Hemodynamics of aortic dissection

Aortic dissection is the most frequent nontraumatic catastrophe that affects the aorta, with an annual incidence exceeding that of spontaneous rupture of aortic aneurysms [1]. Aortic dissection occurs with a frequency of 10-20 cases per million population per year. Approximately 30% (85 of 272 [2], 106 of 325 [3]) of patients with aortic dissection have one or more ischemic complications of the peripheral vasculature, including stroke, paraplegia, loss of peripheral pulses, and compromised renal or mesenteric perfusion. The surgical mortality rates for patients with acute aortic dissection complicated by compromise of a peripheral arterial branch exceed 50% [3]; visceral and renal ischemia are important independent predictors of death as a result of surgery [2]. In the past, the direct propagation of a dissection flap into an aortic branch with the resultant compromise or obstruction of the true lumen was considered to be the basic mechanism for ischemic complications in the peripheral vasculature. This understanding was based on observations of cross-clamped or decompressed aortas without flow and on findings at necropsy. Recently, collapse or obliteration of the true lumen was proposed as another important mechanism for compromise of the aortic branch in aortic dissection [4, 5]. This is based on antemortem cross-sectional imaging studies, including those performed with intravascu- lar ultrasonography, that facilitate an appreciation of the effects of flow on the anatomic relationships between the flap, aortic lumina, and branch vessels [4, 5]. In this setting, the plane of the dissection flap spares the branch vessel. Instead, the flap is positioned in a curtainlike fashion across the origin of the vessel, which causes dynamic obstruction of the branch artery [5]. According to the report by Williams et al. [6], dynamic obstruction due to true-lumen collapse was the cause of the infradiaphragmatic organ or limb ischemia in 20 of 24 patients. Among the 20 patients, 14 had ischemia in multiple organs that involved the mesenteric, renal, and lower-limb circulations. Recently, percutaneous endo-vascular treatment with balloon fenestration and stent placement was introduced to relieve true-lumen collapse and showed promising results [1, 5, 6]. However, there have been few clinical and experimental studies conducted to investigate the causes of true-lumen collapse in aortic dissection and the possible treatment methods to relieve true-lumen collapse or to determine the most effective methods. Patients with chronic dissection often develop late complications mainly related to the patency of the false lumen [7]. In these cases, there is progressive dilatation of the false lumen that can lead to eventual rupture. An acute aortic diameter of greater than 4 cm in type B dissections has been found to be an indicator of possible future rupture [8, 9]. While some studies suggest medically treating dissections with maximum diameters less than 5 cm [10], others support surgery or placement of stent-grafts when the false lumen is greater than 4 cm [8], 5 cm [11], or 6 cm [12] in order to avoid certain rupture in the future. Obviously, there is considerable uncertainty about the critical diameter of the false lumen and how to treat false lumen aneurysms. While formation and development of dissections are not well understood, it is generally accepted that hemodynamics plays a major role in the initiation, acute propagation, and chronic development of dissections. In all three of these stages, hemodynamic effects couple with mechanical and biological processes in the arterial walls. It may be some time before the initiation and propagation mechanics of dissection will be understood as they involve hemodynamic forces interacting with the aortic wall in both its healthy and its diseased state. There are many studies of the hemodynamic effects in aneurysmal growth. In most cases, aortic dilatation evolves slowly over several years (1 mm per year [10]) and can be treated medically. Relatively less effort is being spent on understanding the problem of branch vessel ischemia and, in particular, the special case of true-lumen collapse. Yet, this problem is of critical importance in both acute and chronic dissection and is highly related to hemodynamics.