Background and objectives:COVID-19 related inflammation, endothelial dysfunction and coagulopathy may increase the bleeding risk and lower efficacy of revascularization treatments in patients with acute ischemic stroke. We aimed to evaluate the safety and outcomes of revascularization treatments in patients with acute ischemic stroke and COVID-19.Methods:Retrospective multicenter cohort study of consecutive patients with acute ischemic stroke receiving intravenous thrombolysis (IVT) and/or endovascular treatment (EVT) between March 2020 and June 2021, tested for SARS-CoV-2 infection. With a doubly-robust model combining propensity score weighting and multivariate regression, we studied the association of COVID-19 with intracranial bleeding complications and clinical outcomes. Subgroup analyses were performed according to treatment groups (IVT-only and EVT).Results:Of a total of 15128 included patients from 105 centers, 853 (5.6%) were diagnosed with COVID-19. 5848 (38.7%) patients received IVT-only, and 9280 (61.3%) EVT (with or without IVT). Patients with COVID-19 had a higher rate of symptomatic intracerebral hemorrhage (SICH) (adjusted odds ratio [OR] 1.53; 95% CI 1.16–2.01), symptomatic subarachnoid hemorrhage (SSAH) (OR 1.80; 95% CI 1.20–2.69), SICH and/or SSAH combined (OR 1.56; 95% CI 1.23–1.99), 24-hour (OR 2.47; 95% CI 1.58–3.86) and 3-month mortality (OR 1.88; 95% CI 1.52–2.33).COVID-19 patients also had an unfavorable shift in the distribution of the modified Rankin score at 3 months (OR 1.42; 95% CI 1.26–1.60).Discussion:Patients with acute ischemic stroke and COVID-19 showed higher rates of intracranial bleeding complications and worse clinical outcomes after revascularization treatments than contemporaneous non-COVID-19 treated patients. Current available data does not allow direct conclusions to be drawn on the effectiveness of revascularization treatments in COVID-19 patients, or to establish different treatment recommendations in this subgroup of patients with ischemic stroke. Our findings can be taken into consideration for treatment decisions, patient monitoring and establishing prognosis.
Background and aims Fabry disease (FD) is a rare X-linked lysosomal storage disorder caused by disease-associated variants in the alpha-galactosidase A gene (GLA). FD is a known cause of stroke in younger patients. There are limited data on prevalence of FD and stroke risk in unselected stroke patients. Methods A prospective nationwide study including 35 (78%) of all 45 stroke centers and all consecutive stroke patients admitted during three months. Clinical data were collected in the RES-Q database. FD was diagnosed using dried blood spots in a stepwise manner: in males—enzymatic activity, globotriaosylsphingosine (lyso-Gb3) quantification, if positive followed by GLA gene sequencing; and in females GLA sequencing followed by lyso-Gb3. Results 986 consecutive patients (54% men, mean age 70 years) were included. Observed stroke type was ischemic 79%, transient ischemic attack (TIA) 14%, intracerebral hemorrhage (ICH) 7%, subarachnoid hemorrhage 1% and cerebral venous thrombosis 0.1%. Two (0.2%, 95% CI 0.02–0.7) patients had a pathogenic variant associated with the classical FD phenotype (c.1235_1236delCT and p.G325S). Another fourteen (1.4%, 95% CI 0.08–2.4) patients had a variant of GLA gene considered benign (9 with p.D313Y, one p.A143T, one p.R118C, one p.V199A, one p.R30K and one p.R38G). The index stroke in two carriers of disease-associated variant was ischemic lacunar. In 14 carriers of GLA gene variants 11 strokes were ischemic, two TIA, and one ICH. Patients with positive as compared to negative GLA gene screening were younger (mean 60±SD, min, max, vs 70±SD, min, max, P = 0.02), otherwise there were no differences in other baseline variables. Conclusions The prevalence of FD in unselected adult patients with acute stroke is 0.2%. Both patients who had a pathogenic GLA gene variant were younger than 50 years. Our results support FD screening in patients that had a stroke event before 50 years of age.
Introduction: Dabigatran is direct thrombin inhibitor approved in the prevention of stroke in patients with atrial fibrillation. It was shown in the RELY trial substudy that genetic variants could contribute to interindividual variability in concentrations of the active metabolite of dabigatran and influence the safety of treatment. Carriage of the CES1 rs2244613 minor allele was associated with lower exposure to active metabolite and with a lower bleeding risk compared to wild-type allele. Aim: To determine the influence of gene CES1 polymorphism rs2244613 and through plasmatic concentration of dabigatran on occurrence of major bleeding in stroke patients. Methods: Prospective observational monocentric study in consenting stroke patients initiated on dabigatran. Primary outcome was major bleeding defined using ISTH criteria. DNA analysis of CES1 polymorphism rs2244613 was done with RFLP analysis. Through concentration of dabigatran was measured with liquid chromatography-tandem mass spectrometry (LC-MS/MS) at least 7 days after initiation. Results: 110 patients after cardioembolic stroke, mean age 70,2 (SD 12.7), 56 (50.9%) women, were enrolled. Mean follow-up time was 19.9 months (total 182.2 patient years). 68 (61.8%) patients were wild-type, 37 (33.6%) were minor allele heterozygotes and 5 (4.5%) were homozygous minor allele carriers. Through dabigatran concentration were non-significantly lower in minor allele carriers: 132.8 (SD 98.7) ng/ml in wild-type patients, 112.2 (80.0) in heterozygotes and 95.6 (SD 88.1) in homozygotes. There were 6 episodes of major bleeding, all in patients with wild-type genotype. The patients with dabigatran level above 160 ng/ml (upper quartile) were more likely to have major bleeding, HR 5.74 (95% CI 1.05 - 31.42, p = 0.044). Age and renal function did not correlate with the bleeding. Conclusion: Patients with higher dabigatran concentration had significantly higher major bleeding risk. Minor allele carriers had non-significant trend for having lower through dabigatran level. Personalized dabigatran dosing based on pharmacogenetics and monitoring plasmatic levels should be studied in future trials with the aim to increase the safety of treatment.
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