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34 result(s) for "Mosconi, Maria Giulia"
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Applying the World Stroke Organization roadmap in planning a model for stroke service implementation in Matrouh Governorate-Egypt: a World Stroke Organization young future stroke leaders’ analytical study
BackgroundThe global incidence of stroke is on the rise, primarily due to an increase in the aging population and the prevalence of vascular risk factors among the elderly. However, stroke is a treatable condition if promptly recognized and managed effectively. To optimize stroke management, it is crucial to establish a well-prepared infrastructure comprising adequately trained physicians working in collaboration with multidisciplinary teams. Equipped stroke units, easily accessible emergency medical services with a stroke code, and interconnected telestroke networks, further enhance stroke care delivery. Along with the current study, conducted by a task force from the World Stroke Organization’s Future Stroke Leaders Program, an assessment of the stroke infrastructure within Matrouh governorate in Egypt for stepwise implementation of stroke services, based on the World Stroke Organization’s stroke roadmap took place. The study consisted of two levels: Level One involved analyzing existing gaps that may impede the implementation of stroke services, while Level Two proposed strategies to address these gaps using a problem-solving approach.ResultsThe study identified the Matrouh governorate as a suitable region for stroke service implementation. The region exhibits a blend of urban and rural areas and is geographically distant from major healthcare centers. Matrouh also possesses a diverse population, subject to seasonal variations. Currently, it offers a mix of minimum and essential stroke services, which can be expanded and improved through a step-by-step approach guided by the World Stroke Organization’s stroke roadmap.ConclusionsMapping stroke infrastructures allows for the identification of potential gaps to optimize the potential for implementation of stroke services.
Lessons to be learned in intracerebral haemorrhage research
The 2020 guidelines of the European Society of Cardiology recommend that the decision to start or restart oral anticoagulation in patients with atrial fibrillation after an intracerebral haemorrhage should be considered in consultation with a neurologist or stroke specialist.2 In light of the low level of evidence obtained to date, The Karolinska European Stroke Organisation recommends the inclusion of patients with intracerebral haemorrhage who have atrial fibrillation in ongoing randomised trials.3 In The Lancet Neurology, the SoSTART Collaboration reports results from the Start or STop Anticoagulants Randomised Trial (SoSTART),4 which was designed for survivors of spontaneous intracranial haemorrhage who had atrial fibrillation. In light of the results of SoSTART, the investigators of ongoing randomised trials such as STATICH (NCT03186729), A3ICH (NCT03243175), ASPIRE (NCT03907046), ENRICH-AF (NCT03950076), and PRESTIGE-AF (NCT03996772) have more robust evidence on the safety of anticoagulation after intracerebral haemorrhage that can be shared with eligible patients, their relatives, and caregivers to facilitate the joint decision of enrolment into these trials. Recent studies have confirmed that the underenrolment of women in randomised trials is common in cerebrovascular and cardiovascular diseases.5 To address this underenrolment, the 2016 Motion for a European Parliament Resolution on promoting sex equality in mental health and clinical research called for clinical trials of pharmaceutical products to include sufficient representation of both men and women and for these trials to be inclusive, non-discriminatory, and performed under conditions of equality and inclusion.
Systemic thrombolysis in patients with acute stroke and active cancer: a systematic review and meta-analysis
Cancer patients frequently have concomitant cerebrovascular diseases, which significantly worsen their prognosis. Prospective studies validating intravenous thrombolysis (IVT) safety profile in patients with acute ischemic stroke and active cancer are still lacking. Therefore, we aimed to evaluate IVT’s efficacy and safety profile in acute ischemic stroke patients with comorbid active cancer. We included in a meta-analysis all relevant published studies, including patients with acute ischemic stroke with or without active cancer and receiving IVT, according to recommendations for IVT treatment for acute ischemic stroke. The primary outcomes were: any intracerebral hemorrhage, all-cause mortality, and good functional outcome reported as modified Rankin Scale (mRS) ≤ 2 at the end of the scheduled follow-up period. We included 11 studies in the meta-analysis. IVT was not associated with a significant increase in the incidence of intracerebral hemorrhage (OR 1.35; 95% CI 0.85–2.14; I2 76%), nor with a significant increase in death for any cause (OR 1.26; 95% CI 0.91–1.75; I2 71%); furthermore, IVT did not influence mRS between cancer and non-active cancer stroke patients (OR 0.72; 95% CI 0.35–1.49; I2 59%). IVT seems safe and effective in patients with ischemic stroke and concomitant cancer. Due to the low overall quality of the evidence, high-quality randomized controlled trials with adequate sample sizes are needed.
Immunological Profile of Vasospasm after Subarachnoid Hemorrhage
Subarachnoid hemorrhage (SAH) carries high mortality and disability rates, which are substantially driven by complications. Early brain injury and vasospasm can happen after SAH and are crucial events to prevent and treat to improve prognosis. In recent decades, immunological mechanisms have been implicated in SAH complications, with both innate and adaptive immunity involved in mechanisms of damage after SAH. The purpose of this review is to summarize the immunological profile of vasospasm, highlighting the potential implementation of biomarkers for its prediction and management. Overall, the kinetics of central nervous system (CNS) immune invasion and soluble factors’ production critically differs between patients developing vasospasm compared to those not experiencing this complication. In particular, in people developing vasospasm, a neutrophil increase develops in the first minutes to days and pairs with a mild depletion of CD45+ lymphocytes. Cytokine production is boosted early on after SAH, and a steep increase in interleukin-6, metalloproteinase-9 and vascular endothelial growth factor (VEGF) anticipates the development of vasospasm after SAH. We also highlight the role of microglia and the potential influence of genetic polymorphism in the development of vasospasm and SAH-related complications.
Global thromboelastometry in patients receiving direct oral anticoagulants: the RO-DOA study
Rapidly available tests might be useful to measure the anticoagulant effect of direct oral anticoagulants (DOAs) in emergency situations as bleedings, surgery, or before thrombolysis. The aim of this study was to assess the effects of DOAs on global thromboelastometry (ROTEM). Coagulation parameters assessed at peak and trough in patients with non-valvular atrial fibrillation receiving apixaban, dabigatran or rivaroxaban at steady-state (patients) were compared to those of healthy volunteers (controls). Citrated blood samples were tested by ROTEM using diluted EXTEM assay, with and without the addition of an anti-FXa catcher, and using ECATEM-B, with and without the addition of an anti-FIIa catcher. Overall 30 patients (10 for each DOA) and 15 controls were included. The mean clotting time (CT) of patients at peak and trough were significantly higher compared to controls. The mean CT was significantly shortened after the addition of the anti-FXa catcher to apixaban (p = 0.005 for peak and p = 0.009 for trough) and to rivaroxaban samples (p = 0.005 for both peak and trough) and after the addition of anti-FIIa cather to dabigatran samples (p = 0.005 for both peak and trough). ROC curve analyses showed a good accuracy for CT and for CT/CT + catcher (CTc) in measuring dabigatran anticoagulant activity (AUC 1.000 and 0.993, respectively); for CT, CT/CTc and clot formation time (CFT)/CFT + catcher (CFTc) in measuring both apixaban activity (0.917, 0.880 and 0.880, respectively) and rivaroxaban activity (0.973, 0.987 and 0.860, respectively). In this study the use of ad-hoc designed reagents and catcher molecules was able to accurately identify DOAs activity at ROTEM.
Reperfusion strategies in stroke due to isolated cervical internal carotid artery occlusion: systematic review and treatment comparison
IntroductionDespite intravenous thrombolysis (IVT) and endovascular treatment (EVT) have been demonstrated effective in acute ischemic stroke (AIS) due to large vessel occlusions, there are still no conclusive data to guide treatment in stroke due to cervical internal carotid artery (ICA) occlusion. We systematically reviewed available literature to compare IVT, EVT, and bridging (IVT + EVT) and define optimal treatment.MethodsSystematic review followed predefined protocol (Open-Science-Framework osf.io/bfykj). MEDLINE, EMBASE, and Cochrane CENTRAL were searched. Results were restricted to studies in English, with sample size ≥ 10 and follow-up ≥30 days. Primary outcomes were favorable outcome (mRS ≤ 2), mortality, and symptomatic intracerebral hemorrhage(sICH), defined according to study original report. Newcastle-Ottawa scale was used for bias assessment.ResultsSeven records of 930 screened were included in meta-analysis. Quality of studies was low-to-fair in 5, good in 2. IVT (n = 450) did not differ for favorable outcome and mortality compared to EVT (n = 150), though having lower rate of sICH (OR = 0.4, 95% CI 0.2–0.8). Compared to IVT, bridging (IVT + EVT) was associated with higher rate of favorable outcome (OR = 2.2, 95% CI 1.3–3.7). Compared to EVT, bridging (IVT + EVT) provided higher rate of favorable outcome (OR = 1.9, 95% CI 1.1–3.4), with a marginally increased risk of sICH (OR = 2.1, 95% CI 1–4.4) but similar mortality rates.ConclusionsOur systematic review highlights that, in acute ischemic stroke associated with isolated cervical ICA occlusion, bridging (IVT + EVT) might lead to higher rate of functional independence at follow-up, without increasing mortality. The low quality of available studies prevents from drawing firm conclusions, and randomized-controlled clinical trials are critically needed to define optimal treatment in this AIS subgroup.
SMASH-U classification: a tool for aetiology-oriented management of patients with acute haemorrhagic stroke
Intracerebral haemorrhage (ICH) is responsible for disproportionately high morbidity and mortality rates. The most used ICH classification system is based on the anatomical site. We used SMASH-U, an aetiological based classification system for ICH by predefined criteria: structural vascular lesions (S), medication (M), amyloid angiopathy (A), systemic disease (S), hypertension (H), or undetermined (U). We aimed to correlate SMASH-U classification of our patients to the intra-hospital mortality rates. We performed a single centre retrospective study at the Santa Maria Della Misericordia Hospital, Perugia (Italy) including consecutive patients between January 2009 and July 2017 assigned with 431 ICD-9 (International Classification of Diseases-9). We classified the included patients using SMASH-U criteria, and we analysed the association between SMASH-U aetiology and ICH risk factors to the outcome defined as intra-hospital mortality, using multivariable logistic regression analysis. The higher intra-hospital mortality rate was detected in the systemic disease (36.1%), medication (31.5%), and undetermined (29.4%) groups. At multivariable analysis, medication and systemic disease groups resulted associated with the outcome (odds ratio 3.47; 95% CI 1.15–10.46; P = 0.02 and 3.64; 95% CI 1.47–9.01; P = 0.005, respectively). Furthermore, age and high NIHSS at admission resulted significantly associated with intra-hospital mortality (odds ratio 1.01; 95% CI 1–1.03; P = 0.04 and 1.12; 95% CI 1.03–1.22; P = 0.008, respectively). In our retrospective study, the aetiology-oriented classification system SMASH-U showed to be potentially predictive of intra-hospital mortality of acute haemorrhagic stroke patients and it may support clinicians in the acute ICH management.
Lacunar stroke syndromes as predictors of lacunar and non-lacunar infarcts on neuroimaging: a hospital-based study
Lacunar syndromes are usually caused by small ischemic lesions called lacunar infarcts. However, non-lacunar infarcts account for about 20% of lacunar syndromes. The aim of this study was to identify clinical predictors of lacunar syndromes led by non-lacunar infarcts. The following single centre, observational study was conducted on an analysis of the “Perugia hospital-based Stroke Registry” database enrolling consecutive patients admitted with ischemic stroke during the period 2010–2017. We evaluated patient risk factors and clinical features linked to stroke syndrome (lacunar/non-lacunar) and to cerebral infarction (lacunar/non-lacunar). Lacunar syndromes were diagnosed in 478 (26.6%) out of 1796 patients. In 104 (21.1%) patients, lacunar syndromes were caused by non-lacunar infarcts. Lacunar syndromes with lacunar infarcts were primarily linked to diabetes (27.8% vs 16.3%) and obesity (7.7% vs 0.9%), while lacunar syndromes with non-lacunar infarcts were linked to a higher risk of atrial fibrillation (22.1% vs 9.4%) and higher National Institute of Health Stroke Scale scores on admission (mean 5.5 ± 3.7 vs 4.7 ± 2.8). On multivariate analysis, atrial fibrillation (OR 1.67, 95% CI 1.09–2.31; p = 0.002) and higher NIHSS (OR 1.12 for each point increase, 95% CI 1.09–1.15; p < 0.001) were predictors of non-lacunar infarcts in all stroke cases, while lacunar syndromes were inversely associated with non-lacunar infarcts (OR 0.15, 95% CI 0.11–0.20; p < 0.001). Atrial fibrillation was the only predictor of non-lacunar infarcts in patients with lacunar syndromes (OR 2.62, 95% CI 1.33–5.18; p = 0.005). 21% of patients with lacunar syndromes had non-lacunar infarctions. Atrial fibrillation turned out to be a predictor of lacunar syndrome due to non-lacunar infarct.