Aortic Remodeling and Clinical Outcomes Following Thoracic Endovascular Aortic Repair for Blunt Thoracic Aortic Injury.

BACKGROUND: There is currently limited data assessing the long-term consequences of thoracic endovascular aortic repair (TEVAR) in otherwise healthy aortic segments remote from the site of endograft coverage. The aim of this study is to retrospectively evaluate aortic remodeling and long-term outcomes of blunt thoracic aortic injury (BTAI) patients treated with TEVAR. Our hypothesis is that significant changes to the aorta proximal to the graft-covered segment are suspected following TEVAR. METHODS: An institutional review board-approved retrospective review of patients who underwent TEVAR for BTAI at a level I trauma center from 2004 to 2018 was performed. Forty-six patients were identified and of these, 32 patients with high-resolution computed tomographic angiography imaging follow-up were included in the study. Computed tomographic angiography measurements of aortic dimensions and branch vessels proximal, distal, and adjacent to the stent grafted segment were recorded preprocedure and postprocedure and analyzed. Primary device-related outcomes such as birdbeaking, mural thrombus, stent migration, and persistent endoleak were assessed. Patient outcomes including mortality, graft-related morbidity, and need for secondary interventions were also analyzed. RESULTS: Mean follow-up of the selected patients in the study was 1.52 y (range, 0.06-8.0 y). Following TEVAR, the ascending aortic length increased significantly (mean 5.7 ± 4.6 mm, P < 0.001). The mean diameters of the ascending aorta (1.5 ± 1.5, P < 0.001 mm), the midaortic arch (1.3 ± 1.7 mm, P < 0.001), and proximal and the distal endograft landing zones (1.9 ± 2.1 mm and 2.2 ± 1.6 mm, respectively, P < 0.001) also increased significantly following TEVAR. Clinically relevant device-related outcomes occurred with the presence of endograft infolding and subsequent development of endograft mural thrombus (P < 0.001). The need for secondary intervention following TEVAR for BTAI was associated with endograft mural thrombus (P < 0.05). CONCLUSIONS: TEVAR for BTAI causes significant geometric changes in the aorta proximal to the stented grafted segment of the aorta. Direct consequences of the graft at the stented segment includes mural thrombus development within the endograft which was associated with the need for secondary intervention. Although clinical significance is yet to be determined, post-TEVAR changes in aortic architecture warrant continued aortic surveillance following BTAI.

Chronic + binge alcohol exposure promotes inflammation and alters airway mechanics in the lung.

INTRODUCTION: Alcohol use disorders are major risk factors for the development of and susceptibility to acute respiratory distress syndrome. Although these risks of alcohol consumption on the lung are well described, mechanisms by which alcohol abuse promotes acute lung injury are poorly understood. These gaps in our understanding are due, at least in part, to limitations of animal models to recapitulate human alcohol consumption. Recently, a new model of chronic plus binge alcohol exposure was developed that is hypothesized to better model drinking patterns of individuals with alcohol use disorders. Specifically, this paradigm models chronic consumption coupled with periodic bouts of heavy drinking. The impacts of this alcohol-exposure regimen on the lung are uncharacterized. Therefore, the goal of this study was to examine lung injury and inflammation in a well-characterized experimental model of chronic + binge alcohol exposure. METHODS: 10-week-old male C57Bl6/J mice were administered ethanol-containing (or isocaloric control) liquid diet for 10 days, followed by a single ethanol gavage (5 g/kg). Lung inflammation and pulmonary function were assessed. RESULTS: Ten days of ethanol-containing liquid diet alone (chronic) did not detectably affect any variables measured. However, ethanol diet plus gavage (chronic + binge) caused neutrophils to accumulate in the lung tissue and in the bronchoalveolar lavage fluid 24 h post-binge. This inflammatory cell recruitment was associated with airway hyper-responsiveness to inhaled methacholine, as indicated by elevated resistance, Newtonian resistance, and respiratory resistance. CONCLUSIONS: Taken together, the novel findings reveal that ethanol alone, absent of any secondary inflammatory insult, is sufficient to produce inflammation in the lung. Although these changes were relatively mild, they were associated with functional changes in the central airways. This animal model may be useful in the future for identifying mechanisms by which alcohol abuse sensitizes at-risk individuals to lung injury.