Outcomes and safety of endovascular treatment from 6 to 24 hours in patients with a pre-stroke moderate disability (mRS 3): a multicenter retrospective study.

BACKGROUND: Approximately 30% of patients presenting with acute ischemic stroke (AIS) due to large vessel occlusion have pre-stroke modified Rankin Scale (mRS) scores ≥2. We aimed to investigate the safety and outcomes of endovascular treatment (EVT) in patients with AIS with moderate pre-stroke disability (mRS score 3) in an extended time frame (ie, 6-24 hours from the last time known well). METHODS: Data were collected from five centers in Europe and the USA from January 2018 to January 2023 and included 180 patients who underwent EVT in an extended time frame. Patients were divided into two groups of 90 each (Group 1: pre-mRS 0-2; Group 2: pre-mRS 3; 71% women, mean age 80.3±11.9 years). Primary outcomes were: (1) 3-month good clinical outcome (Group 1: mRS 0-2, Group 2: mRS 0-3) and ΔmRS; (2) any hemorrhagic transformation (HT); and (3) symptomatic HT. Secondary outcomes were successful and complete recanalization after EVT and 3-month mortality. RESULTS: No between-group differences were found in the 3-month good clinical outcome (26.6% vs 25.5%, P=0.974), any HT (26.6% vs 22%, P=0.733), and symptomatic HT (8.9 vs 4.4%, P=0.232). Unexpectedly, ΔmRS was significantly smaller in Group 2 compared with Group 1 (1.64±1.61 vs 2.97±1.69, P<0.001). No between-group differences were found in secondary outcomes. CONCLUSION: Patients with pre-stroke mRS 3 are likely to have similar outcomes after EVT in the extended time frame to those with pre-stroke mRS 0-2, with no difference in safety.

External Validation of SAFE Score to Predict Atrial Fibrillation Diagnosis after Ischemic Stroke: A Retrospective Multicenter Study.

Introduction: The screening for atrial fibrillation (AF) scale (SAFE score) was recently developed to provide a prediction of the diagnosis of AF after an ischemic stroke. It includes 7 items: age ≥ 65 years, bronchopathy, thyroid disease, cortical location of stroke, intracranial large vessel occlusion, NT-ProBNP ≥250 pg/mL, and left atrial enlargement. In the internal validation, a good performance was obtained, with an AUC = 0.88 (95% CI 0.84-0.91) and sensitivity and specificity of 83% and 80%, respectively, for scores ≥ 5. The aim of this study is the external validation of the SAFE score in a multicenter cohort. Methods: A retrospective multicenter study, including consecutive patients with ischemic stroke or transient ischemic attack between 2020 and 2022 with at least 24 hours of cardiac monitoring. Patients with previous AF or AF diagnosed on admission ECG were excluded. Results: Overall, 395 patients were recruited for analysis. The SAFE score obtained an AUC = 0.822 (95% CI 0.778-0.866) with a sensitivity of 87.2%, a specificity of 65.4%, a positive predictive value of 44.1%, and a negative predictive value of 94.3% for a SAFE score ≥ 5, with no significant gender differences. Calibration analysis in the external cohort showed an absence of significant differences between the observed values and those predicted by the model (Hosmer-Lemeshow's test 0.089). Conclusions: The SAFE score showed adequate discriminative ability and calibration, so its external validation is justified. Further validations in other external cohorts or specific subpopulations of stroke patients might be required.

Migraine worsening after COVID-19 and COVID-19 vaccination: Are we facing a nocebo effect?

BACKGROUND AND PURPOSE: In clinical practice patients may report migraine worsening as a consequence of COVID-19 (either infection or vaccines), however, data in this area are lacking. We aimed to investigate the link between COVID-19 and COVID-19 vaccination with migraine worsening and its associated factors. METHODS: An online survey was sent to migraine patients followed up in a Spanish Headache Clinic, collecting demographic data, and information regarding SARS-CoV-2 infection and vaccination. We asked patients if they had noticed worsening of their migraine after these events and assessed concerns about infection, vaccination and migraine worsening. We also extracted data from participants' own electronic diaries (e-diaries), including 1-month data before and after their reported infection and/or vaccination. We compared participants who self-reported migraine worsening since infection or vaccination with those who did not. RESULTS: Of 550 participants, 44.9% (247/550) reported having had COVID-19 at least once and 83.3% (458/550) had been vaccinated. Sixty-one patients reported migraine worsening since COVID-19 and 52 since the vaccination. Among the risk factors for perceived migraine worsening in the two settings (infection and vaccination) was concern about migraine worsening itself (infection: odds ratio [OR] 2.498 [95% CI: 1.02-6.273], p = 0.046; vaccination: OR 17.3 [95% CI: confidence interval 5.3-68], p < 0.001). e-diary information was available for 136 of the 550 patients, 38.2% (52/136) for COVID-19 and 39.7% (54/136) for vaccination. We observed no significant difference in headache frequency 1 month before and after infection or vaccination, even when comparing patients with and without self-reported migraine worsening. CONCLUSIONS: Our preliminary data point to a negligible role of the infection and vaccination on migraine worsening and to the possible presence of a nocebo effect in these settings, as a remarkable proportion of patients had a clear perception of migraine worsening.

Association between non alcoholic fatty liver disease, metabolic and vascular risk. / Asociación entre hígado graso no alcohólico, riesgo metabólico y vascular.

BACKGROUND: Hepatic steatosis is a public health problem with increased incidence and prevalence OBJECTIVE: To determine whether the liver steatosis, as measured by the Fatty Liver Index (FLI), is related to metabolic risk and vascular factors and, if so, to identify the clinical-metabolic factor that explains the higher vascular risk. METHODS: Cross-sectional study including a sample of 531 men who came to the University of Navarra Clinic Check-up Unit. The degree of steatosis was determined by the FLI. The metabolic risk was assessed using a scale based on determinations of HDL, LDL, triglycerides, blood glucose, HOMA-IR, neutrophil/lymphocyte index, and systolic blood pressure. The vascular risk was assessed by the presence of carotid and/or femoral atheromatous plaques. The dose-response association between FLI and both risks was analysed using non-parametric models (splines) and logistic regression. RESULTS: The sample studied had a mean age of 52.70years, with 49.3% having an FLI ≥60, as well as 33.6% with metabolic syndrome, and 43.9% with carotid and/or femoral atheromatous plaques. The relationship between FLI and metabolic risk and vascular was linear (metabolic: non-linear P=.097; linear P<.001; vascular: non-linear P=1.000; linear P=.028). For every 10 units of increase in FLI, the odds of presenting with atheroma plaques increased by 9.7% (OR=1.097; 95% confidence interval 1.010-1.191). When adjusting for triglyceridaemia, the association disappeared (OR=1.001). CONCLUSIONS: Patients with fatty liver disease had an increased metabolic and vascular risk. The increased vascular risk is associated with the triglyceride level. On a clinical level, this study suggests that these patients could benefit from treatment of hypertriglyceridaemia.