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IntroductionThromboinflammatory complications are well described sequalae of Coronavirus Disease 2019 (COVID-19), and there is evidence of both hyperreactive platelet and inflammatory neutrophil biology that contributes to the thromoinflammatory milieu. It has been demonstrated in other thromboinflammatory diseases that the circulating environment may affect cellular behavior, but what role this environment exerts on platelets and neutrophils in COVID-19 remains unknown. We tested the hypotheses that 1) plasma from COVID-19 patients can induce a prothrombotic platelet functional phenotype, and 2) contents released from platelets (platelet releasate) from COVID-19 patients can induce a proinflammatory neutrophil phenotype. MethodsWe treated platelets with COVID-19 patient and disease control plasma, and measured their aggregation response to collagen and adhesion in a microfluidic parallel plate flow chamber coated with collagen and thromboplastin. We exposed healthy neutrophils to platelet releasate from COVID-19 patients and disease controls and measured neutrophil extracellular trap formation and performed RNA sequencing.ResultsWe found that COVID-19 patient plasma promoted auto-aggregation, thereby reducing response to further stimulation ex-vivo. Neither disease condition increased the number of platelets adhered to a collagen and thromboplastin coated parallel plate flow chamber, but both markedly reduced platelet size. COVID-19 patient platelet releasate increased myeloperoxidasedeoxyribonucleic acid complexes and induced changes to neutrophil gene expression.DiscussionTogether these results suggest aspects of the soluble environment circulating platelets, and that the contents released from those neutrophil behavior independent of direct cellular contact.

Objective: To understand arterial remodeling and the pathophysiology of arterial diseases, it is necessary to understand the baseline qualities and variations in arterial structure. Arteries could differ in wall thickness, laminar structure, and laminar fenestration depending on their position within the arterial tree. We endeavored to evaluate and compare the extracellular matrix structure of different arteries throughout the arterial tree, from the aorta to the adductor muscle arteriole, with a particular focus on the internal elastic lamina (IEL). Methods: Arterial segments were harvested from male Sprague-Dawley rats and imaged using multiple modalities. En face scans by multiphoton microscopy were used to compare native-state adventitial collagen undulation and IEL fenestration. Results: Collagen undulation was similar across most examined arteries but straighter in the skeletal muscle arterioles (P < .05). The elastic lamellae showed several differences. The IEL fenestrae were similar in average size among abdominal aorta and celiac, renal, common iliac, and common femoral arteries (range, 14-24 μm2), with wide within-vessel variance (square of the standard deviation, 462-1904 μm4). However, they tended to be smaller (9.08 μm2) and less variable (square of the standard deviation, 88.3 μm4) in the popliteal artery. Fenestrae were greater in number in the superior mesenteric artery (SMA; 6686/mm2; P < .05) and profunda femoris artery (PFA; 11,042/mm2; P < .05) compared with the other examined vessels, which ranged in surface density from 3143/mm2 to 4362/mm2. The SMA and PFA also showed greater total fenestration as a proportion of the IEL surface area (SMA, 15.04%; P < .05; PFA, 24.11%; P < .001) than the other examined arteries (range of means, 4.7%-9.4%). The arteriolar IEL was structurally distinct, comparable to a low-density wireframe. Other structural differences were also noted, including differences in the number of medial lamellae along the arterial tree. Conclusions: We found that vessels at different locations along the arterial tree differ in structure. The SMA, PFA, and intramuscular arterioles have fundamental differences in the extracellular matrix structure compared with other arteries. Location-specific features such as the medial lamellae number and elastic laminar structure might have relevance to physiology and confer vulnerabilities to the development of pathology. : Clinical Relevance: Arterial pathologies affect and depend on elastic fibers and collagen. Medial arterial calcification involves mineral deposition onto elastic fibers and smooth muscle cell osteogenesis, which can be induced by elastin degradation. Degradation or remodeling of the extracellular matrix can be a critical component of atherosclerosis and hypertension. Pathologies can also be site-specific. Aneurysms are most common in the abdominal aorta (Ao), followed by the popliteal artery, which shows age-related changes to wall properties comparable to those in central elastic arteries. Visceral artery aneurysms, however, are rare. Location differences in arterial extracellular matrix structure could inform site-specific differences in arterial pathology.

Angiosome-directed endovascular therapy for the treatment of chronic limb-threatening ischemia (CLTI) remains controversial owing to the overlap of wound angiosomes. Angiographic grading of success has limitations and translesional pressure assessments are seldom performed in the infrapopliteal vessels. Objective criteria to determine revascularization success in tibiopedal vessels have not been well described. Quantifying perfusion to a wound bed after establishing direct or indirect (via collateral) flow after revascularization is an important component for treating CLTI patients yet is seldom performed. We report the use of fluorescent angiography to quantitatively examine perfusion of a diabetic foot ulcer before and after angiosome-directed endovascular therapy.

Introduction: Although parallel graft endovascular aortic repair (pg-EVAR) was initially described as a rescue technique for endovascular aneurysm repairs that unintentionally excluded visceral branches, its use has expanded to include endovascular repairs of paravisceral and thoracoabdominal aneurysms. However, there is limited literature on utilization in emergency repair of ruptured aortic aneurysms which previously underwent elective open repair. Case 1: A 73-year-old man with a remote history of an open AAA repair with a tube graft presented as a transfer with two weeks of worsening left chest pain and was found to have a 6–7 cm contained rupture of a type III thoracoabdominal aortic aneurysm on computed tomography (CT). Due to his anatomy, previous repair, and comorbidities, endovascular repair was preferred over a redo open approach. He was taken for an emergent endovascular repair – a planned sandwich graft with the proximal seal in the mid thoracic aorta and the distal seal in the infrarenal aortic graft. The stenotic celiac artery was nearly occluded, so visceral stents were placed into the superior mesenteric and bilateral renal arteries. His hospital course was complicated by acute kidney injury, deconditioning, and failure to thrive. CT on postoperative day 44 showed a technically successful pg-EVAR with no evidence of endoleak. Case 2: A 69-year-old woman who recently underwent an open AAA repair at an outside facility developed nausea, vomiting, abdominal pain and down-trending hemoglobin while hospitalized for workup of a new coagulopathy. She was found to have a contained rupture of a proximal anastomotic pseudoaneurysm. Due to her recent repair and current medical state, she was brought to the hybrid suite for emergent endovascular repair. The location of the rupture required entire visceral segment coverage, so a pg-EVAR with spinal drainage was planned. Her celiac, superior mesenteric, and left renal arteries were preserved with stents. Her postoperative course was complicated by a hematoma with persistent rebleeding at her brachial access site which resolved following the placement of a covered stent. CT on postoperative day 16 showed a technically successful pg-EVAR with no evidence of endoleak. Discussion: Many patients remain ineligible for conventional EVAR due to anatomic variations and supra-renal aneurysmal disease. Customized branched or fenestrated endografts have been developed to overcome these limitations. However, production time requires weeks, and grafts with greater than two fenestrations are not commercially available in the United States. Because they use readily available devices, parallel graft repairs may be beneficial when urgent repair is needed. There remains a paucity of data on their usage in emergency repairs of aortic aneurysms, particularly in aneurysms that had been previously repaired surgically. The technical success in the two cases detailed here suggest that parallel graft techniques can be used to expeditiously salvage complex emergency aneurysms with successful sealing of parallel grafts into a previous infrarenal aortic graft.

Background Existing evidence indicates Black patients have higher incidence of pulmonary embolism (PE) and PE‐related mortality compared with other races/ethnicities, yet disparities in presenting severity and treatment remain incompletely understood. Methods and Results We retrospectively queried a multihospital healthcare system for all hospitalizations for acute PE (2012–2019). Of 10 329 hospitalizations, 8743 met inclusion criteria. Black patients (14.3%) were significantly younger (54.6±17.8 versus 63.1±16.6 years; P

When a large artery becomes occluded, hemodynamic changes stimulate remodeling of arterial networks to form collateral arteries in a process termed arteriogenesis. However, the structural changes necessary for collateral remodeling have not been defined. We hypothesize that deconstruction of the extracellular matrix is essential to remodel smaller arteries into effective collaterals. Using multiphoton microscopy, we analyzed collagen and elastin structure in maturing collateral arteries isolated from ischemic rat hindlimbs. Collateral arteries harvested at different timepoints showed progressive diameter expansion associated with striking rearrangement of internal elastic lamina (IEL) into a loose fibrous mesh, a pattern persisting at 8 weeks. Despite a 2.5-fold increase in luminal diameter, total elastin content remained unchanged in collaterals compared with control arteries. Among the collateral midzones, baseline elastic fiber content was low. Outward remodeling of these vessels with a 10–20 fold diameter increase was associated with fractures of the elastic fibers and evidence of increased wall tension, as demonstrated by the straightening of the adventitial collagen. Inhibition of lysyl oxidase (LOX) function with β-aminopropionitrile resulted in severe fragmentation or complete loss of continuity of the IEL in developing collaterals. Collateral artery development is associated with permanent redistribution of existing elastic fibers to accommodate diameter growth. We found no evidence of new elastic fiber formation. Stabilization of the arterial wall during outward remodeling is necessary and dependent on LOX activity.

Acute mesenteric ischemia (AMI) is typically treated by open surgery or hybrid techniques. Catheter-based aspiration thrombectomy represents another minimally invasive alternative with a potential additional safety benefit of minimizing the bleeding risk associated with thrombolytics. In this institutional case series, we present five clinical cases of aspiration thrombectomy for high-risk AMI using the Penumbra aspiration system. All patients underwent technically successful endovascular thrombectomy as demonstrated by intraoperative angiography results. However, bowel necrosis and sepsis adversely affected postoperative outcomes. Lack of intraoperative bowel assessment is a limitation of endovascular methods, highlighting the importance of patient selection.