Descending Thoracic Aortic Dissections
Section snippets
Pathophysiology
The principle pathologic mechanism of aortic dissection is a tear in the aortic intima, usually transverse but not completely circumferential, which results in separation between the intimal and medial layers of the aortic wall. Although this usually occurs in pathologic settings (connective tissue disease, atherosclerotic ulcer, and so forth) it can occur in histologically normal aortas also. The most common underlying risk factors for distal dissection are hypertension in conjunction with
Classification
In 1965 DeBakey and colleagues [22] proposed an anatomic classification that is based on the origin and the extent of the dissection (Table 1). Dailey and associates proposed a method based on the inherent different outcomes and operative issues that combined ascending aortic dissections, regardless of origin, as Stanford type A (DeBakey types I and II) and those that originate in and are limited to the descending thoracic aorta (with or without abdominal aortic involvement, DeBakey types IIIa
Presentation
The classic presenting symptom of aortic dissection is abrupt onset of chest pain [6], [25]. With distal dissections the pain is located in the back and characterized in half of cases as tearing but in two thirds additionally as sharp and in approximately one fifth as migratory [6]. In 43% of cases the pain primarily involved or included the abdominal area, raising suspicion of mesenteric ischemia [6]. Unfortunately, if the nature and quality of the pain is not specifically sought after, the
Natural history/medical management
The mortality associated with acute uncomplicated distal aortic dissection managed medically is as low as 10.7%. This figure increases to 31% (or higher) if complications arise that require surgical intervention, particularly during the acute phase [6], [24].
Estrera and colleagues [27] followed 159 consecutive patients, admitted between January 2001 and April 2006, who had acute type B dissection, all initially managed medically. Median time to obtain a systolic blood pressure less than 140 mm
Indications for intervention
There are four indications for acute intervention: rupture, aortic expansion (>5.0 cm), critical vessel malperfusion, and intractable pain. Many authors argue that an aortic diameter in the involved segment of greater than 40 or 45 mm is a reasonable indication for intervention, at least with stent grafts, because of the risk for later aneurysmal development, progressive dissection, or death [8], [36], [41], [51]. Intractable hypertension has been also used as an indication, although as
Operative repair of type B dissection
In contrast to the primacy of open surgical therapy for dissection involving the ascending aorta, the role of open surgery in type B aortic dissection has for years been less well-defined. Enthusiasm for surgical approaches to descending dissection has had peaks and valleys, and with a few notable exceptions, most centers have adopted a protocol of intensive anti-impulse therapy for acute type B dissection [62], [63], [64]. Surgical treatment has for the most part been reserved for complicated
Endovascular management
The recognized difficulties in operative management of acute dissections have led to an increased interest in endovascular approaches, including stent grafting. The enthusiasm was stimulated by the Stanford group's initial report in 1999 [115]. It has been further invigorated by encouraging data in the atherosclerotic aneurysm population, particularly with reduced incidence of spinal cord injury, although how well this translates to the dissection population is still open to question [116].
A
The endovascular procedure
Although probably more comfortable to perform under general anesthesia, especially if very precise imaging is required, endovascular stent grafting for type B dissection has been performed under spinal, epidural, or even local anesthesia [41].
Vascular access can be a major issue. Occasionally a completely percutaneous approach can be used, but this requires confidence in the integrity of the femoral artery, and our bias has been to use this method less frequently than in the setting of
Retrograde dissection
Retrograde dissection, converting a type B case into an acute type A, has been described with virtually all devices, although initially there was a sense that bare metal proximal extension had a higher risk for this [55], [120], [136], [137], [138], [139]. The reported incidence, in larger series of dissection cases, is roughly 0.5% to 3%, but has been reported in as many as 10% [36], [41], [125], [127], [140], [141]. In addition, because most dissections require extension into the arch to
Related conditions
Intramural hematoma (IMH) and penetrating aortic (or atheromatous) ulcer (PAU) complete, with dissection, the triad of acute aortic syndromes [151], [152], [153]. There are some distinct differences between IMH and PAU, however, notably that (1) PAU tends to occur more often in older patients who have extensive calcification, and (2) whereas PAU can be associated with dissection, either often exists alone [151], [154]. Although PAU and IMH probably share cellular processes (such as apoptosis
Combined procedures
There has been increasing interest in performing hybrid operations for the management of atherosclerotic aneurysms, including arch or visceral debranching accompanied by sequential or simultaneous endovascular stent grafting of the diseased aorta, which can be done in some cases without cardiopulmonary bypass [44], [181]. These approaches are being extended to dissection also. In acute type A dissection, which extends into the descending aorta, because of the concern of persistent false lumen
Future development
As is the case with atherosclerotic aneurysmal disease and traumatic rupture, there is ongoing development of medical, surgical, and endovascular therapies for type B dissection. Aggressive β-blockade has been shown to retard aortic root dilation in the case of Marfan disease, and may well have the same benefit in the thoracoabdominal aorta [187]. Understanding the genetic basis for connective tissue disorders, including how variations may predispose to specific complications, may permit better
Summary
Type B dissection represents an acute aortic syndrome, along with PAU and IMH. The cause predominantly involves atherosclerosis and hypertension, but in a significant proportion also involves connective tissue disorders. In the acute setting and in uncomplicated patients, medical management with blood pressure control is the standard of care. Complicated dissection, manifested predominantly by malperfusion syndromes followed by rupture, requires a complication-specific approach. Acute surgical
References (192)
- et al.
Contemporary management of aortic branch compromise resulting from acute aortic dissection
J Vasc Surg
(2001) - et al.
Epidemiology and clinicopathology of aortic dissection
Chest
(2000) - et al.
Vascular complications associated with spontaneous aortic dissection
J Vasc Surg
(1988) - et al.
Endovascular repair of the thoracic aorta: lessons learned
Ann Thorac Surg
(2005) - et al.
Risk factors for aortic dissection: a necropsy study of 161 cases
Am J Cardiol
(1984) - et al.
Early surgical experience with Loeys-Dietz: a new syndrome of aggressive thoracic aortic aneurysm disease
Ann Thorac Surg
(2007) - et al.
Clinical, diagnostic, and management perspectives of aortic dissection
Chest
(2002) - et al.
The dissected aorta: percutaneous treatment of ischemic complications—principles and results
J Vasc Interv Radiol
(1997) - et al.
Surgical management of dissecting aneurysms of the aorta
J Thorac Cardiovasc Surg
(1965) - et al.
Management of acute aortic dissections
Ann Thorac Surg
(1970)