AI Article Synopsis

  • Type A acute aortic dissection (TAAAD) has high morbidity and mortality rates, influenced by factors like the site of intimal rupture and surgical repair extent.
  • Postoperative bleeding is a common complication associated with worse outcomes and is particularly higher in patients with previous cardiac surgeries.
  • Despite advancements in diagnosis and treatment, complications from AAD, including organ ischemia and inflammatory responses, continue to impact recovery negatively, particularly through mechanisms involving endothelial barrier damage and oxidative stress.

Article Abstract

Type A acute aortic dissection (TAAAD) still carries high rates of morbidity and mortality. Outcomes of patients presenting with TAAAD depend on several variables such as the site of intimal rupture, organ malperfusion and extension of surgical repair. Bleeding after surgery for TAAAD is one of the most common complications and it's also associated with worse postoperative outcomes. Previous cardiac operations have been associated with a higher rate of postoperative bleeding and also with worse postoperative outcomes in patients undergoing second elective cardiac operations. According to the Stanford system, the most commonly used system of anatomic classification, type A AAD (TA-AAD: DeBakey type I and II) involves the ascending aorta, irrespective of the site of the intimal tear while type B AAD (TB-AAD) does not involve the ascending aorta and propagates downwards distally from the isthmus. Despite recent substantial diagnostic and therapeutic progress, AAD morbidity and mortality remain still high. Blood malperfusion triggers the propagation of aortic dissection, resulting in the ischemia of involved organs. Meanwhile, an excessive inflammatory response occurs, contributing to the development of oxygen impairment. A recent study suggested that inflammation and coagulation are involved in AAD combined ALI. Endothelial and epithelial barriers are destroyed by increased alveolar-capillary barrier permeability, which is responsible for ALI. Furthermore, inflammatory and oxidative stress-related cellular and metabolic regulatory mechanisms might participate in the AAD course worsened by ALI.

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http://dx.doi.org/10.1016/j.cpcardiol.2023.102242DOI Listing

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