Endovascular thrombectomy in young patients with stroke.

BACKGROUND: Endovascular treatment (ET) is standard of care in patients with acute ischemic stroke due to large vessel occlusion, but data on ET in young patients remain limited. AIM: We aim to compare outcomes for young stroke patients undergoing ET in a matched cohort. METHODS: We analyzed patients from an observational multicenter cohort with acute ischemic stroke and ET, the German Stroke Registry-Endovascular Treatment trial. Baseline characteristics, procedural parameters, and functional outcome at 90 days were compared between young (<50 years) and older (⩾50 years) patients with and without nearest-neighbor 1:1 propensity score matching. RESULTS: Out of 6628 acute ischemic stroke patients treated with ET, 363 (5.5%) were young. Young patients differed with regard to prognostic outcome characteristics. Specifically, National Institutes of Health Stroke Scale (NIHSS) at admission was lower (median 13, interquartile range (IQR) 8-17 vs. 15, IQR 9-19, p < 0.001), and prestroke dependence was less frequent (2.9% vs. 12.2%, p < 0.001) than in older patients. Compared to a matched cohort of older patients, ET was faster (time from groin puncture to flow restoration, 35 vs. 45 min, p < 0.001) and intracranial hemorrhage was less frequent in young patients (10.0% vs. 25.9%, p < 0.001). Good functional outcome (modified Rankin Scale (mRS) 0-2) at 3 months was achieved more frequently in young patients (71.6% vs. 44.1%, p < 0.001), and overall mortality was lower (6.7% vs. 25.4%, p < 0.001). Among previously employed young patients (n = 177), 37.9% returned to work at 3-month follow-up, while 74.1% of the remaining patients were still undergoing rehabilitation. CONCLUSION: Young stroke patients undergoing ET have better outcomes compared to older patients, even when matched for prestroke condition, comorbidities, and stroke severity. Hence, more liberal guidelines to perform ET for younger patients may have to be established by future studies.

Antithrombotic treatment and outcome after endovascular treatment and acute carotid artery stenting in stroke patients with atrial fibrillation.

BACKGROUND: Oral anticoagulation (OAC) is the mainstay of secondary prevention in ischemic stroke patients with atrial fibrillation (AF). However, in AF patients with large vessel occlusion stroke treated by endovascular therapy (ET) and acute carotid artery stenting (CAS), the optimal antithrombotic medication remains unclear. METHODS: This is a subgroup analysis of the German Stroke Registry-Endovascular Treatment (GSR-ET), a prospective multicenter cohort of patients with large vessel occlusion stroke undergoing ET. Patients with AF and CAS during ET were included. We analyzed baseline and periprocedural characteristics, antithrombotic strategies and functional outcome at 90 days. RESULTS: Among 6635 patients in the registry, a total of 82 patients (1.2%, age 77.9 ± 8.0 years, 39% female) with AF and extracranial CAS during ET were included. Antithrombotic medication at admission, during ET, postprocedural and at discharge was highly variable and overall mortality in hospital (21%) and at 90 days (39%) was high. Among discharged patients (n = 65), most frequent antithrombotic regimes were dual antiplatelet therapy (DAPT, 37%), single APT + OAC (25%) and DAPT + OAC (20%). Comparing DAPT to single or dual APT + OAC, clinical characteristics at discharge were similar (median NIHSS 7.5 [interquartile range, 3-10.5] vs 7 [4-11], p = 0.73, mRS 4 [IQR 3-4] vs. 4 [IQR 3-5], p = 0.79), but 90-day mortality was higher without OAC (32 vs 4%, p = 0.02). CONCLUSIONS: In AF patients who underwent ET and CAS, 90-day mortality was higher in patients not receiving OAC. REGISTRATION: https://www. CLINICALTRIALS: gov ; Unique identifier: NCT03356392.

Graded murine wire-induced aortic valve stenosis model mimics human functional and morphological disease phenotype.

Aortic valve stenosis (AS) is the most common valve disease requiring therapeutic intervention. Even though the incidence of AS has been continuously rising and AS is associated with significant morbidity and mortality, to date, no medical treatments have been identified that can modify disease progression. This unmet medical need is likely attributed to an incomplete understanding of the molecular mechanism driving disease development. To investigate the pathophysiology leading to AS, reliable and reproducible animal models that mimic human pathophysiology are needed. We have tested and expanded the protocols of a wire-injury induced AS mouse model. For this model, coronary wires were used to apply shear stress to the aortic valve cusps with increasing intensity. These protocols allowed distinction of mild, moderate and severe wire-injury. Upon moderate or severe injury, AS developed with a significant increase in aortic valve peak blood flow velocity. While moderate injury promoted solitary AS, severe-injury induced mixed aortic valve disease with concomitant mild to moderate aortic regurgitation. The changes in aortic valve function were reflected by dilation and hypertrophy of the left ventricle, as well as a decreased left ventricular ejection fraction. Histological analysis revealed the classic hallmarks of human disease with aortic valve thickening, increased macrophage infiltration, fibrosis and calcification. This new mouse model of AS promotes functional and morphological changes similar to moderate and severe human AS. It can be used to investigate the pathomechanisms contributing to AS development and to test novel therapeutic strategies.