In situ ascending aortic thrombus in a patient with metastatic lung adenocarcinoma and no aortic atherosclerosis or cisplatin exposure: a case report.

BACKGROUND: An ascending aortic thrombus is exceedingly rare. Two instances have been reported in the setting of lung cancer, but only after cisplatin use, which is associated with hypercoagulability. We present the first case of a patient with lung cancer who developed an ascending aortic thrombus without structural risk factors or chemotherapy use. CASE: A 60-year-old white female with significant smoking history presented with several weeks of malaise. A chest computed tomography scan revealed a 2.2-cm right upper lobe mass. As an outpatient, right hilar lymph node immunohistochemistry (IHC) samples via endobronchial ultrasound confirmed thyroid transcription factor-1 adenocarcinoma. After the procedure, the patient endorsed dyspnea and was advised to go to the emergency department. A chest computed tomography angiography identified a new 2.4 × 1.1 × 1.1 cm thrombus within the proximal aortic arch. No pulmonary emboli or intrapulmonary shunts were identified. A hypercoagulable workup was negative. Transthoracic echocardiogram was without left ventricular thrombus, akinesis or hypokinesis, left atrial dilation, or intracardiac shunts. A lower extremity ultrasound was negative for deep vein thrombosis. Given the procedural risk, thrombectomy was deferred. The patient was transitioned to enoxaparin, and a repeat computed tomography for resolution is in process. CONCLUSION: To our knowledge, this is the only case detailing an in situ ascending aortic thrombus in the setting of lung cancer, without structural risk factors, chemotherapy use, or other hypercoagulable comorbidities. Optimal management for an aortic thrombus and malignant disease is less clear. Clinicians should be vigilant for unusual arterial thromboses in patients with high metastatic burden.

Heparanase promotes the onset and progression of atherosclerosis in apolipoprotein E gene knockout mice.

BACKGROUND AND AIMS: Atherosclerosis is the primary underlying cause of myocardial infarction and stroke, which are the major causes of death globally. Heparanase (Hpse) is a pro-inflammatory extracellular matrix degrading enzyme that has been implicated in atherogenesis. However, to date the precise roles of Hpse in atherosclerosis and its mechanisms of action are not well defined. This study aims to provide new insights into the contribution of Hpse in different stages of atherosclerosis in vivo. METHODS: We generated Hpse gene-deficient mice on the atherosclerosis-prone apolipoprotein E gene knockout (ApoE-/-) background to investigate the impact of Hpse gene deficiency on the initiation and progression of atherosclerosis after 6 and 14 weeks high-fat diet feeding, respectively. Atherosclerotic lesion development, blood serum profiles, lesion composition and aortic immune cell populations were evaluated. RESULTS: Hpse-deficient mice exhibited significantly reduced atherosclerotic lesion burden in the aortic sinus and aorta at both time-points, independent of changes in plasma cholesterol levels. A significant reduction in the necrotic core size and an increase in smooth muscle cell content were also observed in advanced atherosclerotic plaques of Hpse-deficient mice. Additionally, Hpse deficiency reduced circulating and aortic levels of VCAM-1 at the initiation and progression stages of disease and circulating MCP-1 levels in the initiation but not progression stage. Moreover, the aortic levels of total leukocytes and dendritic cells in Hpse-deficient ApoE-/- mice were significantly decreased compared to control ApoE-/-mice at both disease stages. CONCLUSIONS: This study identifies Hpse as a key pro-inflammatory enzyme driving the initiation and progression of atherosclerosis and highlighting the potential of Hpse inhibitors as novel anti-inflammatory treatments for cardiovascular disease.

l-thyroxine attenuates extracellular Hsp90α-induced vascular endothelial calcification in diabetes mellitus, as revealed by parallel metabolic profiles.

BACKGROUND AND AIMS: Diabetic atherosclerotic vascular disease is characterized by extensive vascular calcification. However, an elevated blood glucose level alone does not explain this pathogenesis. We investigated the metabolic markers underlying diabetic atherosclerosis and whether extracellular Hsp90α (eHsp90α) triggers vascular endothelial calcification in this particular metabolic environment. METHODS: A parallel human/animal model metabolomics approach was used. We analyzed 40 serum samples collected from 24 patients with atherosclerosis and from the STZ-induced ApoE-/- mouse model. A multivariate statistical analysis of the data was performed, and mouse aortic tissue was collected for the assessment of plaque formation. In vitro, the effects of eHsp90α on endothelial cell calcification were assessed by serum analysis, Western blotting and immunoelectron microscopy. RESULTS: Diabetic ApoE-/- mice showed more severe plaque lesions and calcification damage. Stearamide, oleamide, l-thyroxine, l-homocitrulline and l-citrulline are biomarkers of diabetic ASVD; l-thyroxine was downregulated in both groups, and the thyroid sensitivity index was correlated with serum Hsp90α concentration. In vitro studies showed that eHsp90α increased Runx2 expression in endothelial cells through the LRP1 receptor. l-thyroxine reduced the increase in Runx2 levels caused by eHsp90α and affected the distribution and expression of LRP1 through hydrogen bonding with glutamine at position 1054 in the extracellular segment of LRP1. CONCLUSIONS: This study provides a mechanistic link between characteristic serum metabolites and diabetic atherosclerosis and thus offers new insight into the role of extracellular Hsp90α in promoting vascular calcification.

Anterolateral thoracotomy with partial sternotomy: a feasible approach for treating the complex pathology of the aortic arch.

OBJECTIVES: Our goal was to review our surgical experiences in patients with complex pathologies of the aortic arch who have undergone anterolateral thoracotomy with a partial sternotomy (ALPS). METHODS: From October 2019 to November 2023, a total of 23 patients underwent one-stage repairs of complex pathologies of the aortic arch through the ALPS approach. The mean age was 61.9 ± 16.7 years old. The aortic pathologies were as follows: aorta-related infection in 11 (aorto-oesophageal fistula: 4, graft infection: 6, native aortic infection: 1); aortic dissection in 9 including shaggy aorta in 2, non-dissecting aneurysm in 1, and coarctation of the aorta (CoA) in 2. RESULTS: Eighteen patients underwent aortic replacement from either the sinotubular junction or the ascending aorta to the descending aorta; 1 patient underwent it from the aortic root to the descending aorta (redo Bentall procedure and extensive aortic arch replacement); 3 patients underwent it from the aortic arch between the left carotid artery and left subclavian artery to the descending aorta; and 1 patient underwent a descending aortic replacement. Ten patients underwent omentopexy, latissimus dorsi muscle flap installation or both procedures. The hospital mortality rate was 13.0% (3/23). The overall survival and freedom from aortic events were 73.3%±10.2% and 74.1%±10.2%, respectively, at the 3-year follow-up. There was an absence of aorta-related deaths, and no recurrent infections were identified. CONCLUSIONS: The short-term outcomes using the ALPS approach for the treatment of complex pathologies of the aortic arch were acceptable. Further studies will be required to determine the long-term results.

Initial Triage and Management of Patients with Acute Aortic Syndromes.

The acute aortic syndromes (AAS) are life-threatening vascular compromises within the aortic wall. These include aortic dissection (AD), intramural hematoma (IMH), penetrating aortic ulcer (PAU), and blunt traumatic thoracic aortic injury (BTTAI). While patients classically present with chest pain, the presentation may be highly variable. Timely diagnosis is critical to initiate definitive treatment and maximize chances of survival. In high-risk patients, treatment should begin immediately, even while diagnostic evaluation proceeds. The mainstay of medical therapy is acute reduction of heart rate and blood pressure. Surgical intervention is often required but is informed by patient anatomy and extent of vascular compromise.

Late Outcomes of Surgery Versus Medical Therapy in Patients With Type A Aortic Intramural Hematoma: Meta-Analysis of Reconstructed Time-to-Event Data.

The effect of an initial surgical approach (in comparison with initial medical therapy) in acute type A intramural hematoma remains insufficiently explored. We designed a pooled analysis of Kaplan-Meier-derived individual patient data from studies with follow-up for overall survival (all-cause death). Restricted mean survival time was calculated to evaluate lifetime gain or loss. The Risk of Bias in Non-Randomized Studies of Interventions tool (ROBINS-I) was used to assess risk of bias. The Grading of Recommendations Assessment, Development and Evaluation (GRADE) was applied to assess certainty of evidence. Eight studies met our eligibility criteria, including a total of 654 patients (311 patients treated with surgery and 343 patients treated with medical therapy alone). All the studies were non-randomized and observational. The median follow-up was 4.6 years (interquartile range 1.0 to 7.7). Patients who underwent surgery had a significantly lower risk of mortality compared with patients receiving medical therapy alone (hazard ratio 0.51, 95% confidence interval 0.35 to 0.74, p <0.001). The restricted mean survival time was overall 1.1 years greater with surgery compared with medical therapy, and this difference was statistically significant (p <0.001), which means that surgery is associated with lifetime gain. The overall risk of bias (ROBINS-I) was considered moderate-to-serious and the certainty of evidence (GRADE) was deemed to be low. In conclusion, in the overall follow-up, surgery as the initial approach was associated with better late survival and lifetime gain in comparison with medical therapy alone in the setting of acute type A aortic intramural hematoma; however, high-quality randomized trials are warranted to establish the efficacy of the surgical strategy.

Interleukin-1 receptor accessory protein blockade limits the development of atherosclerosis and reduces plaque inflammation.

AIMS: The interleukin-1 receptor accessory protein (IL1RAP) is a co-receptor required for signalling through the IL-1, IL-33, and IL-36 receptors. Using a novel anti-IL1RAP-blocking antibody, we investigated the role of IL1RAP in atherosclerosis. METHODS AND RESULTS: Single-cell RNA sequencing data from human atherosclerotic plaques revealed the expression of IL1RAP and several IL1RAP-related cytokines and receptors, including IL1B and IL33. Histological analysis showed the presence of IL1RAP in both the plaque and adventitia, and flow cytometry of murine atherosclerotic aortas revealed IL1RAP expression on plaque leucocytes, including neutrophils and macrophages. High-cholesterol diet fed apolipoprotein E-deficient (Apoe-/-) mice were treated with a novel non-depleting IL1RAP-blocking antibody or isotype control for the last 6 weeks of diet. IL1RAP blockade in mice resulted in a 20% reduction in subvalvular plaque size and limited the accumulation of neutrophils and monocytes/macrophages in plaques and of T cells in adventitia, compared with control mice. Indicative of reduced plaque inflammation, the expression of several genes related to leucocyte recruitment, including Cxcl1 and Cxcl2, was reduced in brachiocephalic arteries of anti-IL1RAP-treated mice, and the expression of these chemokines in human plaques was mainly restricted to CD68+ myeloid cells. Furthermore, in vitro studies demonstrated that IL-1, IL-33, and IL-36 induced CXCL1 release from both macrophages and fibroblasts, which could be mitigated by IL1RAP blockade. CONCLUSION: Limiting IL1RAP-dependent cytokine signalling pathways in atherosclerotic mice reduces plaque burden and plaque inflammation, potentially by limiting plaque chemokine production.

Calcifications in the descending thoracic aorta predict postoperative anastomotic leakages after esophagectomy for cancer.

BACKGROUND: Anastomotic leak is one of the most feared complications of esophagectomy. Previous studies have suggested a potential link between aortic calcifications detected on routine preoperative CT scans and increased risk of anastomotic leak after esophagectomy. This study aims to investigate whether clinicians' assessment of aortic calcifications can predict the occurrence of anastomotic leaks in patients undergoing esophagectomy for cancer. METHODS: A long-term follow-up was conducted on consecutive patients with esophageal cancer who underwent elective open esophagectomy at a Finnish tertiary hospital. Aortic calcifications were evaluated based on CT scans and categorized on a 0-3 scale reflecting the number of calcifications in the affected segment of the aorta. Reviewers assessing the calcifications were blinded to clinical details and postoperative outcomes. RESULTS: The study included 97 patients (median age: 64 years and range: 43-78; 20% female), with a median follow-up time of 1307 (2-1540) days. Among them, 22 patients (23%) had postoperative anastomotic leak. We observed a significant association between calcifications in the descending aorta and a higher risk of anastomotic leak (p = 0.007), as well as an earlier occurrence of leak postoperatively (p = 0.013). However, there was no association between aortic calcifications and increased mortality. CONCLUSIONS: Presence of calcifications in the descending aorta is independently associated with an increased risk of anastomotic leaks following esophagectomy for cancer. Identifying patients at higher risk for this complication could facilitate appropriate pre- and postoperative interventions, as well as enable earlier diagnosis and treatment to mitigate the severity of the complication.

[Cost-revenue aspects of endovascular treatment of distal aortic arch pathologies with respect to the introduction of a new thoracic side-branch prosthesis]. / Kosten-Erlös-Aspekte der endovaskulären Versorgung distaler Aortenbogenpathologien im Hinblick auf die Einführung einer neuen thorakalen Seitenarmprothese.

BACKGROUND: The standard vascular surgical procedure (SV) for the treatment of distal aortic arch pathologies involves a hybrid approach using a left carotid-subclavian bypass and thoracic endovascular aortic repair. Considering the introduction of a thoracic side branch prosthesis (TBE), the aim of this study was to analyze the cost-revenue aspects of both procedures. MATERIAL AND METHODS: A retrospective analysis was conducted on cases treated by SV from 2017 to 2022. To draw conclusions regarding the use of TBE, the main diagnoses and procedures of SV were recoded based on current classifications (ICD/OPS 2023) for revenue calculations and regrouped according to aG-DRG 2023. An OPS modification and regrouping were performed for modeling TBE revenues. RESULTS: A total of 13 cases were identified (mean age 62.5 ± 13.8 years; 10 males). After regrouping, the following DRGs were obtained: F42Z in N = 5, F51A in N = 4, F08B in N = 2, and F07A and F36B each in N = 1. The total revenue after regrouping was €â€¯666,514.13, including an additional payment (ZE) of €â€¯132,729.14. With the modeled application of TBE, a total revenue of €â€¯659,212.19 was achieved. Compared to SV, this represents a revenue decrease of €â€¯16,886.71 (changed DRG), but with an increase in ZE revenue by €â€¯65,559.78 (different ZE). The use of TBE resulted in a saving of 74 occupancy days, including 13.5 days in intensive care. CONCLUSION: A cost coverage seems probable with a change in the procedure, despite the yet to be determined pricing of TBE. This is highly dependent on the coding quality and the future development of ZE, given the annually changing DRG relative weights. Precise and transparent performance and cost documentation are essential for determining the pricing.

Multifaceted roles of Meg3 in cellular senescence and atherosclerosis.

BACKGROUND AND AIMS: Long noncoding RNAs are involved in the pathogenesis of atherosclerosis. As long noncoding RNAs maternally expressed gene 3 (Meg3) prevents cellular senescence of hepatic vascular endothelium and obesity-induced insulin resistance, we decided to examine its role in cellular senescence and atherosclerosis. METHODS AND RESULTS: By analyzing our data and human and mouse data from the Gene Expression Omnibus database, we found that Meg3 expression was reduced in humans and mice with cardiovascular disease, indicating its potential role in atherosclerosis. In Ldlr-/- mice fed a Western diet for 12 weeks, Meg3 silencing by chemically modified antisense oligonucleotides attenuated the formation of atherosclerotic lesions by 34.9% and 20.1% in male and female mice, respectively, revealed by en-face Oil Red O staining, which did not correlate with changes in plasma lipid profiles. Real-time quantitative PCR analysis of cellular senescence markers p21 and p16 revealed that Meg3 deficiency aggravates hepatic cellular senescence but not cellular senescence at aortic roots. Human Meg3 transgenic mice were generated to examine the role of Meg3 gain-of-function in the development of atherosclerosis induced by PCSK9 overexpression. Meg3 overexpression promotes atherosclerotic lesion formation by 29.2% in Meg3 knock-in mice independent of its effects on lipid profiles. Meg3 overexpression inhibits hepatic cellular senescence, while it promotes aortic cellular senescence likely by impairing mitochondrial function and delaying cell cycle progression. CONCLUSIONS: Our data demonstrate that Meg3 promotes the formation of atherosclerotic lesions independent of its effects on plasma lipid profiles. In addition, Meg3 regulates cellular senescence in a tissue-specific manner during atherosclerosis. Thus, we demonstrated that Meg3 has multifaceted roles in cellular senescence and atherosclerosis.

Predictive factors of thoracic aortic calcification in patients candidate for cardiac surgery.

BACKGROUND: The presence of the severe thoracic aortic calcification (TAC) in cardiac surgery patients is associated with adverse post-operative outcome. However, the relationship between cardiovascular risk factors and aortic plaque burden remains unknown. The objective of this study was to determine the predictive factors of TAC in patients candidate for cardiac surgery. METHODS: Patients who underwent thoracic CT scan prior to cardiac surgery between August 2020 to April 2021 were included. Of 556 patients, 209 (36.7%) had a thoracic aortic calcium score (TACS) ≥ 400 mm [3] and were compare with the remaining patients. Predictors of severe TAC were assessed through stepwise multivariable logistic regression analysis. RESULTS: The patients with TACS ≥ 400 had a higher mean age (67.3 ± 7.1 vs. 55.7 ± 10.6; p < 0.001) with a higher frequency of diabetes mellitus (40.7% vs. 30.8%; p = 0.018), dyslipidemia (49.8% vs. 38.6%; p = 0.010), hypertension (60.8% vs. 44.7%; p < 0.001), opium addiction (18.2% vs. 11.2%; p = 0.023), peripheral vascular disease (PVD) (7.7% vs. 2.3%; p = 0.005) as compared with TACS < 400. The multiple determinants of TAC were PVD (OR = 2.86) followed by opium addiction, diabetes and age. CONCLUSIONS: Thoracic CT scan prior to cardiac surgery for patients with older age, diabetes, opium addiction and PVD is recommended. Our study could serve as a foundation for future research endeavors aimed at establishing a risk score for TAC.

Identification of key genes for atherosclerosis in different arterial beds.

Atherosclerosis (AS) is the pathologic basis of various cardiovascular and cerebrovascular events, with a high degree of heterogeneity among different arterial beds. However, mechanistic differences between arterial beds remain unexplored. The aim of this study was to explore key genes and potential mechanistic differences between AS in different arterial beds through bioinformatics analysis. Carotid atherosclerosis (CAS), femoral atherosclerosis (FAS), infrapopliteal atherosclerosis (IPAS), abdominal aortic atherosclerosis (AAS), and AS-specific differentially expressed genes (DEGs) were screened from the GSE100927 and GSE57691 datasets. Immune infiltration analysis was used to identify AS immune cell infiltration differences. Unsupervised cluster analysis of AS samples from different regions based on macrophage polarization gene expression profiles. Weighted gene co-expression network analysis (WGCNA) was performed to identify the most relevant module genes with AS. Hub genes were then screened by LASSO regression, SVM-REF, and single-gene differential analysis, and a nomogram was constructed to predict the risk of AS development. The results showed that differential expression analysis identified 5, 4, 121, and 62 CAS, FAS, IPAS, AAS-specific DEGs, and 42 AS-common DEGs, respectively. Immune infiltration analysis demonstrated that the degree of macrophage and mast cell enrichment differed significantly in different regions of AS. The CAS, FAS, IPAS, and AAS could be distinguished into two different biologically functional and stable molecular clusters based on macrophage polarization gene expression profiles, especially for cardiomyopathy and glycolipid metabolic processes. Hub genes for 6 AS (ADAP2, CSF3R, FABP5, ITGAX, MYOC, and SPP1), 4 IPAS (CLECL1, DIO2, F2RL2, and GUCY1A2), and 3 AAS (RPL21, RPL26, and RPL10A) were obtained based on module gene, gender stratification, machine learning algorithms, and single-gene difference analysis, respectively, and these genes were effective in differentiating between different regions of AS. This study demonstrates that there are similarities and heterogeneities in the pathogenesis of AS between different arterial beds.

3-D transesophageal echocardiography aids in assessment of embolic stroke due to aortic atherosclerotic plaque: A case series.

Atherosclerosis is the most common cause of heart disease and stroke. Plaque thickness ≥4 mm in the ascending aorta or aortic arch is strongly correlated with cerebral embolic events and ischemic stroke. However, despite imaging workup, the cause of embolic stroke remains unidentified in many patients. Transesophageal echocardiography (TEE) is the preferred echocardiographic method for the evaluation of cardiac source of emboli. 2D TEE imaging evaluates aortic root and aortic arch in a single plane or two planes with biplane imaging. However, 2D TEE often fails to detect mobile or complex components in the ascending aorta and aortic arch plaques. The routine availability of 3D TEE in current ultrasound systems may significantly improve the assessment of aortic plaques as a potential embolic source. In this case series, we present four consecutive patients with stroke who underwent TEE by a single cardiologist for possible cardioembolic source. Some of these patients may have been labelled as "cryptogenic stroke" or "embolic stroke of undetermined source" (ESUS) due to the presence of insignificant or nonmobile ascending aortic or aortic arch plaques on 2D TEE imaging. In our four consecutive patients with ESUS who underwent TEE by a single operator, 3D TEE showed complex aortic arch plaques with ulceration with mobile components and established these plaques as the likely source of embolic stroke.

Computed Tomography Angiography for Aortic Diseases.

Aortic pathologies encompass a heterogeneous group of disorders, including acute aortic syndrome, traumatic aortic injury , aneurysm, aortitis, and atherosclerosis. The clinical manifestations of these disorders can be varied and non-specific, ranging from acute presentations in the emergency department to chronic incidental findings in an outpatient setting. Given the non-specific nature of their clinical presentations, the reliance on non-invasive imaging for screening, definitive diagnosis, therapeutic strategy planning, and post-intervention surveillance has become paramount. Commonly used imaging modalities include ultrasound, computed tomography (CT), and MR imaging. Among these modalities, computed tomography angiography (CTA) has emerged as a first-line imaging modality owing to its excellent anatomic detail, widespread availability, established imaging protocols, evidence-proven indications, and rapid acquisition time.

Deficiency of lncRNA MERRICAL abrogates macrophage chemotaxis and diabetes-associated atherosclerosis.

Diabetes-associated atherosclerosis involves excessive immune cell recruitment and plaque formation. However, the mechanisms remain poorly understood. Transcriptomic analysis of the aortic intima in Ldlr-/- mice on a high-fat, high-sucrose-containing (HFSC) diet identifies a macrophage-enriched nuclear long noncoding RNA (lncRNA), MERRICAL (macrophage-enriched lncRNA regulates inflammation, chemotaxis, and atherosclerosis). MERRICAL expression increases by 249% in intimal lesions during progression. lncRNA-mRNA pair genomic mapping reveals that MERRICAL positively correlates with the chemokines Ccl3 and Ccl4. MERRICAL-deficient macrophages exhibit lower Ccl3 and Ccl4 expression, chemotaxis, and inflammatory responses. Mechanistically, MERRICAL guides the WDR5-MLL1 complex to activate CCL3 and CCL4 transcription via H3K4me3 modification. MERRICAL deficiency in HFSC diet-fed Ldlr-/- mice reduces lesion formation by 74% in the aortic sinus and 86% in the descending aorta by inhibiting leukocyte recruitment into the aortic wall and pro-inflammatory responses. These findings unveil a regulatory mechanism whereby a macrophage-enriched lncRNA potently inhibits chemotactic responses, alleviating lesion progression in diabetes.

The Impact of Pregnancy in Patients with Thoracic Aortic Disease: Epidemiology, Risk Assessment, and Management Considerations.

Thoracic aortic disease (TAD) poses substantial risks during pregnancy, particularly for women with genetic conditions such as Marfan syndrome, Loeys-Dietz syndrome, and vascular Ehlers-Danlos syndrome. This review examines the epidemiology, risk assessment, and management of TAD in pregnancy. Preconception counseling is vital considering the hereditary nature of TAD and potential pregnancy-related complications. Genetic testing and imaging surveillance aid in risk assessment. Medical management, including beta-blockade and strict blood pressure control, is essential throughout pregnancy. Surgical interventions may be necessary in certain cases. A multidisciplinary approach involving cardiologists, obstetricians, cardiac surgeons, anesthesiologists, and other specialists with expertise in cardio-obstetrics is essential for optimal outcomes. Patient education and shared decision-making play vital roles in navigating the complexities of TAD in pregnancy and improving maternal and neonatal outcomes.

Evaluation of intramural hematoma: a novel use of 18F-fluorodeoxyglucose positron emission tomography/magnetic resonance imaging.

BACKGROUND: Aortic intramural hematoma (IMH) is one of the typical entities of acute aortic syndrome and probably accounts for 5-25% of all cases. The ulcer-like projections (ULP), which are described as a focal, blood-filled pouch protruding into the hematoma of the aortic wall, are regarded as one of the high-risk imaging features of IMH and may cause initial medical treatment failure and death. CASE PRESENTATION: We present a case report of an acute type B IMH patient with impaired renal function and newly developed ULP in the acute phase. The 18F-fluorodeoxyglucose positron emission tomography/magnetic resonance imaging (18F-FDG PET/MR) was performed to evaluate the condition of aortic hematoma. The 18F-FDG focal uptake along the aortic wall of the hematoma was normal compared to the background (SUVmax 2.17; SUVSVC 1.6; TBR 1.35). We considered the IMH stable in such cases and opted for medical treatment and watchful observation. Six months after discharge, the patient's recovery was satisfactory, and aortic remodeling was ideal. CONCLUSIONS: The 18F-FDG PET/MR is a novel tool to evaluate the risk of IMH patients and thus provides information for therapy selection.

Acute aortic occlusion: A narrative review for emergency clinicians.

INTRODUCTION: Acute aortic occlusion (AAO) is a rare but serious condition associated with significant morbidity and mortality. OBJECTIVE: This review provides an emergency medicine focused evaluation of AAO, including presentation, assessment, and emergency department (ED) management based on current evidence. DISCUSSION: AAO refers to obstruction of blood flow through the aorta due to either thrombosis or embolism. This condition primarily affects older adults ages 60-70 with cardiovascular comorbidities and most commonly presents with signs and symptoms of acute limb ischemia, though the gastrointestinal tract, kidneys, and spinal cord may be affected. The first line imaging modality includes computed tomography angiography of the chest, abdomen, and pelvis. ED resuscitative management consists of avoiding extremes of blood pressure or heart rate, maintaining normal oxygen saturation and euvolemic status, anticoagulation with heparin, and pain control. Emergent consultation with the vascular surgery specialist is recommended to establish a plan for restoration of perfusion to ischemic tissues via endovascular or open techniques. High rates of baseline comorbidities present in the affected population as well as ischemic and reperfusion injuries place AAO patients at high risk for complications in an immediate and delayed fashion after surgical management. CONCLUSIONS: An understanding of AAO can assist emergency clinicians in diagnosing and managing this rare but devastating disease.