerebral artery remodeling following transient brain ischemia is linked to early postischemic hyperemia: A target of uric acid treatment

Onetti, Yara; Dantas, Ana Paula; Pérez, Belén; Cugota, Roger; Chamorro, Ángel; Planas, Anna M.; Vila, Elisabet; Jiménez‐Altayó, Francesc

doi:10.1152/ajpheart.00001.2015

Cited by 70 publications

(76 citation statements)

References 38 publications

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“…23,24 Moreover, brain ischemia also induces by itself changes in the arterial wall structure and function that are mediated by inflammatory and oxidative stress-related mechanisms. 25,26 Taken together, these observations give support to the potential benefit of therapies aimed to prevent and modulate vessel injury by targeting inflammation and oxidative stress. 22 This study is not without limitations.…”

Section: March 2017mentioning

confidence: 74%

Vessel Wall Enhancement and Blood–Cerebrospinal Fluid Barrier Disruption After Mechanical Thrombectomy in Acute Ischemic Stroke

Renú¹,

Laredo²,

López-Rueda³

et al. 2017

Stroke

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T he most effective treatment approach in acute ischemic stroke is early reperfusion, which includes the administration of the r-tPA (recombinant tissue-type plasminogen activator) or the use of mechanical thrombectomy (MT). 1 However, less than half of patients who are treated obtain permanent clinical benefits.1 Early blood-brain barrier (BBB) disruption is one of the main mechanisms implicated in reperfusion ineffectiveness, and it has been associated to the severity of ischemia, adverse effects of thrombolytic drugs, and thrombectomy-related direct vessel damage.2 In experimental brain ischemia, MT causes direct vessel injury in the intimal and medial layers of the arterial wall.3-5 Besides direct mechanical injury, ischemia itself, thrombus inflammatory components, and r-tPA-related toxicity may also compromise the integrity of the endothelial surface.6 Overall, these changes may result in increased endothelial permeability and can be imaged with contrast-enhanced magnetic resonance imaging (MRI). 7,8 Likewise, postgadolinium enhancement of the cerebrospinal fluid space visible on postcontrast fluidattenuated inversion recovery (FLAIR) is an established neuroimaging marker of blood-cerebrospinal fluid barrier (BCSFB) or BBB disruption. In acute ischemic stroke, it has been associated with increased risk of hemorrhage, poor clinical outcome, r-tPA-induced reperfusion injury, and poor early neurological recovery after MT.9-12 However, whether there is a link between vessel wall enhancement and diffuse BCSFB disruption has not been studied previously. Thus, clarifying this potential relationship may be of relevance for Background and Purpose-Less than half of acute ischemic stroke patients treated with mechanical thrombectomy obtain permanent clinical benefits. Consequently, there is an urgent need to identify mechanisms implicated in the limited efficacy of early reperfusion. We evaluated the predictors and prognostic significance of vessel wall permeability impairment and its association with blood-cerebrospinal fluid barrier (BCSFB) disruption after acute stroke treated with thrombectomy. Methods-A prospective cohort of acute stroke patients treated with stent retrievers was analyzed. Vessel wall permeability impairment was identified as gadolinium vessel wall enhancement (GVE) in a 24-to 48-hour follow-up contrast-enhanced magnetic resonance imaging, and severe BCSFB disruption was defined as subarachnoid hemorrhage or gadolinium sulcal enhancement (present across >10 slices). Infarct volume was evaluated in follow-up magnetic resonance imaging, and clinical outcome was evaluated with the modified Rankin Scale at day 90. Results-A total of 60 patients (median National Institutes of Health Stroke Scale score, 18) were analyzed, of whom 28 (47%) received intravenous alteplase before mechanical thrombectomy. Overall, 34 (57%) patients had GVE and 27 (45%) had severe BCSFB disruption. GVE was significantly associated with alteplase use before thrombectomy and with more stent retriever passes, along with the pr...

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Section: March 2017mentioning

confidence: 74%

Vessel Wall Enhancement and Blood–Cerebrospinal Fluid Barrier Disruption After Mechanical Thrombectomy in Acute Ischemic Stroke

Renú¹,

Laredo²,

López-Rueda³

et al. 2017

Stroke

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“…The neuroprotective function of SUA can be explained from the following aspects. First, UA is the main endogenous antioxidant in human plasma, its multiple effects include scavenging hydroxyl radicals, hydrogen peroxide, and peroxynitrite and prevent lipid peroxidation [45], and these effects mainly take place within the walls of the brain vessels [46]. Second, it has been argued that SUA could be a compensatory mechanism to counteract oxidative damage related to atherosclerosis and aging in humans [47].…”

Section: Discussionmentioning

confidence: 99%

U-Shaped Relationship Between Functional Outcome and Serum Uric Acid in Ischemic Stroke

Yang

Zhang

et al. 2018

Cell Physiol Biochem

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Background/Aims: We sought to assess a consecutive number of patients with first-ever acute ischemic stroke (AIS), the clinical relevance in regard to functional outcome of the serum uric acid (SUA) measured at admission. Methods: In 2 prospective centers for observational study, serum concentrations of SUA were measured on admission in the serum of 710 consecutive patients with AIS. SUA concentrations were determined by high-performance liquid chromatography. SUA, NIH stroke scale (NIHSS), and conventional risk factors were evaluated to determine their value to predict functional outcome within 3 months. Results: During the follow-up, an unfavorable functional outcome (defined as a mRS score > 2) was found in 219 (30.8%) patients. The unfavorable functional outcome distribution across the SUA quartiles ranged between 12.4% (third quartile) and 50.6% (first quartile). After adjusting for all other significant outcome predictors, SUA concentration remained an independent unfavorable outcome predictor with an adjusted OR of 0.996 (95% CI, 0.993-0.998; P< 0.001). Conclusions: The data show that the U-shaped nature of the exposure-risk relationship was more prominent when the data were assessed in deciles (based on the SUA values). This model predicted the lowest relative risk of unfavorable outcome in the 67th percentile (corresponding to 309 µmol/L). SUA was significantly associated with the risk of poor functional outcomes in Chinese patients with stroke.

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“…Several treatments modulating inflammatory and immune responses to brain ischemia have entered pre-clinical trials with different and sometimes contrasting results (Table 5) [10,210,211,212,213,214,215,216,217,218,219,220,221,222,223,224,225,226,227,228,229,230,231,232,233,234,235,236,237,238,239,240,241,242,243,244,245,246,247,248,249,250,251,252,253]. …”

Section: Anti-inflammatory Treatments In Is: Evidence From Pre-climentioning

confidence: 99%

Update on Inflammatory Biomarkers and Treatments in Ischemic Stroke

Bonaventura

Liberale

Vecchiè

et al. 2016

IJMS

133

114

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After an acute ischemic stroke (AIS), inflammatory processes are able to concomitantly induce both beneficial and detrimental effects. In this narrative review, we updated evidence on the inflammatory pathways and mediators that are investigated as promising therapeutic targets. We searched for papers on PubMed and MEDLINE up to August 2016. The terms searched alone or in combination were: ischemic stroke, inflammation, oxidative stress, ischemia reperfusion, innate immunity, adaptive immunity, autoimmunity. Inflammation in AIS is characterized by a storm of cytokines, chemokines, and Damage-Associated Molecular Patterns (DAMPs) released by several cells contributing to exacerbate the tissue injury both in the acute and reparative phases. Interestingly, many biomarkers have been studied, but none of these reflected the complexity of systemic immune response. Reperfusion therapies showed a good efficacy in the recovery after an AIS. New therapies appear promising both in pre-clinical and clinical studies, but still need more detailed studies to be translated in the ordinary clinical practice. In spite of clinical progresses, no beneficial long-term interventions targeting inflammation are currently available. Our knowledge about cells, biomarkers, and inflammatory markers is growing and is hoped to better evaluate the impact of new treatments, such as monoclonal antibodies and cell-based therapies.

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Middle cerebral artery remodeling following transient brain ischemia is linked to early postischemic hyperemia: A target of uric acid treatment

Cited by 70 publications

References 38 publications

Vessel Wall Enhancement and Blood–Cerebrospinal Fluid Barrier Disruption After Mechanical Thrombectomy in Acute Ischemic Stroke

Vessel Wall Enhancement and Blood–Cerebrospinal Fluid Barrier Disruption After Mechanical Thrombectomy in Acute Ischemic Stroke

U-Shaped Relationship Between Functional Outcome and Serum Uric Acid in Ischemic Stroke

Update on Inflammatory Biomarkers and Treatments in Ischemic Stroke

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