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International Immunopharmacology Sep 2023Aortic dissection, characterized by severe intramural hematoma formation and acute endometrial rupture, is caused by excessive bleeding within the aortic wall or a... (Review)
Review
Aortic dissection, characterized by severe intramural hematoma formation and acute endometrial rupture, is caused by excessive bleeding within the aortic wall or a severe tear within the intimal layer of the aorta, which subsequently promotes the separation or dissection in the layers of the aortic wall. Epidemiological surveys showed that aortic dissection was most observed among those patients from 55 to 80 years of age, with a prevalence of approximately 40 cases per 100,000 individuals per year, posing serious risks to future health and leading to high mortality. Other risk factors of aortic dissection progression contained dyslipidemia, hypertension, and genetic disorders, such as Marfan syndrome. Currently, emerging evidence indicates the pathological progression of aortic dissection is significantly complicated, which is correlated with the aberrant infiltration of pro-inflammatory cells into the aortic wall, subsequently facilitating the apoptosis of vascular smooth muscle cells (VSMCs) and inducing the aberrant expression of pro-inflammatory cytokines, including tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interferon (IF). Other pro-inflammatory-related cytokines, including the colony-stimulating factor (CSF), chemotactic factor, and growth factor (GF), played an essential function in facilitating aortic dissection. Multiple studies focused on the important relationship between pro-inflammatory cytokines and aortic dissection, which could deepen the understanding of aortic dissection and further guide the therapeutic strategies in clinical practice. The present review elucidated pro-inflammatory cytokines' functions in modulating the risk of aortic dissection are summarized. Moreover, the emerging evidence that aimed to elucidate the potential mechanisms wherebyvarious pro-inflammatory cytokines affected the pathological development of aortic dissection was also listed.
Topics: Humans; Cytokines; Aortic Dissection; Interferons; Aorta; Tumor Necrosis Factor-alpha
PubMed: 37480750
DOI: 10.1016/j.intimp.2023.110618 -
Vascular Dec 2023The indication, timing, and choice of the treatment modality for penetrating aortic ulcers (PAUs) and intramural hematoma (IMH) are frequently challenging. This article... (Review)
Review
OBJECTIVES
The indication, timing, and choice of the treatment modality for penetrating aortic ulcers (PAUs) and intramural hematoma (IMH) are frequently challenging. This article reviews these pathologies and their relation to aortic dissection and proposes a diagnostic and treatment algorithm.
METHODS
A review of literature on diagnosis and treatment of PAU and IMH was conducted. The PubMed database was searched using the terms "penetrating aortic ulcer" and "aortic intramural hematoma". Articles were reviewed and the studies involving diagnosis and management of PAU and IMH were included. We subsequently proposed a management algorithm for PAU and IMH based on available evidence.
RESULTS
PAU and IMH are distinct entities from aortic dissection, although they carry a significant risk of progression into dissection, aneurysm, and rupture. PAU and IMH originating in zone 0 of the aorta generally require surgical treatment. When the origin is beyond zone 0, a trial of medical therapy is recommended. Progression of disease on imaging studies, persistent uncontrolled pain, and certain high-risk features warrant surgery. High-risk features signaling risk of disease progression include PAU with IMH, PAU depth more than 10 mm, PAU diameter more than 20 mm, IMH thickness more than 10 mm, and maximum initial aortic diameter more than 40 mm.
CONCLUSIONS
High-quality evidence regarding the treatment of PAU and IMH is lacking. These entities can have a malignant course when they are present with associated symptoms and/or when they have associated high-risk features on imaging. An aggressive surgical approach is necessary in that group of patients.
Topics: Humans; Aortic Intramural Hematoma; Penetrating Atherosclerotic Ulcer; Aorta; Aortic Dissection; Hematoma
PubMed: 35578772
DOI: 10.1177/17085381221102785 -
Annals of Vascular Surgery Aug 2023Intramural hematoma (IMH) is one of the acute aortic syndromes along with acute aortic dissection and penetrating aortic ulcer. The three conditions can occur alone or... (Review)
Review
Intramural hematoma (IMH) is one of the acute aortic syndromes along with acute aortic dissection and penetrating aortic ulcer. The three conditions can occur alone or in combination with overlapping presentation. Medical, open surgical, and endovascular treatment is tailored depending on clinical presentation, timing, and location within the aorta. Among patients who present with acute IMH affecting the ascending aorta (Type A), urgent open surgical repair is considered the primary line of treatment in patients who are suitable candidates and unstable. The management of IMH in the descending aorta and aortic arch (Type B) is similar to that applied to treat acute dissections in the same segment. Medical treatment with sequential imaging is recommended in patients with uncomplicated course, and endovascular repair is indicated in patients with rupture, persistent pain, end-organ ischemia, or rapid aortic enlargement. This review discusses the ideal timing for treatment of IMH.
Topics: Humans; Aortic Intramural Hematoma; Treatment Outcome; Aortic Diseases; Aortic Dissection; Hematoma; Aorta, Thoracic
PubMed: 36309166
DOI: 10.1016/j.avsg.2022.09.041 -
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 -
Arteriosclerosis, Thrombosis, and... Sep 2023Transmural failure of the aorta is responsible for substantial morbidity and mortality; it occurs when mechanical stress exceeds strength. The aortic root and ascending...
BACKGROUND
Transmural failure of the aorta is responsible for substantial morbidity and mortality; it occurs when mechanical stress exceeds strength. The aortic root and ascending aorta are susceptible to dissection and rupture in Marfan syndrome, a connective tissue disorder characterized by a progressive reduction in elastic fiber integrity. Whereas competent elastic fibers endow the aorta with compliance and resilience, cross-linked collagen fibers confer stiffness and strength. We hypothesized that postnatal reductions in matrix cross-linking increase aortopathy when turnover rates are high.
METHODS
We combined ex vivo biaxial mechanical testing with multimodality histological examinations to quantify expected age- and sex-dependent structural vulnerability of the ascending aorta in Marfan versus wild-type mice without and with 4-week exposures to β-aminopropionitrile, an inhibitor of lysyl oxidase-mediated cross-linking of newly synthesized elastic and collagen fibers.
RESULTS
We found a strong β-aminopropionitrile-associated sexual dimorphism in aortic dilatation in Marfan mice and aortic rupture in wild-type mice, with dilatation correlating with compromised elastic fiber integrity and rupture correlating with compromised collagen fibril organization. A lower incidence of rupture of β-aminopropionitrile-exposed Marfan aortas associated with increased lysyl oxidase, suggesting a compensatory remodeling of collagen that slows disease progression in the otherwise compromised aorta.
CONCLUSIONS
Collagen fiber structure and function in the Marfan aorta are augmented, in part, by increased lysyl oxidase in female and especially male mice, which improves structural integrity, particularly via fibrils in the adventitia. Preserving or promoting collagen cross-linking may represent a therapeutic target for an otherwise vulnerable aorta.
Topics: Animals; Female; Male; Mice; Aminopropionitrile; Collagen; Dilatation; Disease Models, Animal; Extracellular Matrix; Fibrillin-1; Marfan Syndrome; Mice, Inbred C57BL; Protein-Lysine 6-Oxidase
PubMed: 37470181
DOI: 10.1161/ATVBAHA.123.319122 -
Medical Science Monitor : International... Feb 2024Aortic root aneurysms are one of the most common aortic root diseases, involving the aortic valve, aortic sinus, bilateral coronary arteries, and part of the ascending... (Review)
Review
Aortic root aneurysms are one of the most common aortic root diseases, involving the aortic valve, aortic sinus, bilateral coronary arteries, and part of the ascending aorta. It is a life-threatening aortic disease with a high mortality rate of approximately 90%, due to aortic aneurysm rupture. Aortic valve insufficiency is one of the most common complications of aortic root aneurysms that can lead to acute left heart failure. The etiology of aortic root aneurysms is not yet completely clear and is mainly related to genetic diseases, such as Marfan syndrome and atherosclerosis. It can also occur secondary to aortic valve stenosis or a bivalve deformity. Surgery is the primary treatment for aortic root aneurysms, and aortic root replacement is a classic surgical method. However, the incidences of perioperative complications and mortality are relatively high, particularly in high-risk patients. In recent years, the anatomical structure of the aortic root has been gradually refined, and an in-depth understanding of root aneurysms has led to individualized treatment methods. Conservative drug therapy (ß-receptor blockers, angiotensin-converting enzyme inhibitors, or angiotensin receptor blockers), Bentall and modified Bentall surgeries (Button technology, Cabrol surgery, and modified Cabrol surgery), valve-sparing aortic root replacement (David and Yacoub), personalized external aortic root support, and endovascular intervention therapy have significantly improved the perioperative and long-term survival rates of patients with aortic root aneurysms. However, different treatment methods have their own advantages and disadvantages. This review aimed to summarize the current research progress and treatment of aortic root aneurysms.
Topics: Humans; Aortic Root Aneurysm; Aorta; Aortic Aneurysm, Thoracic; Marfan Syndrome; Aortic Valve Insufficiency; Aortic Valve; Aortic Diseases; Treatment Outcome
PubMed: 38332569
DOI: 10.12659/MSM.943216 -
International Journal of Molecular... Sep 2023Marfan syndrome causes a hereditary form of thoracic aortic aneurysms with worse outcomes in male compared to female patients. In this study, we examine the effects of...
Marfan syndrome causes a hereditary form of thoracic aortic aneurysms with worse outcomes in male compared to female patients. In this study, we examine the effects of 17 β-estradiol on aortic dilation and rupture in a Marfan mouse model. Marfan male mice were administered 17 β-estradiol, and the growth in the aortic root, along with the risk of aortic rupture, was measured. Transcriptomic profiling was used to identify enriched pathways from 17 β-estradiol treatments. Aortic smooth muscle cells were then treated with cytokines to validate functional mechanisms. We show that 17 β-estradiol decreased the size and rate of aortic root dilation and improved survival from rupture. The Marfan transcriptome was enriched in inflammatory genes, and the addition of 17 β-estradiol modulated a set of genes that function through TNFα mediated NF-κB signaling. In addition, 17 β-estradiol suppressed the induction of these TNFα induced genes in aortic smooth muscle cells in vitro in an NF-κB dependent manner, and 17 β-estradiol decreased the formation of adventitial inflammatory foci in aortic roots in vivo. In conclusion, 17 β-estradiol protects against the dilation and rupture of aortic roots in Marfan male mice through the inhibition of TNFα-NF-κB signaling.
Topics: Female; Male; Animals; Mice; Estradiol; Tumor Necrosis Factor-alpha; Aorta, Thoracic; NF-kappa B; Dilatation; Marfan Syndrome
PubMed: 37686377
DOI: 10.3390/ijms241713571