Ascending and descending
Ascending
Descending
Stanford type A
Stanford type A
Stanford type B
DeBakey type I
DeBakey type II
Debakey type III
The Stanford system is categorized as type A or type B. Type A dissection involves the ascending aorta with any variable amount extending into the aortic arch and descending aorta. Type B dissection involves the descending aorta only. The Stanford system has become increasingly popular in recent years due to its ability to predict disease prognosis and guide therapeutic strategies. As our understanding of aortic pathologies have progressed there is an increased need for qualifiers that account for clinical status at the time of presentation as this has been shown to correlate with overall survival [10–12]. The group from the University of Pennsylvania has proposed a PENN classification system of type A dissections that accounts for clinical presentation and extent of dissection. In this system class A refers to dissection without aortic branch malperfusion or circulatory collapse. Class B refers to branch vessel malperfusion (e.g. stroke, ischemic limb, etc.). Class C refers to circulatory collapse with or without cardiac involvement. Class B and C refers to patients with circulatory collapse with branch vessel malperfusion (Table 3.2). The PENN classification system provides valuable prognosis data for clinicians that the Stanford and DeBakey systems fail to deliver [13, 14].
Table 3.2
Penn clinical classification of type A dissections
Clinical presentation | Definition of clinical presentation class |
|---|---|
Class A | Clinical presentation characterized by Absence of branch vessel malperfusion or circulatory collapse |
Class B | Clinical presentation characterized by Branch vessel malperfusion with ischemia e.g. stroke; ischemia extremity |
Class C | Clinical presentation characterized by Circulatory collapse with or without cardiac involvement |
Class B and C | Clinical presentation characterized by both Branch vessel malperfusion and Circulatory collapse |
Emergent surgical repair is the gold standard for management of type A aortic dissection [3, 4, 6, 15, 16]. The standard operation entails aortic root reconstruction, valve resuspension, ascending aorta and hemiarch reconstruction. One of the major principles of repair is resection of the primary tear site, with stabilization of the true lumen flow. Untreated distal extent of dissection has been associated with poorer long-term outcomes. Recently, the use of antegrade stenting and TEVAR as an adjunct has become increasingly utilized and shown to improve long-term survival and decrease the need for subsequent distal aortic intervention [17–23]. RTAD are a subgroup of aortic dissection that can be categorized as spontaneous or iatrogenic. Patients with Spontaneous RTAD have historically been considered a high-risk endeavor. However, as surgical techniques for simultaneous treatment of the ascending and descending aorta have evolved, the surgical risk has decreased accordingly [20, 24, 25]. Iatrogenic RTAD have become an increasingly prevalent condition with an increasing body of literature dedicated to the description and proposed treatment strategies. Iatrogenic RTAD has been described after all forms of endovascular interventions involving the descending aorta; however, it is most commonly described after TEVAR for type B aneurysms and dissections. The rate of RTAD is currently believed to occur in 1–2 % of all patients undergoing TEVAR, and risk factors for its development include oversizing of thoracic stents, balloon manipulation of the proximal stent graft, and wire injury. Presentation of the RTAD can vary from intra-operative detection to several months post-procedure [17, 26–29].
Search Strategy
A literature search of English language publications from 1990 to 2013 was used to identity published data on diagnosis, natural history, and treatment of type A aortic dissection originating distal to the left subclavian artery (Table 3.3). Select studies dated prior to 1990 were utilized to provide historical context. Databases searched included PubMed, Embase, Medline, and Cochrane Evidence Based Medicine. Terms used in the search were; “type A aortic dissection” OR “type A dissection” OR “retrograde aortic dissection” OR “Debakey type IIId” OR “aortic dissection after TEVAR” OR “iatrogenic aortic dissection” OR “Prognosis of iatrogenic type A dissection” OR “Prognosis of retrograde type A dissection” AND/OR “medical management”. The data was classified using the GRADE system.
Table 3.3
PICO table for management of retrograde type A dissections
P (patients) | I (intervention) | C (comparator group) | O (outcomes measured) |
|---|---|---|---|
Patients with retrograde type A aortic dissections | Open surgical repair | Medical therapy or endovascular repair | Perioperative mortality and morbidity |
Results
Clinical Relevance of Type A Aortic Dissections Originating Distal to the Left Subclavian Artery
Spontaneous Type A Retrograde Dissection
Spontaneous RTAD are a subtype of type A dissection whose incidence and natural history are incompletely understood (Fig. 3.1). Studies suggest varying rates of RTAD. Ruel and colleagues published the first series formally classifying RTAD in 1975 showing 9 (10 %) of 91 with type A dissections having intimal flaps in the descending aorta [9]. In 1984 Miller et al. reported 5 (10 %) of 48 cases with descending aorta intimal flaps [30]. More recent studies in 1993 and 1994 by Erbel et al. [31] and Lansman et al. [32] demonstrated rates of 27 % (22 of 82) and 7 % (5 of 69) cases respectively. Lansman published a second report in 1999 where the rate of RTAD was found to be 6 % [33]. In a 2003 study by Kaji and colleagues comparing outcomes of antegrade and retrograde type A dissection found 27 of 109 (25 %) cases to have intimal tears in the descending aorta (Table 3.4) [34]. The most recent study, performed by Kim and colleagues at a single institution between 1999 and 2011 found the rate of retrograde dissection to be 9.1 % (49 of 538) [35].
Fig. 3.1
CT scan demonstrating patient with a Type B IMH and retrograde involvement of hematoma in the ascending aorta
Table 3.4
Incidence and mortality of spontaneous type A retrograde dissection
Author (year) | Incidence | Mortality | Study type (evidence quality) |
|---|---|---|---|
Ruel (1975) | 9/91 10 % | 8/9 89 % | Case series (low) |
Miller (1984) | 5/48 10 % | Not recorded | Case series (low) |
Erbel (1993) | 22/82 27 % | 10/22 45 % | Case series (low) |
Lansman (1994) | 6/69 9 % | 0/6 0 % | Case series (low) |
Lansman (1999) | 8/139 6 % | 0/8 0 % | Case series (low) |
Kaji (2003) | 27/109 25 % | 4/27 15 % | Case series (low) |
Kim (2014) | 49/538 9.1 % | 4/49 8 % | Case series (low) |
Total: | 125/1076 11.6 % | 26/121 21 % |
Iatrogenic Retrograde Type A Dissections
Iatrogenic RTAD is one of the most catastrophic complications of TEVAR (Figs. 3.2 and 3.3). As indications and overall number of TEVAR cases continues to expand, it is likely that the prevalence of iatrogenic RTAD will increase. Current literature suggests varying incidence between 1 and 6.8 % [36–39]. A review of the European Registry on Endovascular Aortic Repair Complications found an overall rate of iatrogenic dissection to be 1.33 %, with an associated mortality of 42 %. Time of onset in this study varied from intraoperative to 1050 days post-TEVAR [27]. A single center study from the University of Pennsylvania in 2013 examining reintervention after TEVAR found the rate of iatrogenic RTAD to be 1.3 % (9 of 680), with associated operative mortality of 22 % (2 of 9) [39]. In 2008, Langer and colleagues reported the incidence of RTAD after TEVAR to be 1.8 % (2 of 106) [37]. A study by Neuhauser et al. in 2005 showed a rate of type A retrograde dissection after TEVAR to be 6.8 % (5 of 73), with a median time of RTAD detection to be at 20 days (range 2–124 days). The associated mortality in this report was 40 % [38]. In 2011, Dumfarth and colleagues examined 421 patients who underwent TEVAR at two institutions and found that 5 (1.1 %) patients developed RTAD [26]. A 2009 study in China by Dong and colleagues examined a single center experience where 11 (2.4 %) of 443 patients undergoing TEVAR developed RTAD with associated mortality of 27.3 % [40].
Fig. 3.2
(a, b) Series of angiograms performed after TEVAR showing retrograde dissection
Fig. 3.3
Patient with a retrograde type A IMH who presented 4 weeks after a TEVAR for chronic type B aneurysm with CT scan demonstrating the entry tear (a: arrow) and extensive IMH (b: arrow)
Risk Factors for Spontaneous Type A Retrograde Dissection
Spontaneous Type A Retrograde Dissection
Known risk factors for Spontaneous RTAD are currently believed to be identical to those of antegrade dissections. Hypertension, atherosclerosis, preexisting aortic aneurysm, aortic ulcer, connective tissue disease, advanced age, and biscuspid aortic valve disease have all been associated with increased risk [1, 6, 12, 16, 41–44]. No literature specifically focusing on patient risk factors for de novo RTAD was found in the preparation of this chapter.
Iatrogenic Type A Retrograde Dissection
The primary risk factor for the development of iatrogenic RTAD is endovascular manipulation of the aortic arch and DTA, most commonly, during TEVAR and hybrid surgical procedures [26, 27, 39, 45–48]. A study by Eggebrecht and colleagues examining the European registry on endovascular repair complications found the majority of iatrogenic RTAD to be caused by stent graft injury to the aorta (N = 29, 60 %). Other causes included guidewire/sheath injury (N = 7, 15 %), as well as progression of underlying disease (N = 7, 15 %) [27]. Other factors associated with increased risk for development of iatrogenic RTAD include balloon manipulation of the stent graft (especially in the proximal portion of the graft) the use of proximal stents with bare metal springs, oversizing the stent graft, steep aortic arch angulation (>60o) [49], connective tissue disease [40], fragile aorta, ascending aorta diameter >40 mm, progression of aortic disease [48], and patients with connective tissue disease (Table 3.5) [26, 49].
Table 3.5
Risk factors for RTAD during TEVAR
Stent graft injury | Guidewire injury |
Sheath injury
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