RESUMEN
BACKGROUND AND PURPOSE: There are very few published data on the patency of carotid stents implanted during thrombectomies for tandem lesions in the anterior circulation. We aimed to communicate our experience of stenting in the acute setting with systematic follow-up of stent patency and discuss predictors and clinical repercussions of delayed stent thrombosis. MATERIALS AND METHODS: We performed a retrospective study of stroke thrombectomies in a single center between January 2009 and April 2018. Patient files were reviewed to extract patient characteristics, procedural details, imaging studies, and clinical information. Predictors of delayed stent thrombosis and clinical outcome at discharge were analyzed using univariate and multivariate analyses. RESULTS: We identified 81 patients treated for tandem lesions: 63 (77.7%) atheromas, 17 (20.9%) dissections, and 1 (1.2%) carotid web. TICI 2b-3 recanalization was achieved in 70 (86.4%) cases. Thirty-five patients (43.2%) were independent (mRS score ≤ 2) at discharge. Among 73 patients with intracranial recanalization and patent stents at the end of the procedure, delayed stent thrombosis was observed in 14 (19.1%). Among 59 patients with patent stents, 44 had further imaging controls (median, 105 days; range, 2-2407 days) and 1 (1.6%) had 50% in-stent stenosis with no retreatment. Stent occlusion rates were 11/39 (28.2%) for periprocedural aspirin treatment versus 3/34 (8.8%) for aspirin and clopidogrel (P = .04). Delayed stent thrombosis was independently associated with higher admission NIHSS scores (OR, 1.1; 95% CI, 1.01-1.28), diabetes (OR, 6.07; 95% CI, 1.2-30.6), and the presence of in-stent thrombus on the final angiographic run (OR, 6.2; 95% CI, 1.4-27.97). Delayed stent thrombosis (OR, 19.78; 95% CI, 2.78-296.83), higher admission NIHSS scores (OR, 1.27, 95% CI, 1.12-1.51), and symptomatic hemorrhagic transformation (OR, 23.65; 95% CI, 1.85-3478.94) were independent predictors of unfavorable clinical outcome at discharge. CONCLUSIONS: We observed a non-negligible rate of delayed stent thrombosis with significant negative impact on clinical outcome. Future studies should systematically measure and report stent patency rates.
Asunto(s)
Estenosis Carotídea/terapia , Complicaciones Posoperatorias/etiología , Accidente Cerebrovascular/terapia , Trombectomía/métodos , Trombosis/etiología , Adulto , Anciano , Anciano de 80 o más Años , Estenosis Carotídea/complicaciones , Femenino , Humanos , Masculino , Persona de Mediana Edad , Estudios Retrospectivos , Stents , Accidente Cerebrovascular/etiología , Trombosis/epidemiología , Resultado del TratamientoRESUMEN
Single-nucleotide polymorphisms (SNPs) in CACNA1C, the α1C subunit of the voltage-gated L-type calcium channel Cav1.2, rank among the most consistent and replicable genetics findings in psychiatry and have been associated with schizophrenia, bipolar disorder and major depression. However, genetic variants of complex diseases often only confer a marginal increase in disease risk, which is additionally influenced by the environment. Here we show that embryonic deletion of Cacna1c in forebrain glutamatergic neurons promotes the manifestation of endophenotypes related to psychiatric disorders including cognitive decline, impaired synaptic plasticity, reduced sociability, hyperactivity and increased anxiety. Additional analyses revealed that depletion of Cacna1c during embryonic development also increases the susceptibility to chronic stress, which suggest that Cav1.2 interacts with the environment to shape disease vulnerability. Remarkably, this was not observed when Cacna1c was deleted in glutamatergic neurons during adulthood, where the later deletion even improved cognitive flexibility, strengthened synaptic plasticity and induced stress resilience. In a parallel gene × environment design in humans, we additionally demonstrate that SNPs in CACNA1C significantly interact with adverse life events to alter the risk to develop symptoms of psychiatric disorders. Overall, our results further validate Cacna1c as a cross-disorder risk gene in mice and humans, and additionally suggest a differential role for Cav1.2 during development and adulthood in shaping cognition, sociability, emotional behavior and stress susceptibility. This may prompt the consideration for pharmacological manipulation of Cav1.2 in neuropsychiatric disorders with developmental and/or stress-related origins.