Aortic Rupture

Aortic aneurysm is a chronic aortic disease affected by many factors. Although it is generally asymptomatic, it poses a significant threat to human life due to a high risk of rupture. Because of its strong concealment, it is difficult to diagnose the disease in the early stage. At present, there are no effective drugs for the treatment of aneurysms. Surgical intervention and endovascular treatment are the only therapies. Although current studies have discovered that inflammatory responses as well as the production and activation of various proteases promote aortic aneurysm, the specific mechanisms remain unclear. Researchers are further exploring the pathogenesis of aneurysms to find new targets for diagnosis and treatment. To better understand aortic aneurysm, this review elaborates on the discovery history of aortic aneurysm, main classification and clinical manifestations, related molecular mechanisms, clinical cohort studies and animal models, with the ultimate goal of providing insights into the treatment of this devastating disease. The underlying problem with aneurysm disease is weakening of the aortic wall, leading to progressive dilation. If not treated in time, the aortic aneurysm eventually ruptures. An aortic aneurysm is a local enlargement of an artery caused by a weakening of the aortic wall. The disease is usually asymptomatic but leads to high mortality due to the risk of artery rupture.

Aortic aneurysm is a chronic disease characterized by localized expansion of the aorta, including the ascending aorta, arch, descending aorta, and abdominal aorta. Although aortic aneurysms are generally asymptomatic, they can threaten human health by sudden death due to aortic rupture. Aortic aneurysms are estimated to lead to 150,000 ~ 200,000 deaths per year worldwide. Currently, there are no effective drugs to prevent the growth or rupture of aortic aneurysms; surgical repair or endovascular repair is the only option for treating this condition. The pathogenic mechanisms and therapeutic targets for aortic aneurysms have been examined over the past decade; however, there are unknown pathogenic mechanisms involved in cellular heterogeneity and plasticity, the complexity of the transforming growth factor-β signaling pathway, inflammation, cell death, intramural neovascularization, and intercellular communication. This review summarizes the latest research findings and current pathogenic mechanisms of aortic aneurysms, which may enhance our understanding of aortic aneurysms.

Inherited thoracic aortopathies denote a group of congenital conditions that predispose to disease of the thoracic aorta. Aortic wall weakness and abnormal aortic hemodynamic profiles predispose these patients to dilatation of the thoracic aorta, which is generally silent but can precipitate aortic dissection or rupture with devastating and often fatal consequences. Current strategies to assess the future risk of aortic dissection or rupture are based primarily on monitoring aortic diameter. However, diameter alone is a poor predictor of risk, with many patients experiencing dissection or rupture below current intervention thresholds. Developing tools that improve the risk assessment of those with aortopathy is internationally regarded as a research priority. A robust understanding of the molecular pathways that lead to aortic wall weakness is required to identify biomarkers and therapeutic targets that could improve patient management. Here, we summarize the current understanding of the genetically determined mechanisms underlying inherited aortopathies and critically appraise the available blood biomarkers, imaging techniques, and therapeutic targets that have shown promise for improving the management of patients with these important and potentially fatal conditions.

BackgroundRuptured abdominal aortic aneurysm (RAAA) remains a medical catastrophe. Although early outcomes improved, contemporary data integrating early and long-term survival, and postdischarge care needs across sex- and age groups is limited.MethodsThis nationwide cohort included Dutch RAAA repairs between 2014 and 2023. Dutch Surgical Aneurysm Audit data were linked to Statistics Netherlands registries. Outcomes included 90-day mortality, long-term survival, and postdischarge care.ResultsOf the 3642 patients, 15.2% were women, who were older (76.3 vs. 74.0 y) and more often required open repair (61.4% vs. 54.0%). Ninety-day mortality increased with age and was higher in women (39.1% vs. 29.1%), but female sex was not independently associated with early mortality after adjustment.Among 90-day survivors, absolute long-term survival was similar, but relative survival was lower in women (5-year relative survival 68.0% vs. 78.3%). Women were less often discharged home (42.4% vs. 56.7%) and more frequently required early homecare (47.7% vs. 34.7%). Reinterventions were more common after EVAR than open repair and occurred less frequently in women.ConclusionIn this nationwide linked audit-registry analysis, outcomes after RAAA repair improved substantially, despite lower estimated in-hospital turndown rates than in earlier eras. The higher early mortality in women WAS reflected by differences in age, presentation severity, and repair type - possibly reflecting less favorable aneurysm anatomy. Female sex also associated with an increased long-term excess mortality and greater postdischarge dependency. These findings indicate that optimization of care for women with a RAAA is not confined to perioperative mortality, but extends across the entire care pathway.