Department of Anesthesiology and Critical Care, University of Pennsylvania School of Medicine, Philadelphia, PA, USA.
J Cardiothorac Vasc Anesth. 2010 Feb;24(1):198-207. doi: 10.1053/j.jvca.2009.09.018. Epub 2009 Dec 14.
Significant innovations have defined the approach to the proximal thoracic aorta. Aortic proteolysis predisposes to dissection and aneurysm. Losartan may prevent aortic root dilation in Marfan syndrome. The Loeys-Dietz syndrome mandates early aortic intervention. Because genetic aortopathies have a multicenter registry, further aortic molecular advances are likely. Acute intramural hematoma (IMH) may be due to aortic dissection with unrecognized microintimal tears. Type-A IMH is often a surgical emergency, whereas type-B IMH often requires medical management. Because preoperative ischemia predicts mortality in type-A dissection, it is logical to classify this disease by ischemic presentation. Because advanced age worsens the outcome in type-A dissection, transcatheter interventions should be urgently developed for this high-risk subgroup. Aortic arch repairs shorter than 45 minutes in duration are safely performed under deep hypothermic circulatory arrest with/without perfusion adjuncts. Bilateral antegrade cerebral perfusion (ACP) offers the best neuroprotection for complex repairs longer than 45 minutes. Axillary artery cannulation improves outcomes in proximal thoracic aortic procedures. Contralateral hemispheric ischemia is possible with unilateral ACP because cross-cerebral perfusion may be inadequate. Arch repair with ACP and moderate HCA is safe and effective and represents a research opportunity for pharmacologic ischemic preconditioning. Antegrade thoracic aortic stenting for DeBakey 1 dissection thromboses the distal false lumen to improve long-term aortic outcomes. Endovascular arch repair is feasible and may soon be done off-pump. These described innovations have collectively ushered in a paradigm shift in diseases affecting the ascending aorta and aortic arch.
在近端胸主动脉的处理方面已经出现了显著的创新。主动脉蛋白水解作用使夹层和动脉瘤易于发生。氯沙坦可能预防马凡综合征的主动脉根部扩张。Loeys-Dietz 综合征需要早期进行主动脉干预。由于遗传性主动脉疾病有一个多中心登记处,因此可能会有进一步的主动脉分子进展。急性壁内血肿(IMH)可能是由于未识别的微小内膜撕裂导致的主动脉夹层。A型 IMH 通常是手术急症,而 B 型 IMH 通常需要药物治疗。由于术前缺血预测 A 型夹层的死亡率,因此根据缺血表现对这种疾病进行分类是合理的。由于高龄使 A 型夹层的预后恶化,因此应紧急为这一高危亚组开发经导管介入治疗。在深低温循环停搏下进行持续时间短于 45 分钟的主动脉弓修复是安全的,可使用或不使用灌注辅助设备。双侧顺行性脑灌注(ACP)为超过 45 分钟的复杂修复提供最佳的神经保护。腋动脉插管可改善近端胸主动脉手术的结果。由于交叉脑灌注可能不足,单侧 ACP 可能导致对侧半球缺血。在 ACP 和中度 HCA 下进行弓部修复是安全有效的,并且代表了进行药物缺血预处理的研究机会。对于 Debakey 1 型夹层血栓形成的胸主动脉顺行支架置入术可改善主动脉长期预后。血管内弓部修复是可行的,并且可能很快就能在无泵情况下进行。这些描述的创新共同带来了影响升主动脉和主动脉弓疾病的范式转变。