Can remote endarterectomy expand access to kidney transplantation in patients with severe iliac calcification?

Severe iliac artery calcification in patients with end-stage renal disease is a common barrier to listing for kidney transplant. While few surgical solutions to iliac calcification have been reported, improving treatment may thus improve access to transplant care. Here we present two cases of a novel application of remote endarterectomy of the external iliac artery to facilitate listing for renal transplant. Both patients were listed following remote endarterectomy, followed by successful renal transplants using the treated vessels.

Evaluating the Safety of Transcarotid Artery Revascularization under Local Anesthesia Prior to Coronary Artery Bypass Grafting Surgery.

BACKGROUND: Controversy exists regarding the timing of intervention for patients with critical coronary artery disease (CAD) awaiting coronary artery bypass and severe carotid artery stenosis (CAS). Transcarotid artery revascularization (TCAR) is a minimally invasive revascularization alternative through direct transcervical carotid access that minimizes the chance of arch manipulation and consequent antegrade embolic stroke rate. While the TCAR procedure can be performed under local anesthesia (monitored anesthesia care [MAC]) versus general anesthesia, the hemodynamic benefits of local anesthesia in patients with severe CAD are significant. Patients receiving staged TCAR-coronary artery bypass grafting (CABG) have high-risk cardiovascular disease and require accurate perioperative neurological and hemodynamic evaluation that can be safely provided with local anesthesia. METHODS: In this retrospective single-center study, 14 patients were systematically identified to have undergone staged TCAR prior to CABG surgery from December 2018 to October 2021. All patients underwent TCAR with local anesthesia and minimal sedation. Relevant patient demographics, medical and surgical history, preoperative covariates, and type of anesthesia administered were obtained from patients' charts. CAD was confirmed by either carotid duplex imaging or computed tomography angiography (CTA) of the head/neck. RESULTS: Staged TCAR-CABG interventions were performed on 14 patients (64% male; mean age 65.0 years). No major adverse cardiac events were reported including transient ischemic attack (TIA), stroke, myocardial infarction (MI), or TCAR-related death in the interval between their TCAR and CABG as well as in a 12-month follow-up period. One patient required to return to the operating room (OR) for evacuation of a neck hematoma. CONCLUSIONS: This study demonstrated high success rate of TCAR under local anesthesia prior to CABG (100%) with no incidence of perioperative stroke, MI, or death at 1-month, 6-month, and 12-month follow-up intervals. The authors support the use of staged TCAR-CABG with local anesthesia as a safe and promising treatment option for patients with high-grade cardiac disease, high risk of stroke, or multiple comorbidities that preclude a carotid endarterectomy (CEA).

Depletion of CD4 and CD8 Positive T Cells Impairs Venous Thrombus Resolution in Mice.

Resolution of deep venous thrombosis involves coordinated inflammatory processes. T cells regulate inflammation in vivo and modulate vascular remodeling in other settings, but their role in venous thrombus resolution remains undefined. To determine the role of T cells in venous thrombus resolution in vivo, stasis induced thrombi were created by vena cava ligation in outbred CD-1 mice. CD4 and CD8 positive T cells, as determined by flow cytometry, were present in thrombi both during thrombus formation and resolution. Depletion of the CD4 and CD8 positive T cells by antibody treatment selectively impaired thrombus resolution compared to animals treated with isotype control antibodies, without an effect on venous thrombus formation. Quantitation of intra-thrombus macrophage numbers, fibrinolytic marker expression, and gelatinolytic activity by zymography revealed that T cell depletion decreased the number of macrophages, reduced the expression of fibrinolytic marker urokinase plasminogen activator (uPA), and decreased the activity of matrix metalloprotinease-9 (MMP-9). These data implicate CD4 and CD8 positive T cells in functionally contributing to venous thrombus resolution, thus representing a potential therapeutic target, but also underscoring potential risks involved in T cell depletion used clinically for solid organ and hematopoietic transplantation procedures.

Myeloid p53 regulates macrophage polarization and venous thrombus resolution by inflammatory vascular remodeling in mice.

Deep venous thrombosis (DVT) remains a common and serious cardiovascular problem with both fatal and long-term consequences. The consequences of DVT include the development of postthrombotic syndrome in 25% to 60% of DVT patients. Despite the clinical importance of venous thrombus resolution, the cellular and molecular mediators involved are poorly understood, and currently there is no molecular therapy to accelerate this process. Several lines of evidence suggest that a complex and interrelated array of molecular signaling processes are involved in the inflammatory vascular remodeling associated with the resolution of DVT. Here, we have identified a role for the tumor suppressor gene p53 in regulating venous thrombus resolution. Using the stasis model of venous thrombosis and resolution in mice, we found that genetic deficiency of p53 or pharmacologic inhibition by pifithrin impairs thrombus resolution and is associated with increased fibrosis and altered expression of matrix metalloproteinase-2. The effect of p53 loss was mediated by cells of the myeloid lineage, resulting in enhanced polarization of the cytokine milieu toward an M1-like phenotype. Furthermore, augmentation of p53 activity using the pharmacological agonist of p53, quinacrine, accelerates venous thrombus resolution in a p53-dependent manner, even after establishment of thrombosis. Together, these studies define mechanisms by which p53 regulates thrombus resolution by increasing inflammatory vascular remodeling of venous thrombi in vivo, and the potential therapeutic application of a p53 agonist as a treatment to accelerate this process in patients with DVT.

The myristoylated alanine-rich C kinase substrate differentially regulates kinase interacting with stathmin in vascular smooth muscle and endothelial cells and potentiates intimal hyperplasia formation.

OBJECTIVE: Restenosis limits the durability of all cardiovascular reconstructions. Vascular smooth muscle cell (VSMC) proliferation drives this process, but an intact, functional endothelium is necessary for vessel patency. Current strategies to prevent restenosis employ antiproliferative agents that affect both VSMCs and endothelial cells (ECs). Knockdown of the myristoylated alanine-rich C kinase substrate (MARCKS) arrests VSMC proliferation and paradoxically potentiates EC proliferation. MARCKS knockdown decreases expression of the kinase interacting with stathmin (KIS), increasing p27kip1 expression, arresting VSMC proliferation. Here, we seek to determine how MARCKS influences KIS protein expression in these two cell types. METHODS: Primary human coronary artery VSMCs and ECs were used for in vitro experiments. MARCKS was depleted by transfection with small interfering RNA. Messenger RNA was quantitated with the real-time reverse transcription polymerase chain reaction. Protein expression was determined by Western blot analysis. Ubiquitination was determined with immunoprecipitation. MARCKS and KIS binding was assessed with co-immunoprecipitation. Intimal hyperplasia was induced in CL57/B6 mice with a femoral artery wire injury. MARCKS was knocked down in vivo by application of 10 µM of small interfering RNA targeting MARCKS suspended in 30% Pluronic F-127 gel. Intimal hyperplasia formation was assessed by measurement of the intimal thickness on cross sections of the injured artery. Re-endothelialization was determined by quantitating the binding of Evans blue dye to the injured artery. RESULTS: MARCKS knockdown did not affect KIS messenger RNA expression in either cell type. In the presence of cycloheximide, MARCKS knockdown in VSMCs decreased KIS protein stability but had no effect in ECs. The effect of MARCKS knockdown on KIS stability was abrogated by the 26s proteasome inhibitor MG-132. MARCKS binds to KIS in VSMCs but not in ECs. MARCKS knockdown significantly increased the level of ubiquitinated KIS in VSMCs but not in ECs. MARCKS knockdown in vivo resulted in decreased KIS expression. Furthermore, MARCKS knockdown in vivo resulted in decreased 5-ethynyl-2'-deoxyuridine integration and significantly reduced intimal thickening. MARCKS knockdown enhanced endothelial barrier function recovery 4 days after injury. CONCLUSIONS: MARCKS differentially regulates the KIS protein stability in VSMCs and ECs. The difference in stability is due to differential ubiquitination of KIS in these two cell types. The differential interaction of MARCKS and KIS provides a possible explanation for the observed difference in ubiquitination. The effect of MARCKS knockdown on KIS expression persists in vivo, potentiates recovery of the endothelium, and abrogates intimal hyperplasia formation.

Considerations beyond Stenosis for Carotid Endarterectomy in Treating Free-Floating Thrombus of the Carotid Artery.

BACKGROUND: Free-floating thrombus (FFT) of the carotid artery is an uncommon condition that can present with neurologic symptoms, often in the setting of ischemic stroke. The literature pertaining to the incidence and optimal treatment of this condition is limited. Herein, we report our contemporary experience with FFT across a range of degrees of carotid stenosis. METHODS: Medical records and imaging studies from a single academic medical center from January 2016 to July 2018 were retrospectively reviewed. Patient demographics, presentation, treatment, and follow-up were abstracted. RESULTS: Six cases of FFT of the carotid artery with and without hemodynamically significant atherosclerotic disease were identified. All cases presented with ischemic stroke; one case had a hemorrhagic conversion. In each case, the FFT was visualized by at least one imaging modality including computed tomography angiography, magnetic resonance angiography, and duplex ultrasound. Three patients had >50% carotid stenosis and three had <50%. All cases were treated with endarterectomy. Four of the six patients received preoperative anticoagulation. There were no postoperative complications. Median follow-up was 252 days, with one case lost to follow-up. Four of the six patients have been without restenosis, recurrence of the thrombus, nor worsening or recurrent stroke on follow-up. The fifth patient developed restenosis but remained clinically stable. CONCLUSIONS: Although current society guidelines do not recommend carotid endarterectomy as first-line treatment for symptomatic patients with <50% stenosis, it may be indicated in the context of FFT.

Tumor suppressor protein p53 negatively regulates ischemia-induced angiogenesis and arteriogenesis.

OBJECTIVE: The tumor suppressor protein p53 regulates angiogenesis and is a key regulatory mediator of cellular apoptosis, proliferation, and growth. p53 expression is induced in response to ischemia; however, its role in regulating ischemia-induced angiogenesis and arteriogenesis remains undefined. The objective of this study was to define the role of p53 in regulating ischemia-induced angiogenesis and arteriogenesis and to identify mechanisms by which this regulation occurs in vivo. METHODS: Surgically induced hindlimb ischemia or mesenteric artery ligation was performed in wild-type (p53+/+) and p53 knockout (p53-/-) mice. Limb perfusion and revascularization were assessed by laser Doppler perfusion imaging, capillary density, and collateral artery development. Mesenteric collateral artery flow and development were determined by arterial flow measurement and by histologic analysis, respectively. An in vitro aortic ring assay was performed on p53+/+ and p53-/- aortic tissue to evaluate endothelial function. The p53 inhibitor and activator pifithrin-α and quinacrine, respectively, were used to modulate p53 activity in vivo after ischemia. RESULTS: Absence of p53 in mice resulted in increased limb perfusion (P < .05), capillary density (P < .05), and collateral artery development (P < .05) after induction of hindlimb ischemia. In the nonischemic mesenteric artery ligation model of arteriogenesis, p53 expression was induced in collateral arteries and increased arterial blood flow in mice lacking p53 (P < .05). Lack of p53 decreased apoptosis in ischemic hindlimb tissue (P < .05) and increased proangiogenic factors hypoxia-inducible factor 1α and vascular endothelial growth factor (VEGF). Endothelial cell outgrowth in vitro increased in the absence of p53 (P < .05). Pharmacologic augmentation of p53 expression after ischemia impaired perfusion and collateral artery formation and decreased VEGF levels (P < .05). Conversely, inhibition of p53 with pifithrin-α augmented limb perfusion (P < .05) and collateral artery formation (P < .05) and increased protein levels of hypoxia-inducible factor 1α and VEGF. Pharmacologic augmentation and inhibition of p53 had no significant effect in mice lacking p53. CONCLUSIONS: p53 negatively regulates ischemia-induced angiogenesis and arteriogenesis. Inhibition of p53 increases ischemia-induced arteriogenesis and limb perfusion and thus represents a potential therapeutic strategy for arterial occlusive disease.

Flow Reduction-Aided Thrombin Injection for Complex Femoral Pseudoaneurysms: Case Series and Review of the Literature.

BACKGROUND: Peripheral pseudoaneurysms are a known complication of vascular access procedures. Complex lesions-those with short, wide necks or other complex arrangements-would conventionally require open repair, but we believe that even these lesions could be managed with an endovascular approach. METHODS: Four patients with complex pseudoaneurysms were offered an open repair or thrombin injection with the use of flow-reducing balloons. RESULTS: In our series of 4 patients with complex pseudoaneurysms, all were safely treated with percutaneous thrombin injection in conjunction with endovascular flow reduction. All patients recovered from their procedures without incident and are free from recurrence at follow-up. CONCLUSIONS: Flow reduction-aided thrombin injection may have particular utility in complex femoral pseudoaneurysms, especially in a patient population that may not tolerate open repair. High-risk lesions may merit special consideration for this technique, and further study is warranted.

Implications of concomitant hypogastric artery embolization with endovascular repair of infrarenal abdominal aortic aneurysms.

OBJECTIVE: Hypogastric artery embolization (HAE) is associated with significant risk of ischemic complications. We assessed the impact of HAE on 30-day outcomes of endovascular aneurysm repair (EVAR) of infrarenal abdominal aortic aneurysms. METHODS: We queried the American College of Surgeons National Surgical Quality Improvement Program database from 2011 to 2014 to identify and to compare clinical features, operative details, and 30-day outcomes of EVAR with those of concomitant HAE with EVAR (HAE + EVAR). Multivariate analysis was performed to determine preoperative and intraoperative factors associated with development of significant complications observed in patients with HAE + EVAR. RESULTS: In a cohort of 5881 patients, 387 (6.6%) underwent HAE + EVAR. Compared with EVAR, a higher incidence of ischemic colitis (2.6% vs 0.9%; P = .002), renal failure requiring dialysis (2.8% vs 1%; P = .001), pneumonia (2.6% vs 1.3%; P = .039), and perioperative blood transfusion (17% vs 13%; P = .024) was noted after HAE + EVAR. Thirty-day thromboembolic events, strokes, myocardial infarction, lower extremity ischemia, reoperation, and readmission rates were not significantly different (P > .05). Mortality at 30 days in HAE + EVAR patients was 4.1% compared with 2.5% with EVAR (P = .044). HAE was independently associated with increased risk of colonic ischemia (adjusted odds ratio, 2.98; 95% confidence interval, 1.44-6.14; P = .003) and renal failure requiring dialysis (adjusted odds ratio, 2.22; 95% confidence interval, 1.09-4.53; P = .029). However, HAE was not an independent predictor of mortality. Average length of hospital stay was 4 ± 8.5 days after HAE + EVAR vs 3.3 ± 5.9 days after EVAR (P = .001). CONCLUSIONS: Concomitant HAE with EVAR is associated with longer and more complicated hospital stays. Ischemic colitis is a rare complication of EVAR. HAE increases the risk of ischemic colitis and renal failure requiring dialysis. This study highlights the importance of hypogastric artery preservation during EVAR.

Management and outcomes of carotid artery extension of aortic dissections.

BACKGROUND: Aortic dissection (AD) is the most common aortic catastrophe. Carotid artery dissection due to extension of AD (CAEAD) is one severe complication of this condition. Despite years of refinement in the techniques for repair of AD, the optimal management strategy for CAEAD remains yet to be described. We hypothesized that CAEAD eventually resolves on antiplatelet therapy with a low but not insignificant risk of cerebrovascular accident (CVA). METHODS: This was a single-institution retrospective review of patients admitted with nontraumatic coincident aortic and carotid dissection between 2001 and 2013. RESULTS: CAEAD was present in 38 patients (24 men [53%]). The median age was 59.5 years (range, 25-85 years). A Stanford type A AD was diagnosed in 36 patients (95%). CVA or transient ischemic attack was identified in 11 patients (29%). Eight were potentially attributable to the carotid lesion. Two of these eight strokes resulted in death. Of the 11 CVAs and transient ischemic attacks, 8 were evident at presentation, 2 were diagnosed postoperatively during hospitalization, and 1 was diagnosed during early follow-up. Only one of these three postadmission strokes was attributable to the carotid lesion. Nonoperative management of aortic and carotid dissections was pursued in 9 patients (24%), 26 (68%) underwent open repair, and 4 (11%) had endovascular management of AD (2 thoracic endovascular aortic repair, 2 endovascular fenestrations), including 1 patient with a staged hybrid procedure (frozen elephant trunk). There were eight inpatient deaths (21%) and nine deaths in the follow-up period. Of the 30 patients who survived to discharge, 24 (80%) were managed with antiplatelet therapy. At a median follow-up of 14.5 months in 22 patients with follow-up computed tomography scans available, a minority of lesions had resolved, and only one CVA was reported. CONCLUSIONS: This study found that CAEAD was associated almost exclusively with type A AD, was typically unilateral, most often on the left, and usually persisted at follow-up. Many CAEAD patients presented with CVA and experienced significant early mortality. Notably, not all CVA events were attributable to the CAEAD. CVAs were not common after admission, and there appeared to be a low risk of new or subsequent stroke during follow-up with routine antiplatelet and antihypertensive therapy.

A Defined Protocol to Resolving Cannulation Failure during Endovenous Ablation Procedures.

During endovenous ablation for the treatment of insufficient veins, failure to cannulate the entirety of the refluxing vein with the treatment catheter prevents technically successful ablation. In this technique report, we describe a defined protocol to overcome cannulation failure of axial veins for endovenous ablation. This protocol utilizes commonly available adjunctive techniques including ultrasound-guided digital compression, the use of a guidewire, the use of a guide catheter, and placement of a second puncture site in a step-wise fashion to overcome varying degrees of tortuosity or obstruction. The sequential application of these techniques as described in this report allows endovenous ablation to be applied to patients with challenging venous anatomy.

Open and Endovascular Management of Inferior Mesenteric Artery Aneurysms: A Report of Two Cases.

Inferior mesenteric artery (IMA) aneurysms are a rare entity, attributing to 1% of Splanchnic aneurysms (Edogawa S, Shibuya T, Kurose K et al. Inferior mesenteric artery aneurysm: case report and literature review. Ann Vasc Dis 2013;6:98-101), often found incidentally on evaluation for other intra-abdominal pathologies. Similar to other visceral arterial aneurysms, there is an estimated 20-50% risk of potentially fatal rupture and repair is generally recommended. We report 2 patients with IMA aneurysms, using them as cases to illustrate feasibility of both open and endovascular management options. Patient 1 is a 69-year-old male with bilateral claudication found to have an asymptomatic 20-mm IMA aneurysm. This patient underwent aortobifemoral bypass with branch polytetrafluoroethylene graft to distal IMA after excision of IMA aneurysm. Patient 2 is a 32-year-old male who underwent an ex vivo renal artery aneurysm repair and was noted on routine follow-up to have an incidental saccular 1.5-cm IMA aneurysm for which he underwent endovascular coil embolization. Both patients had an unremarkable postoperative course with a notable absence of stigmata of bowel ischemia.

Percutaneous Treatment of Multiple Recurrent Thromboembolization from a Descending Thoracic Aortic Intimal Sarcoma.

Aortic intimal sarcomas are rare tumors that may result in distal embolic ischemia. Here, we present a patient who presented with crescendo lower extremity and mesenteric ischemic events from malignant macroembolism. Management with percutaneous pharmacomechanical thromboembolectomy enabled restoration of distal perfusion and minimally invasive collection of tumor sample to confirm the suspected diagnosis of aortic sarcoma. The patient underwent definitive aortectomy and reconstruction and is recovering well.

A new aortic injury score predicts early rupture more accurately than clinical assessment.

OBJECTIVE: The optimal timing for repair of a high-grade blunt thoracic aortic injury (BTAI) is uncertain. Delayed repair is common and associated with improved outcomes, but some lesions may rupture during observation. To determine optimal patient selection for appropriate management, we developed a pilot clinical risk score to evaluate aortic stability and predict rupture. METHODS: Patients presenting in stable condition with Society for Vascular Surgery grade III or IV BTAI diagnosed on computed tomography (CT) were retrospectively reviewed. To determine clinical and radiographic factors associated with aortic rupture, patients progressing to aortic rupture (defined by contrast extravasation on CT or on operative or autopsy findings) were compared with those who had no intervention ≤48 hours of admission. A model targeting 100% sensitivity for rupture was generated and internally validated by bootstrap analysis. Clinical utility was tested by comparison with clinical assessment by surgeons experienced in BTAI management who were provided with CT images and clinical data but were blinded to outcome. RESULTS: The derivation cohort included 18 patients whose aorta ruptured and 31 with stable BTAI. There was no difference in age, gender, injury mechanism, nonchest injury severity, blood pressure, or Glasgow Coma Scale on admission between patient groups. As dichotomous factors, admission lactate >4 mM, posterior mediastinal hematoma >10 mm, and lesion/normal aortic diameter ratio >1.4 on the admission CT were independently associated with aortic rupture. The model had an area under the receiver operator curve of .97, and in the presence of any two factors, was 100% sensitive and 84% specific for predicting aortic rupture. No aortic lesions ruptured in patients with fewer than two factors. In contrast, clinical assessment had lower accuracy (65% vs 90% total accuracy, P < .01). CONCLUSIONS: This novel risk score can be applied on admission using clinically relevant factors that incorporate patient physiology, size of the aortic lesion, and extent of the mediastinal hematoma. The model reliably identifies and distinguishes patients with high-grade BTAI who are at risk for early rupture from those with stable lesions. Although preliminary, because it is more accurate than clinical assessment alone, the score may improve patient selection for emergency or delayed intervention.

Management and outcomes of blunt common and external iliac arterial injuries.

OBJECTIVE: Blunt iliac arterial injuries (BIAI) require complex management but are rare and poorly studied. We investigated the presentation, management, and outcomes of patients with blunt common or external iliac arterial injuries. METHODS: We identified and reviewed 112 patients with BIAI admitted between 2000 and 2011 at a Level I trauma center. Patients with common/external iliac artery injuries (CE group) were primarily analyzed, with patients with injuries of the internal iliac artery or its major branches (IB group) included for comparison of pelvic arterial trauma. RESULTS: Twenty-four patients had CE and 88 had IB injuries. Mean ages (45 ± 19 years) and gender (86% male) were similar between groups. The mean injury severity score was 40 ± 14 (CE, 36 ± 15; IB, 40 ± 14; P = .19), indicating severe trauma. Twenty (83%) of the CE patients presented with signs of leg malperfusion. Admission factors associated with CE injury were crush mechanism of injury (37% vs 17%; P = .03) and pelvic soft tissue trauma (50% vs 15%; P < .01). The CE group had higher early mortality rates, both within 3 hours of admission (50% vs 19%; P = .04) and prior to iliac intervention (42% vs 3%; P < .01). Among those surviving to management, CE patients were more likely to undergo open repair or revascularization (68% vs 3%; P < .01) and had a higher rate of leg amputation (50% vs 6%; P < .01), with 8/12 (67%) culminating in hemipelvectomy. Risk factors for amputation included leg malperfusion, high-grade pelvic fractures, pelvic soft tissue trauma, and increasing leg injury severity. Overall mortality was 40%, and was similar between the injury groups. Among CE patients, need for amputation, pelvic fractures, and wounds were associated with inpatient mortality. CONCLUSIONS: This is the largest series to date of blunt CE injuries and demonstrates distinct clinical features and outcomes for these patients. They have high risk for early death and proximal leg amputation. CE injury is specifically associated with serious open pelvic soft tissue injury, which, along with high-grade pelvic fractures, is a risk factor for amputation and death. On-demand emergent endovascular intervention may play an important role in improving management of these complex injuries.

Time-dependent ultrastructural changes during venous thrombogenesis and thrombus resolution.

BACKGROUND: Deep vein thrombosis is a common vascular event that can result in debilitating morbidity and even death due to pulmonary embolism. Clinically, patients with faster resolution of a venous thrombus have improved prognosis, but the detailed structural information regarding changes that occur in a resolving thrombus over time is lacking. OBJECTIVES: To define the spatial-morphologic characteristics of venous thrombus formation, propagation, and resolution at the submicron level over time. METHODS: Using a murine model of stasis-induced deep vein thrombosis along with scanning electron microscopy and immunohistology, we determine the specific structural, compositional, and morphologic characteristics of venous thrombi formed after 4 days and identify the changes that take place during resolution by day 7. Comparison is made with the structure and composition of venous thrombi formed in mice genetically deficient in plasminogen activator inhibitor type 1. RESULTS: As venous thrombus resolution progresses, fibrin exists in different structural forms, and there are dynamic cellular changes in the compositions of leukocytes, platelet aggregates, and red blood cells. Intrathrombus microvesicles are present that are not evident by histology, and red blood cells in the form of polyhedrocytes are an indicator of clot contraction. Structural evidence of fibrinolysis is observed early during thrombogenesis and is accelerated by plasminogen activator inhibitor type 1 deficiency. CONCLUSION: The results reveal unique, detailed ultrastructural and compositional insights along with documentation of the dynamic changes that occur during accelerated resolution that are not evident by standard pathologic procedures and can be applied to inform diagnosis and effectiveness of thrombolytic treatments to improve patient outcomes.

Risk factors and treatment interventions associated with incomplete thrombus resolution and pulmonary hypertension after pulmonary embolism.

BACKGROUND: Residual pulmonary vascular occlusion (RPVO) affects one half of patients after a pulmonary embolism (PE). The relationship between the risk factors and therapeutic interventions for the development of RPVO and chronic thromboembolic pulmonary hypertension is unknown. METHODS: This retrospective review included PE patients within a 26-month period who had baseline and follow-up imaging studies (ie, computed tomography [CT], ventilation/perfusion scans, transthoracic echocardiography) available. We collected the incidence of RPVO, percentage of pulmonary artery occlusion (%PAO), baseline CT %PAO, most recent CT %PAO, and difference between the baseline and most recent %PAO on CT (Δ%PAO). RESULTS: A total of 354 patients had imaging reports available; 197 with CT and 315 with transthoracic echocardiography. The median follow-up time was 144 days (interquartile range [IQR], 102-186 days). RPVO was present in 38.9% of the 354 patients. The median Δ%PAO was -10.0% (IQR, -32% to -1.2%). Fewer patients with a provoked PE developed RPVO (P ≤ .01), and the initial troponin level was lower in patients who developed RPVO (P = .03). The initial thrombus was larger in the patients who received advanced intervention vs anticoagulation (baseline CT %PAO: median, 61.2%; [IQR, 27.5%-75.0%] vs median, 12.5% [IQR, 2.5%-40.0%]; P ≤ .0001). Catheter-directed thrombolysis (CDT; median Δ%PAO, -47.5%; IQR, -63.7% to -8.7%) and surgical pulmonary embolectomy (SPE; median Δ%PAO, -42.5; IQR, -68.1% to -18.7%) had the largest thrombus reduction compared with anticoagulation (P = .01). Of the 354 patients, 76 developed pulmonary hypertension; however, only 14 received pulmonary hypertension medications and 12 underwent pulmonary thromboendarterectomy. Cancer (odds ratio [OR], 1.7) and planned prolonged anticoagulation (>1 year; OR, 2.20) increased the risk of RPVO. In contrast, the risk was lower for men (OR, 0.61), patients with recent surgery (OR, 0.33), and patients treated with SPE (OR, 0.42). A larger Δ%PAO was found in men (coefficient, -8.94), patients with a lower body mass index (coefficient, -0.66), patients treated with CDT (coefficient, -18.12), and patients treated with SPE (coefficient, -21.69). A lower Δ%PAO was found in African-American patients (coefficient, 7.31). CONCLUSIONS: The use of CDT and SPE showed long-term benefit in thrombus reduction.

Patterns and management of blunt abdominal aortic injury.

BACKGROUND: Blunt abdominal aortic injury (BAAI) is historically associated with significant morbidity and mortality. Our institutional experience was analyzed to define current patterns of injury and to help guide management. METHODS: Adult patients with BAAI between January 2000 and July 2011 were identified from our trauma registry. Medical, radiographic, and autopsy records were reviewed for relevant clinical data. Management and outcomes were compared between patients with minimal aortic injury limited to the intima (MAI) compared to more significant aortic injury (SAI). RESULTS: Nine patients had MAI and 8 had SAI, including 2 dissections, 2 pseudoaneurysms, 2 branch avulsions, 1 thrombosis, and 1 transection. The MAI and SAI groups had similar demographics and patterns of injury, and all patients had significant polytrauma, with a mean injury severity score of 42. More MAI than SAI patients were managed nonoperatively (100% vs. 38%; P=0.01). All observed patients underwent repeat imaging during the index admission, 85% within 72 hours, and no observed lesions led to malperfusion, death, or progression during the index admission. One MAI progressed to a pseudoaneurysm within 8 months. Five SAI patients underwent aortic-related repairs, including 2 endovascular stent grafts, 2 open primary repairs, and 1 axillobifemoral bypass. Overall, 15 (88%) patients underwent procedures for any injury-9 required laparotomy (53%) and 2 underwent thoracotomy. There were 6 (35%) deaths, 2 attributable to aortic injury-1 from hemorrhage and 1 from hyperkalemic cardiac arrest after prolonged ischemia from infrarenal aortic occlusion. Among patients who survived the initial resuscitation, SAI was associated with a significantly higher mortality rate compared to MAI (50% vs. 0%; P=0.03). CONCLUSIONS: Patients with MAI are at low risk of complications and may be considered for observation. Patients with SAI requiring intervention manifest clinically and/or radiographically at presentation. Those not associated with bleeding, malperfusion, or thromboembolism may be observed with interval imaging. For all observed patients, long-term surveillance is required to document complete resolution or stability, because even MAI can progress to a more complex lesion.

Utilizing an office based laboratory (OBL) during the COVID-19 pandemic for vascular surgical patients.

COVID-19 pandemic brought new challenges in healthcare including the need to create tiered class recommendations about which types patients to treat urgently and which surgical cases to defer. This is a report of a single center's Office Based Laboratory (OBL) system to prioritize vascular patients and preserve acute care resources and personnel. In reviewing three months of data, it appears that by continuing to provide the urgent care needed for this chronically ill population, the insurmountable backup of surgical procedures is prevented in the operating room once elective surgeries resumed. The OBL was able to continue providing care at the same pre-pandemic rate to a large intercity population.

Intravascular ultrasound imaging for diagnosis and characterization of the popliteal compression syndrome.

Objective: Functional popliteal artery entrapment syndrome (fPAES) is a rare form of nonatherosclerotic claudication most often seen in young athletic patients. Diagnosis remains challenging, with various imaging modalities showing equivocal or subtle findings that may be missed. We sought to critically examine and quantitate the utility of intravascular ultrasound (IVUS) imaging, a common diagnostic tool for vascular compression syndromes, in diagnosis and characterization of fPAES. Methods: Patients presenting to a single tertiary care center between 2019 and 2022 with symptoms of PAES but without an anatomic etiology or equivocal workup were selected. Angiogram and IVUS with maneuvers were performed on affected extremities at rest, active plantarflexion/dorsiflexion, and plantarflexion/dorsiflexion against resistance. IVUS examination was recorded using a pull-back technique from the tibial vessels to the superficial femoral artery. The degree, length, and anatomic location of compression using the two imaging modalities were compared. Results: Angiogram and IVUS with maneuvers were performed on 17 lower extremities (9 left, 8 right) in 15 patients (88% female; mean age, 21.2 years). Evidence of arterial compression on angiography was noted in 88.2% (n = 15) of limbs (66.7% complete contrast cessation and 20% popliteal artery tapering); 13.3% (n = 2) only demonstrated sluggish flow as possible evidence of compression. Arterial compression was seen on IVUS imaging in 15 of 17 limbs, and all completely compressed around the IVUS catheter. The IVUS-measured mean length of compression was 10.5 cm ± 4.2 (median, 11 cm; range, 4-23 cm). Compression involved only the popliteal vessels in 86.7% (n = 13); one patient had both popliteal and tibioperoneal trunk compression, whereas another had tibioperoneal trunk and peroneal artery compression. Popliteal vein compression was 100%. The contrast cessation point on angiography and the proximal point of compression on IVUS imaging differed in 80% of cases (P < .05). The distal extent of compression was unable to be determined by angiogram findings but was clearly delineated by IVUS imaging in all cases. Conclusions: IVUS imaging is a more sensitive diagnostic and descriptive imaging modality compared with angiogram in patients with possible fPAES. IVUS and angiogram findings are greatly discordant; moreover, IVUS imaging can provide detailed information such as the precise extent and anatomic location of the arterial compression, which may be useful in aiding surgical planning. IVUS imaging should be considered the gold standard for diagnosing and characterizing fPAES before intervention planning.