The Impact of Frailty on Outcomes of Proximal Aortic Aneurysm Surgery: A Nationwide Analysis.

(1) Background: This study examines frailty's impact on proximal aortic surgery outcomes. (2) Methods: All patients with a thoracic aortic aneurysm who underwent aortic root, ascending aorta, or arch surgery from the 2016-2017 National Inpatient Sample were included. Frailty was defined by the Adjusted Clinical Groups Frailty Indicator. Outcomes of interest included in-hospital mortality and a composite of death, stroke, acute kidney injury (AKI), and major bleeding (MACE). (3) Results: Among 5745 patients, 405 (7.0%) met frailty criteria. Frail patients were older, with higher rates of chronic pulmonary disease, diabetes, and chronic kidney disease. There was no difference in in-hospital death (4.9% vs. 2.4%, p = 0.169); however, the frail group exhibited higher rates of stroke and AKI. Frail patients had a longer length of stay (17 vs. 8 days), and higher rates of non-home discharge (74.1% vs. 54.3%) than non-frail patients (both p < 0.001). Sensitivity analysis confirmed increased morbidity and mortality in frail individuals. After adjusting for patient comorbidities and hospital characteristics, frailty independently predicted MACE (OR 4.29 [1.88-9.78], p = 0.001), while age alone did not (OR 1.00 [0.99-1.02], p = 0.568). Urban teaching center status predicted a lower risk of MACE (OR 0.27 [0.08-0.94], p = 0.039). (4) Conclusions: Frailty is associated with increased morbidity in proximal aortic surgery and is a more significant predictor of mortality than age. Coordinated treatment in urban institutions may enhance outcomes for this high-risk group.

Early Failure of a Bioprosthetic Valve in the Pulmonary Position Causing Panic.

An asymptomatic 26-year-old woman with repaired tetralogy of Fallot and a bioprosthetic pulmonary valve presented with a large thrombosis occluding most of her right ventricular outflow tract and main pulmonary arteries. Our pulmonary embolism response team was emergently consulted, resulting in considerable discussion regarding the treatment modality given the large size and high-risk nature of the thrombosis. Ultimately, she was started on a heparin infusion until she could undergo open thrombectomy and pulmonary valve repeat replacement. The patient's asymptomatic presentation, despite the considerable clot burden, complicated our approach to management but ultimately led to a measured and timely intervention.

Amyloid Beta Peptides Block New Synapse Assembly by Nogo Receptor-Mediated Inhibition of T-Type Calcium Channels.

Compelling evidence links amyloid beta (Aß) peptide accumulation in the brains of Alzheimer's disease (AD) patients with the emergence of learning and memory deficits, yet a clear understanding of the events that drive this synaptic pathology are lacking. We present evidence that neurons exposed to Aß are unable to form new synapses, resulting in learning deficits in vivo. We demonstrate the Nogo receptor family (NgR1-3) acts as Aß receptors mediating an inhibition of synapse assembly, plasticity, and learning. Live imaging studies reveal Aß activates NgRs on the dendritic shaft of neurons, triggering an inhibition of calcium signaling. We define T-type calcium channels as a target of Aß-NgR signaling, mediating Aß's inhibitory effects on calcium, synapse assembly, plasticity, and learning. These studies highlight deficits in new synapse assembly as a potential initiator of cognitive pathology in AD, and pinpoint calcium dysregulation mediated by NgRs and T-type channels as key components. VIDEO ABSTRACT.