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Vascular Specialist International Sep 2023Aortic endograft infection (AEI) is a rare but life-threatening complication of endovascular aneurysm repair (EVAR). The clinical features of AEI range from generalized... (Review)
Review
Aortic endograft infection (AEI) is a rare but life-threatening complication of endovascular aneurysm repair (EVAR). The clinical features of AEI range from generalized weakness and mild fever to fatal aortic rupture or sepsis. The diagnosis of AEI usually depends on clinical manifestations, laboratory tests, and imaging studies. Management of Aortic Graft Infection Collaboration (MAGIC) criteria are often used to diagnose AEI. Surgical removal of the infected endograft, restoration of aortic blood flow, and antimicrobial therapy are the main components of AEI treatment. After removing an infected endograft, in situ aortic reconstruction is often performed instead of an extra-anatomic bypass. Various biological and prosthetic aortic grafts have been used in aortic reconstruction to avoid reinfection, rupture, or occlusion. Each type of graft has its own merits and disadvantages. In patients with an unacceptably high surgical risk and no evidence of an aortic fistula, conservative treatment can be an alternative. Treatment results are determined by bacterial virulence, patient status, including the presence of an aortic fistula, and hospital factors. Considering the severity of this condition, the best strategy is prevention. When encountering a patient with AEI, current practice emphasizes a multidisciplinary team approach to achieve an optimal outcome.
PubMed: 37732343
DOI: 10.5758/vsi.230071 -
British Journal of Pharmacology Mar 2022Abdominal aortic aneurysm (AAA) rupture is estimated to cause 200,000 deaths each year. Currently, the only treatment for AAA is surgical repair; however, this is only... (Review)
Review
Abdominal aortic aneurysm (AAA) rupture is estimated to cause 200,000 deaths each year. Currently, the only treatment for AAA is surgical repair; however, this is only indicated for large asymptomatic, symptomatic or ruptured aneurysms, is not always durable, and is associated with a risk of serious perioperative complications. As a result, patients with small asymptomatic aneurysms or who are otherwise unfit for surgery are treated conservatively, but up to 70% of small aneurysms continue to grow, increasing the risk of rupture. There is thus an urgent need to develop drug therapies effective at slowing AAA growth. This review describes the commonly used mouse models for AAA. Recent research in these models highlights key roles for pathways involved in inflammation and cell turnover in AAA pathogenesis. There is also evidence for long non-coding RNAs and thrombosis in aneurysm pathology. Further well-designed research in clinically relevant models is expected to be translated into effective AAA drugs. LINKED ARTICLES: This article is part of a themed issue on Preclinical Models for Cardiovascular disease research (BJP 75th Anniversary). To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v179.5/issuetoc.
Topics: Animals; Aortic Aneurysm, Abdominal; Aortic Rupture; Disease Models, Animal; Humans; Mice
PubMed: 32914434
DOI: 10.1111/bph.15260 -
Clinical Practice and Cases in... Nov 2023Acute aortic syndrome (AAS) includes the disease processes of aortic dissection, penetrating atherosclerotic ulcer, and intramural hematoma. This case demonstrates an...
INTRODUCTION
Acute aortic syndrome (AAS) includes the disease processes of aortic dissection, penetrating atherosclerotic ulcer, and intramural hematoma. This case demonstrates an atypical presentation of the disease and offers approaches to potentially prevent missed diagnoses.
CASE REPORT
An 87-year-old female with hypertension and Alzheimer's dementia presented to the emergency department with stable vital signs and a chief complaint of throat pain. Initial work-up was significant for ischemia on electrocardiogram and elevated troponin. Computed tomography of the soft tissue neck revealed evidence of a ruptured aorta.
CONCLUSION
Aortic rupture is a fatal complication of AAS. In an elderly patient with a history of hypertension, ischemic changes on electrocardiogram, and nonspecific pain, AAS should be on the emergency physician's differential even in the setting of a benign or limited history and exam.
PubMed: 38353194
DOI: 10.5811/cpcem.1349 -
BMC Cardiovascular Disorders Oct 2022The incidence and mortality of aortic dissection (AD) are increasing. In pathological studies, macrophages, T lymphocytes and dendritic cells were found in the tunica...
BACKGROUND
The incidence and mortality of aortic dissection (AD) are increasing. In pathological studies, macrophages, T lymphocytes and dendritic cells were found in the tunica media of the aorta. Acetaldehyde dehydrogenase 2 (ALDH) gene polymorphisms are associated with a high incidence of hypertension in Asian populations. However, there is no clear evidence of the relationship between ALDH and aortic dissection in Asians. The aim of this study was to investigate the incidence of aortic dissection in different ALDH genotypes and explore changes in the vasculature.
MATERIALS AND METHODS
Three-week-old male mice were administered freshly prepared β-aminopropionitrile solution dissolved in drinking water (1 g/kg/d) for 28 days to induce TAD. An animal ultrasound imaging system was used to observe the formation of arterial dissection and changes in cardiac function. Subsequently, mice were euthanized by cervical dislocation. The aortas were fixed for HE staining and EVG staining to observe aortic elastic fiber tears and pseudoluma formation under a microscope.
RESULTS
Knockout of ALDH mitigated β-aminopropionitrile-induced TAD formation in animal studies. Ultrasound results showed that ALDH knockout reduced the degree of ascending aortic widening and the incidence of aortic dissection rupture. Pathological sections of multiple aortic segments showed that the protective effect of ALDH knockout was observed in not only the ascending aorta but also the aortic arch and descending aorta. The expression levels of genes related to NK CD56bright cells, Th17 cells, T cells and T helper cells were decreased in ALDH knockout mice treated with β-aminopropionitrile for 28 days.
CONCLUSION
ALDH knockout protects against aortic dissection by altering the inflammatory response and immune response and protecting elastic fibers.
Topics: Aldehyde Dehydrogenase, Mitochondrial; Aminopropionitrile; Aortic Dissection; Animals; Aortic Aneurysm, Thoracic; Aortic Rupture; Disease Models, Animal; Drinking Water; Male; Mice; Mice, Inbred C57BL; Mice, Knockout
PubMed: 36229771
DOI: 10.1186/s12872-022-02874-5 -
The Journal of Thoracic and... Mar 2022Aortic aneurysm and dissection are major life-threatening complications of Marfan syndrome. Avoiding factors that promote aortic damage is critical in managing the care...
OBJECTIVE
Aortic aneurysm and dissection are major life-threatening complications of Marfan syndrome. Avoiding factors that promote aortic damage is critical in managing the care of these patients. Findings from clinical and animal studies raise concerns regarding fluoroquinolone use in patients at risk for aortic aneurysm and dissection. Therefore, we examined the effects of ciprofloxacin on aortic aneurysm and dissection development in Marfan mice.
METHODS
Eight-week-old Marfan mice (Fbn1) were given ciprofloxacin (100 mg/kg/d; n = 51) or vehicle (n = 59) for 4 weeks. Mice were monitored for 16 weeks. Aortic diameters were measured by using ultrasonography, and aortic structure was examined by using histopathologic and immunostaining analyses.
RESULTS
Vehicle-treated Fbn1 mice showed progressive aortic enlargement, with aortic rupture occurring in 5% of these mice. Compared with vehicle-treated Fbn1 mice, ciprofloxacin-treated Fbn1 mice showed accelerated aortic enlargement (P = .01) and increased incidences of aortic dissection (25% vs 47%, P = .03) and rupture (5% vs 25%, P = .005). Furthermore, ciprofloxacin-treated Fbn1 mice had higher levels of elastic fiber fragmentation, matrix metalloproteinase expression, and apoptosis than did vehicle-treated Fbn1 mice.
CONCLUSIONS
Ciprofloxacin accelerates aortic root enlargement and increases the incidence of aortic dissection and rupture in Marfan mice, partially by suppressing lysyl oxidase expression and further compromising the inherited defect in aortic elastic fibers. Our findings substantiate that ciprofloxacin should be avoided in patients with Marfan syndrome.
Topics: Aortic Dissection; Animals; Anti-Bacterial Agents; Aorta; Aortic Aneurysm; Aortic Rupture; Apoptosis; Ciprofloxacin; Dilatation, Pathologic; Disease Progression; Elastic Tissue; Extracellular Matrix Proteins; Female; Fibrillin-1; Genetic Predisposition to Disease; Male; Matrix Metalloproteinases; Mice, Knockout; Phenotype; Protein-Lysine 6-Oxidase; Vascular Remodeling; Mice
PubMed: 34586071
DOI: 10.1016/j.jtcvs.2020.09.069 -
Hypertension (Dallas, Tex. : 1979) Apr 2022
Topics: Aldosterone; Aortic Dissection; Aortic Aneurysm; Aortic Rupture; Humans
PubMed: 35263159
DOI: 10.1161/HYPERTENSIONAHA.122.18888 -
European Radiology Dec 2019Acute aortic syndromes comprise a group of potentially fatal conditions that result from weakening of the aortic vessel wall. Pre-emptive surgical intervention is... (Review)
Review
Acute aortic syndromes comprise a group of potentially fatal conditions that result from weakening of the aortic vessel wall. Pre-emptive surgical intervention is currently reserved for patients with severe aortic dilatation, although abundant evidence describes the occurrence of dissection and rupture in aortas with diameters below surgical thresholds. Modern imaging techniques (such as hybrid PET-CT and 4D flow MRI) afford the non-invasive assessment of anatomic, hemodynamic, and molecular features of the aorta, and may provide for a more accurate selection of patients who will benefit from preventative surgical intervention. In the current review, we summarize evidence and considerations regarding predictive aortic imaging and highlight evolving imaging modalities that have shown promise to improve risk assessment for the occurrence of dissection and rupture. KEY POINTS: • Guidelines for the preventative management of aortic disease depend on maximal vessel diameters, while these have shown to be poor predictors for the occurrence of catastrophic acute aortic events. • Evolving imaging modalities (such as 4D flow MRI and hybrid PET-CT) afford a more comprehensive insight into anatomic, hemodynamic, and molecular features of the aorta and have shown promise to detect vessel wall instability at an early stage.
Topics: Aortic Dissection; Aorta; Aortic Aneurysm; Aortic Rupture; Humans; Imaging, Three-Dimensional; Magnetic Resonance Imaging; Positron Emission Tomography Computed Tomography; Risk Assessment
PubMed: 31278573
DOI: 10.1007/s00330-019-06320-7 -
Journal of the American Heart... Apr 2022Background The biological mechanism of action for osteoprotegerin, a soluble decoy receptor for the receptor activator of nuclear factor-kappa B ligand in the vascular...
Background The biological mechanism of action for osteoprotegerin, a soluble decoy receptor for the receptor activator of nuclear factor-kappa B ligand in the vascular structure, has not been elucidated. The study aim was to determine if osteoprotegerin affects aortic structural integrity in angiotensin II (Ang II)-induced hypertension. Methods and Results Mortality was higher (<0.0001 by log-rank test) in 8-week-old male homozygotes of osteoprotegerin gene-knockout mice given subcutaneous administration of Ang II for 28 days, with an incidence of 21% fatal aortic rupture and 23% aortic dissection, than in age-matched wild-type mice. Ang II-infused aorta of wild-type mice showed that osteoprotegerin immunoreactivity was present with proteoglycan. The absence of osteoprotegerin was associated with decreased medial and adventitial thickness and increased numbers of elastin breaks as well as with increased periostin expression and soluble receptor activator of nuclear factor-kappa B ligand concentrations. PEGylated human recombinant osteoprotegerin administration decreased all-cause mortality (<0.001 by log-rank test), the incidence of fatal aortic rupture (=0.08), and aortic dissection (<0.001) with decreasing numbers of elastin breaks, periostin expressions, and soluble receptor activator of nuclear factor-kappa B ligand concentrations in Ang II-infused osteoprotegerin gene-knockout mice. Conclusions These data suggest that osteoprotegerin protects against aortic rupture and dissection in Ang II-induced hypertension by inhibiting receptor activator of nuclear factor-kappa B ligand activity and periostin expression.
Topics: Aortic Dissection; Angiotensin II; Animals; Aortic Rupture; Disease Models, Animal; Elastin; Hypertension; Male; Mice; Mice, Inbred C57BL; Mice, Knockout; Osteoprotegerin; RANK Ligand
PubMed: 35411794
DOI: 10.1161/JAHA.122.025336 -
International Journal of Molecular... Sep 2020Abdominal aortic aneurysm (AAA) rupture is an important cause of death in older adults. In clinical practice, the most established predictor of AAA rupture is maximum... (Review)
Review
Abdominal aortic aneurysm (AAA) rupture is an important cause of death in older adults. In clinical practice, the most established predictor of AAA rupture is maximum AAA diameter. Aortic diameter is commonly used to assess AAA severity in mouse models studies. AAA rupture occurs when the stress (force per unit area) on the aneurysm wall exceeds wall strength. Previous research suggests that aortic wall structure and strength, biomechanical forces on the aorta and cellular and proteolytic composition of the AAA wall influence the risk of AAA rupture. Mouse models offer an opportunity to study the association of these factors with AAA rupture in a way not currently possible in patients. Such studies could provide data to support the use of novel surrogate markers of AAA rupture in patients. In this review, the currently available mouse models of AAA and their relevance to the study of AAA rupture are discussed. The review highlights the limitations of mouse models and suggests novel approaches that could be incorporated in future experimental AAA studies to generate clinically relevant results.
Topics: Animals; Aorta, Abdominal; Aortic Aneurysm, Abdominal; Aortic Rupture; Biomechanical Phenomena; Computer Simulation; Disease Models, Animal; Humans; Mice; Models, Cardiovascular; Risk Factors; Stress, Mechanical
PubMed: 33008131
DOI: 10.3390/ijms21197250 -
Biomedicines Dec 2023Aortic aneurysms are responsible for significant morbidity and mortality. Despite their clinical significance, there remain critical knowledge gaps in the pathogenesis... (Review)
Review
Aortic aneurysms are responsible for significant morbidity and mortality. Despite their clinical significance, there remain critical knowledge gaps in the pathogenesis of aneurysm disease and the mechanisms involved in aortic rupture. Recent studies have drawn attention to the role of reactive oxygen species (ROS) and their down-stream effectors in chronic cardiovascular diseases and specifically in the pathogenesis of aortic aneurysm formation. This review will discuss current mechanisms of ROS in mediating aortic aneurysms, the failure of endogenous antioxidant systems in chronic vascular diseases, and their relation to the development of aortic aneurysms.
PubMed: 38275364
DOI: 10.3390/biomedicines12010003