Journal of Vascular Surgery
Volume 43, Issue 2, Supplement , Pages A30-A43, February 2006

Aortic dissection: Perspectives in the era of stent-graft repair

  • Marvin D. Atkins Jr, MD

      Affiliations

    • Massachusetts General Hospital, Boston, Mass
    • ,
  • James H. Black III, MD

      Affiliations

    • Johns Hopkins Hospital, Baltimore, Md
    • ,
  • Richard P. Cambria, MD

      Affiliations

    • Massachusetts General Hospital, Boston, Mass
    • Corresponding Author InformationCorrespondence: Richard P. Cambria, MD, Massachusetts General Hospital, WACC 458, 15 Parkman Street, Boston, MA 02114

Received 14 October 2005; accepted 17 October 2005.

Article Outline

 

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Introduction 

Acute aortic dissection is the most common catastrophe affecting the aorta, with an incidence exceeding that of ruptured abdominal aortic aneurysm (AAA).1 The mortality rate in the acute phase of the disease has traditionally been quoted as 1% per hour in the absence of treatment. Earlier studies confirmed a 75% mortality rate without treatment within the first 2 weeks after the onset of symptoms.2 Despite advances in the diagnosis and medical, surgical, and endovascular management of aortic dissection, the morbidity and mortality remain significant, with an overall mortality of 27% reported in the International Registry of Aortic Dissection (IRAD).3

The treatment paradigm for acute aortic dissection is likely to change in the near future with the emergence of endovascular stent-graft technologies. A thorough understanding of the clinical presentation, classification, and pathologic anatomy of aortic dissection is, of course, a necessary prerequisite for either open surgical or endovascular treatment. This review focuses on the clinical features of aortic dissection and recent advances in the surgical and endovascular management of distal aortic dissection and its associated complications, such as malperfusion syndromes.

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General features 

The pathognomonic aortic dissection lesion begins with a tear in the aortic intima media, allowing access for the surging blood column to the aortic intramural space. Histopathology within this area of the aortic wall may reveal deterioration of medial collagen and elastin fibers, although it is important to emphasize that aortic dissection can occur in a histologically normal aorta. The typical tear is transverse and does not involve the entire circumference of the aorta. The intimomedial layer is cleaved both longitudinally and circumferentially for a variable distance.4 The flow of blood is usually antegrade within the aortic wall; however, retrograde flow and dissection may occur.

The so-called false lumen, adventitially bound, represents the blood-filled space between the dissected layers of the aortic wall. Depending on the circumference involved, dilation of the false channel may diminish the true lumen. Fenestrations within the intimal flap downstream, typically occurring where branch ostia are cleaved off by the dissecting process, lead to sites of re-entry for flow into the true lumen, thus maintaining false lumen patency.

The usual pattern for the dissection plane in descending aortic dissection is down the left posterolateral aspect of the aorta. The celiac, superior mesenteric, and right renal arteries typically emanate from the true lumen and the left renal artery arises from the false lumen, but variations in this pattern are frequently encountered.5, 6 The intimal flap, through a variety of mechanisms, may partially, intermittently, or completely obstruct distal perfusion to the aorta or any branch vessel.

Aortic dissection is classified as acute or chronic based upon the duration of symptoms at presentation. Aortic dissection diagnosed ≤2 weeks of the onset of symptoms, when most life-threatening complications occur, is considered acute; beyond this time frame, chronic. Anatomically, three classification schemes within the literature have been used to describe aortic dissection based on entry tear site and proximal or distal involvement. Sixty-five percent of intimal tears occur in the ascending aorta, 20% in the descending aorta, 10% in the aortic arch, and 5% in the abdominal aorta.3 The classification scheme proposed by DeBakey et al7 in 1965 is most commonly used and specifically delineates the extent of the descending aortic dissection according to the following classification (Fig 1):

•Type I: dissection originates in the ascending aorta and extends through the aortic arch and into the descending aorta or abdominal aorta, or both, for a varying distance.

•Type II: dissection originates in and is confined to the ascending aorta.

•Type III: dissection originates in the descending aorta and is limited to it in Type IIIa; Type IIIb involves descending and variable extents of the abdominal aorta.

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  • Fig 1. 

    DeBakey and Stanford classification schemes for acute aortic dissection. The principle distinction between proximal and distal dissections is the involvement of the ascending aorta.

The second classification scheme, proposed by Dailey et al,8 simplifies aortic dissection into Stanford type A, including dissections that include the ascending aorta (DeBakey type I and II) irrespective of the site of origin, and type B, which originate in and are confined to the descending aorta.8 The most recent classification scheme further simplifies aortic dissection into the anatomic categories “proximal” and “distal,” equivalent to Stanford type A and B.

Determination of the aortic entry tear or involvement, or both, of the ascending aorta is the most important determinant for proximal cardioaortic complications and has specific treatment implications. Typically, involvement of the ascending aorta implies that the entry tear has occurred in the proximal ascending aorta, but rarely, the ascending aorta can be involved with retrograde dissection from a more distal entry tear.

Rapid classification is essential in the management of aortic dissection, as proximal dissections usually require emergent graft replacement of the ascending aorta owing to the high risk of cardioaortic complications, namely aortic rupture, cardiac tamponade, acute aortic insufficiency, or coronary artery ostial occlusion. Distal dissections currently are managed medically unless specific complications such as malperfusion syndrome complicate the dissection.

The incidence of acute aortic dissection is reported to be 14 to 20 million each year.1, 9 Men are more frequently afflicted, with a male-to-female ratio of 5:1.2, 9 The peak incidence is 50 to 60 years of age for proximal dissection and 60 to 70 years for distal dissections.3 Two thirds of acute aortic dissections are proximal (DeBakey I, II, Stanford A), and the remaining third are distal dissections (Fig 2).10

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  • Fig 2. 

    Demographic and clinical features of 512 patients with acute aortic dissection classified by the DeBakey system. The distribution of dissection extent, demographic features, and incidence of peripheral vascular complications were similar over the 35-year period (1965 to 1999) in which these patients were treated. Patients with type III dissections tend to be older and almost universally hypertensive. As anticipated, vascular complications tend to cluster among the more extensive type I and IIIb dissections. HBP, High blood pressure; VC, vascular complications. (Adapted from Lauterbach SR, Cambria RP, Brewster DC, et al: Contemporary management of aortic branch compromise resulting from acute aortic dissection. J Vasc Surg 2001;33:1185-92 and Cambria RP, Brewster DC, Gertler J, et al: Vascular complications associated with spontaneous aortic dissection. J Vasc Surg 1988;7:199-209.)

Started in 1996, the IRAD database is an ongoing, multinational, academic medical center registry of consecutive patients with acute aortic dissection. The IRAD study found an overall mortality of 27.4% for all types of aortic dissection, including 26% for surgical treatment of proximal dissection and 58% for medical management alone, although it may be inferred that patients in the latter group were not surgical candidates because of advanced age, comorbidities, or refusal to consent. In distal aortic dissection, mortality was 10.7% with medical therapy but rose to 31% in the presence of complications requiring intervention3; clearly, patients in these two treatment groups were not comparable.

Branch vessel involvement, termed malperfusion syndrome when ischemic complications arise, is a frequent indication for surgery in aortic dissection and occurs in 30% to 42% of patients.11, 12, 13 False lumen thrombosis occurs in 2% to 3% of medically treated patients and in only 15% to 30% of surgically treated patients. Continued false lumen patency is a risk factor for recurrent dissection or aneurysmal degeneration, or both, and remains a significant issue despite surgical therapy.14 Progression to aneurysm formation ≤4 years of initial diagnosis occurs in 30% to 50% of patients with distal dissection who are treated medically.15, 16

The most common associated risk factors for the development of aortic dissection include hypertension and advanced age. This association is strongest for patients with distal aortic dissection, who tended to be older and universally hypertensive (Fig 2). Aortic wall structural abnormalities and the presence of a bicuspid aortic valve are also well-established risks. Patients with connective tissue disorders such as Ehlers-Danlos and Marfan syndrome are prone to develop cystic medial degeneration of the aortic wall. Marfan syndrome accounts for 5% of all aortic dissections and is the leading cause of aortic dissection in patients aged <40.17 Cocaine ingestion and pregnancy associated with hypertension and preeclampsia are rare causes of acute aortic dissection in otherwise healthy individuals.4

Our cumulative experience affords a perspective over a 35-year period involving 512 patients with acute aortic dissection.10 The overall mortality rate in the interval 1990 to 1999 was significantly lower compared with an earlier report from 1965 to1986 (18% vs 37%, P < .006).11 Nearly a third of the patients had evidence of branch occlusion; 17 (32%) of these 53 patients underwent peripheral vascular intervention to restore circulation. In discerning the factors associated with improved results over time, several variables were important:

1.Aortic rupture occurred in just 6% of patients vs 18% in the prior interval. Presumably, patients were being diagnosed and referred more promptly.

2.The impact of branch occlusion on mortality was no longer significant, implying that earlier recognition and treatment of malperfusion syndromes had improved overall results.

3.Overall mortality in surgical repair of proximal dissection had improved from 33% to 15% because of advances in cardiac surgical techniques.

4.The presence of mesenteric ischemia receives treatment priority in virtually all patients and constitutes an exception to prompt central aortic repair of type A dissection. Deeb et al18 emphasized the importance of treating mesenteric ischemia first and delaying central aortic repair, which resulted in improvements in mortality from 87% to 37%.

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Clinical presentation 

The most common presenting symptom is pain, reported in >93% of the IRAD patients, with 85% specifying an abrupt onset.3, 19 The pain was typically described as anterior in location in type A dissection but was more often experienced in the back in type B dissection.3 Unlike the classic description of the character of the pain in aortic dissection as ripping or tearing (50%), the pain is more often described as sharp (68%), and less often as migratory (19%). Typically, the pain is severe, causing the patient to seek medical attention within minutes to hours of onset. The localization of pain to the abdomen was reported by 21% of patients in type A dissection and 43% of patients in type B dissection.3 In such patients, a high index of suspicion for mesenteric vascular compromise is warranted.

The control of pain by antihypertensive therapy is considered to be of paramount importance in the early management of acute aortic dissection, and the recurrence of pain has been considered to imply failure of medical therapy. Januzzi et al20 studied 53 patients who experienced recurrent pain after diagnosis of type B aortic dissection; repeat imaging studies revealed no change in aortic diameter and no radiographic evidence of worsening. Overall, only 2 (4%) of the 53 patients had a complicated hospital course. These observations led the authors to conclude that among patients with early recurrent pain after type B aortic dissection, in the absence of clinical or radiographic signs of pathoanatomic changes, a conservative strategy of continued medical management was a reasonable approach.20

Syncope may complicate the presentation of acute aortic dissection in 5% to 10% of patients, and its presence often indicates the development of cardiac tamponade or involvement of the brachiocephalic vessels.21 Overall, patients in the IRAD study presenting with syncope were more likely have a type A dissection than a type B dissection (19% vs 3%, P < .001) and were more likely to have cardiac tamponade (28% vs 8%, P < .001). Similarly, they were more likely to have a stroke (18% vs 4%, P < .001) and more likely to die in the hospital (34% vs 23%, P = .01). Although patients presenting with syncope had a higher rate of severe complications (tamponade, stroke, death), almost half had none of the aforementioned complications to explain their loss of consciousness.21

Spinal cord ischemia from the interruption of intercostal vessels is clearly more common with type B aortic dissections and may occur in 2% to 3% of all patients. On the initial physical examination, hypertension is present in 70% of type B dissections but only in 25% to 35% of type A dissections (Fig 2). The presence of hypotension complicating a type B dissection is rare, seen in <5% of patients. In contrast, hypotension may be present in 25% of dissections that involve the ascending aorta, potentially as a result of aortic valve disruption or cardiac tamponade.3 The malperfusion of brachiocephalic vessels by the dissection may falsely depress brachial cuff pressures. Refractory hypertension in the course of medical management of type B aortic dissections is common, occurring in 64% patients with involvement of the descending aorta.22 However, it is usually not associated with renal artery compromise or aortic dilatation and, therefore, continued medical therapy is indicated.

Pulse deficits are common and occur in 30% to 50% patients in whom the aortic arch or thoracoabdominal aorta, or both, is involved.11, 12, 13 In the IRAD population, the involvement of the brachiocephalic trunk was noted in 14.5% of all patients, left common carotid artery in 6.0%, left subclavian in 14.5%, and femoral arteries in 13% to 14.0%.23 Patients presenting with pulse deficits more often had neurologic deficits, coma, and hypotension. Carotid pulse deficits, not surprisingly, were strongly correlated with fatal stroke, consistent with prior observations.10 The number of pulse deficits was clearly associated with increased mortality. Within 24 hours of presentation, 9.4% of patients with no deficits died, 15.8% of patients with one or two deficits died, and 35.3% of patients with three or more deficits died.23

In regard to isolated lower-extremity pulse deficits, mortality due to lower-extremity ischemia or its sequelae is uncommon.11 Nonetheless, leg ischemia caused by acute dissection was a marker of extensive dissection and may be accompanied by other compromised vascular territories. Indeed, the clinical course of the peripheral ischemia can be quite variable, and up to one third of this group may demonstrate spontaneous resolution of their pulse deficits.11 Clearly, rapid bedside pulse examination can provide important information in the diagnosis of acute aortic dissection and identify those at risk for complications.

In our previous report of patients treated during the 1990s, those with peripheral branch obstruction had a 23% mortality rate compared with 16% for those without obstruction (P = .26). In contrast to the IRAD study findings, the presence of peripheral vascular complications did not increase mortality.11 This finding was thought to be due to a more timely diagnosis, prompt initiation of therapy, and the recognition of the importance and appropriate treatment of peripheral vascular complications.

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Related conditions of the thoracic aorta 

Intramural hematoma (IMH) and penetrating atheromatous ulcer (PAU) are two closely related (possibly the same) aortic syndromes that commonly cause diagnostic confusion with classic aortic dissection. Both are manifestations of degenerative aortic pathology, typically occurring in older patients with significant hypertension.

IMH of the thoracic aorta has been characterized as a distinct clinical entity whose distinguishing radiographic features are the absence of a definable intimal flap (as seen with classic aortic dissection) or penetrating ulceration.24, 25 The extent of this IMH is variable both in terms of length and circumference of the aorta involved and prograde vs antegrade propagation.

The etiology of IMH was initially thought to involve spontaneous rupture of the vasa vasorum within the medial layers of the aortic wall. More consistent with our own observations, a PAU phenomenon is usually the origin of IMH and whether or not the ulcer-like projection is radiographically demonstrated is merely serendipity. PAU is used to describe these lesions when a cap-like projection of contrast is seen on computed tomographic (CT) scan beyond the usual luminal aortic boundary.

The natural history of IMH and PAU has been reported to include progression to aortic dissection, false aneurysm, rupture, or spontaneous regression.26 The IRAD database examined 1010 patients with acute aortic syndromes, of whom 5.7% were found to have IMH. IMH affected the descending aorta in 60% of cases, whereas classic aortic dissection more commonly affected the ascending aorta (65% of cases). The overall mortality of IMH was similar to that for classic aortic dissection, 20.7% vs 23.9%, both for proximal (39.1% vs 29.9%) and distal (8.3% vs 13.1%) locations. Among the 51 patients whose initial diagnostic study revealed IMH, 8 (16%) progressed to aortic dissection on a second imaging study.

A normal aortic diameter in the acute phase was the best predictor of IMH regression without complications. The IRAD investigators recommended prompt surgical therapy for IMH involvement of the ascending aorta. Intense medical therapy alone (goal of systolic blood pressure <120/80, heart rate <60) was recommended for involvement of the arch and descending aorta.27

A recent report of 35 patients with IMH detailed a highly significant correlation of progression based on initial aortic diameter and the thickness of the hematoma. Those patients with an initial aortic diameter >40 mm had a 30-fold increased risk of progression to either aneurysm formation or rupture. Aortic wall thickness >1 cm (ie, the extent of intramural clot) was also associated with a ninefold increased risk of progression. This suggests that the degree of separation of the aortic wall layers contributes to chronic aneurysmal degeneration.28

Although such focal pathology is potentially ideally suited for stent-graft repair treatment, most patients with IMH or PAU of the descending aorta do not require intervention. Indications for intervention include aortic diameter >6 cm, rupture, impending rupture, or major progression in size despite medical therapy. Those patients with involvement of the ascending aorta are usually treated surgically because of the high risk of cardioaortic complications. Follow-up of patients with IMH or PAU treated medically should be frequent, especially those with evidence of aneurysmal dilation, the strongest predictor of future need for intervention (Fig 3).

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Pathogenesis of malperfusion syndromes 

Aortic branch compromise, often termed malperfusion syndrome when vascular beds are critically compromised, may occur in aortic dissection through several mechanisms. One or more vascular beds may be simultaneously affected. Branch vessel obstruction is often subtotal, waxing and waning in severity after symptom onset. It should be emphasized that the terms aortic branch compromise and malperfusion syndrome do not equate, as partial aortic branch obstruction may not result in critical ischemia. Aortic branch compromise may complicate aortic dissection in up to 31% of patients.11, 12, 13 We documented that such aortic branch compromise was associated with an increased early mortality.10 Virtually any aortic branch can be affected, and as intuitively suspected, the morbid clinical events will vary as a function of the vascular territory involved. Mesenteric vessel involvement is associated with intestinal infarction, whereas subclavian or lower-extremity occlusive events, or both, are often well tolerated (Fig 4).

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  • Fig 4. 

    Distribution of peripheral vascular complications in 512 patients over a 35-year period (1965 to 1999) treated at the Massachusetts General Hospital. Peripheral vascular complications are classified by aortic branch site. Differences between site occlusions and clinical events represent asymptomatic occlusions. HBP, high blood pressure.

Identifying the mechanisms of branch compromise is critical to formulating effective treatment modalities. In the minutes after an aortic dissection is initiated, the true lumen collapses to a variable degree and the false lumen expands.29 The adventitially bound outer wall of the false lumen must expand to a larger diameter to accommodate the same wall tension at any given blood pressure, as governed by the law of Laplace. The true lumen, which contains most of the elastic components of the aortic wall, undergoes radial elastic collapse.29 The degree to which the true lumen recoils and the false lumen expands (ie, their respective cross-sectional area) is therefore dependent on the percentage of the total aortic circumference involved with the dissection.

Two mechanisms for aortic branch vessel compromise have been identified, each of which has specific treatment implications in the management of malperfusion syndromes. In dynamic obstruction, the compressed true lumen is unable to provide adequate flow volume or the dissection flap may prolapse into the vessel ostium, which remains anatomically intact. This is the more common mechanism of branch compromise, being responsible for some 80% of malperfusion syndromes.30 The severity of true lumen collapse and the degree of the aortic-level ostial vessel occlusion is determined by the circumference of the aorta dissected, the blood pressure, heart rate, and peripheral resistance of the outflow vessel. Pulse deficits based on dynamic obstruction may wax and wane over time because of the variability of the aforementioned variables (Fig 5, A to C).31, 32

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  • Fig 5. 

    Mechanisms of aortic branch obstruction in acute dissection. A, In dynamic obstruction, the septum may prolapse into the vessel ostium during the cardiac cycle, and the compressed true lumen flow is inadequate to perfuse branch vessel ostia, which remain anatomically intact. B, Near complete circumferential dissection with static obstruction. The cleavage plane of the dissection extends into the ostium and compromises inflow. Thrombosis beyond the compromised ostia may further worsen perfusion. C, Spontaneous perfusion of aortic branches perfused from the false lumen occurs if the dissecting process tears the ostia away from the true lumen. Such spontaneous “fenestrations” often account for persistent false lumen flow. F, false lumen; T, true lumen.

In acute dissection, the false lumen is highly thrombogenic as a result of the exposed adventitial and medial layers. Thrombus formation may occur in the blind end of the dissection column. If the blind end or the propagating end of the dissection column enters and constricts the ostia of a branch vessel, organ injury can occur by thrombosis or hypoperfusion of the involved vessel. This mechanism for malperfusion syndrome involves the dissecting process extending into the branch vessel proper, narrowing it to a variable degree—the so-called static obstruction.30 This mechanism is unlikely to resolve with restoration of aortic true lumen flow alone, and some manipulation of the vessel itself (ie, stent, bypass graft) will typically be required.

More common than static obstruction is the dissection process itself shearing the aortic intima media around the vessel ostium, with the vessel anatomy remaining intact and flow provided by the false lumen (Fig 5, C.) Most branches perfused from the false lumen do not show evidence of ongoing malperfusion as long as there is distal decompression and continued false lumen flow.

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Diagnostic studies 

In most environments, a contrast-enhanced, fine-cut CT scan of the entire aorta is the preferred diagnostic modality. The findings of aortic dissection on chest radiography are nonspecific and rarely diagnostic. The most common abnormality seen in aortic dissection is widening of the aortic silhouette, appearing in 60% to 90% of cases.3

Aortography 

Formerly the gold standard for the diagnosis of aortic dissection, with a sensitivity of 88% and a specificity of 94%, aortography has largely yielded to axial imaging studies.33, 34 False negative aortograms may occur when thrombosis of the false lumen has occurred, in the presence of an intramural hematoma, or when equal flow into the true and false lumen obscures delineation. The aortographic findings considered supportive of a diagnosis of aortic dissection include distortion of the normal contrast column, flow reversal or stasis into a false channel, failure of major branches to fill, and aortic valvular regurgitation. Most contemporary diagnostic algorithms have de-emphasized the role of aortography.

Furthermore, pressurized contrast injections into either lumen in the presence of aortic dissection can, in fact, lead to diagnostic confusion with respect to malperfusion syndromes. For example, branch ostia are anatomically normal in circumstances of dynamic obstruction and true lumen typically appears normal with injections. Therefore, in contemporary practice, aortography is unnecessary before surgical repair of proximal dissection and is essentially not used as a diagnostic modality.35 It is used as a component of an interventional treatment strategy in the endovascular management of dissection.

Transesophageal echocardiography 

The sensitivity of transesophageal echocardiography (TEE) has been reported to be as high as 98%, and the specificity ranges from 63% to 96%.36 The advantages of TEE include wide availability, ease of use, and bedside capability. In addition, TEE is able to detect entry tear sites, false lumen flow and thrombus, involvement of the arch or coronary arteries, degrees of aortic valvular regurgitation, and pericardial effusions. The addition of color flow Doppler patterns may decrease false positives by recognizing differential flow velocities in the true and false lumens.

The chief limitations of TEE are the anatomic blind spot in the distal ascending aorta and arch secondary to the air-filled trachea and left main stem bronchus, and the inability to document dissection extension beyond the diaphragm. Despite these shortcomings, TEE can be particularly useful in delineating dissection and relevant surgical pathology in the ascending aorta. Moreover, in the unstable patient with a suspected acute dissection in the ascending aorta, TEE may be performed in the operating room to expedite diagnosis and definitive therapy. In the IRAD study, TEE was second in most frequent usage after CT in the diagnosis and work-up of an acute aortic dissection.36

Computed tomography 

All patients with suspected acute aortic dissection should be thoroughly evaluated with both chest and abdominal dynamic, contrast-enhanced fine-cut CT scanning. CT scanning has a reported sensitivity of 83% to 95% and a specificity of 87% to 100% for the diagnosis of acute aortic dissection.37 The chief limitation is the ascending aorta, where the sensitivity may drop to <80%, but this is readily overcome by the addition of TEE.

Three-dimensional CT scan reconstructions can aid in treatment planning, but axial imaging affords the best opportunity to detect topographic relationships of the true and false lumens and potential aortic branch compromise. In most cases, the true lumen may be localized by its continuity with an undissected segment of the aorta. The presence of intraluminal thrombus is a fairly good marker of the false lumen, but in patients with a concomitant degenerative aneurysm, thrombus may be present in the true lumen.

The finding of greatest significance was the observation in the descending thoracic aorta of the false lumen being larger than the true lumen in >90% of cases (P < .05), and this simple guideline is clinically quite useful.38 A compressed true lumen is perhaps the key radiographic finding, which should substantially raise the index of suspicion for renal/visceral/lower extremity malperfusion syndrome.

Indeed, it may be appropriate if open surgical intervention is chosen as the revascularization procedure to proceed directly to surgery after CT alone in circumstances where the clinical or laboratory signs, or both, dictate the need for urgent revascularization. Compared with other modalities, CT scanning is the least operator dependent, provides useful anatomic correlates for surgical and endovascular therapy, and most reliably collects information for follow-up analysis and measurement (Fig 6).

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Principles of treatment 

Prompt institution of intravenous antihypertensive medications to lower systemic blood pressure and pulse (dP/dT) is a key element of initial therapy for all patients, with the goal of stabilizing the extent of the dissection, reducing intimal flap mobility, relieving dynamic aortic branch obstruction, and decreasing the risk of rupture. Mortality in the acute phase of a proximal dissection may exceed 1% per hour related to the central cardioaortic complications of tamponade, acute aortic valvular insufficiency, and coronary obstruction. Thus, prompt graft replacement with or without aortic valve repair or replacement is the treatment of choice for most patients with type A aortic dissection.

For patients with type B dissections, the catastrophic complication of rupture is uncommon, except in those patients who present with advanced false lumen dilatation or the equivalent of aneurysm formation at the aortic entry site.31 Furthermore, in stable patients with uncomplicated type B dissections, surgical therapy has not demonstrated superiority over medical or interventional therapy.19

Aortic branch compromise by the propagating false lumen and subsequent malperfusion syndrome may complicate the initial presentation of patients with extensive type B dissections. A complication-specific approach involving open surgical and endovascular options to treat such malperfusion syndromes is advocated and reviewed below. The application of stent-graft repair at the entry tear may alter this paradigm in the near future.

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Surgical therapy 

Graft replacement of ascending aortic dissection 

A complete review of the surgical literature and state-of-the-art management of acute type A dissection is beyond the scope of this review. Urgent surgical repair of acute type A dissection is the treatment of choice for all patients unless major neurologic deficits or peripheral vascular complications of the dissection pose greater overall risk (ie, visceral ischemia) than the threat of proximal rupture. The IRAD study group found an overall operative mortality of 25.1% in patients with proximal aortic dissection.3 Improvements in cardiac surgery, including the use of circulatory arrest, improved cerebral protection, avoidance of routine aortic valve replacement, and the avoidance of extensive arch resections have led to improvements in outcome. The mortality rate in several large referral centers, including our own, is about 15%.10, 39

Graft replacement of descending aortic dissection 

Threatened or actual rupture at the aortic intimal tear in the proximal descending aorta remains, in our view, the only indication for acute graft replacement in distal dissection. Unless an extensive aneurysm is present, resection should be confined to the proximal descending aorta, as mortality and spinal cord ischemia risk increase dramatically with extensive aortic replacement in the setting of an acute dissection. The mortality rate for the open repair of acute type B aortic dissection has ranged from 6% to 69% in several large series (Table). In a series of nearly 100 type B dissection patients over the course of a decade, we applied this approach only once.10 In addition, central aortic grafting may be unsuccessful in alleviating distal malperfusion syndromes, depending on the mechanism of obstruction, the anatomic complexity of the dissection, and the successful obliteration of false lumen flow (Table).

Table. Results of graft replacement of acute type B aortic dissection
AuthorPeriodAdjuncts (% pts)Patients (N)Mortality (%)Paraplegia/Paraparesis
Jex1962-1983PB(66)294524
Verdant1974-1994NA52120
Glower1975-1988
PB(44)

GS(39)

1918NA
Miller1977-1982PB(NA)261325
Neya1979-1991PB(NA)1369NA
Fann1983-1992PB(100)1741NA
Svennson1986-1989PB(NA)67625
Coselli1986-1994
PB(NA)

CSF(NA)

28147

PB, partial bypass; NA, not available; GS, Gott shunt; CSF, cerebrospinal fluid drainage.

(Adapted from Black JH, Cambria RP. Aortic dissection: perspectives for the Vascular/Endovascular Surgeon. In: Rutherford R, editor. Rutherford’s Textbook of Vascular Surgery, 6th ed. Philadelphia: Elsevier Saunders; 2005.)

Surgical treatment of malperfusion syndromes 

Because dynamic obstruction at the aortic level is the most common mechanism of malperfusion syndromes (see Fig 5), surgical fenestration has been the most commonly applied procedure.31 This technique involves wide resection of the dissected septum to relieve aortic obstruction by equalizing flow between the true and false lumens.

A fundamental consideration is whether aortic clamping and the fenestration are confined to the infrarenal aorta. It may be desirable to extend the septectomy into the visceral segment, permitting direct inspection and repair of the ostia of the mesenteric and renal vessels.40 The interposition of a short-segment polyester graft in the infrarenal aorta facilitates reconstruction of the aortic layers at the distal anastomosis with the double-layer Teflon felt technique.

We extend the fenestration/septectomy into the visceral aortic segment when there is evidence of total absence of visceral artery flow, when the dissected septum extends directly to or beyond a vital branch orifice, or when there is radiographic evidence of intussuscepted septum into a renal or mesenteric vessel. Such an approach also permits direct repair of a static obstruction, for example, where the branch vessel itself is dissected. This can be accomplished by circumferential suture of the vessel intima to the aortic wall at the ostia. Because continuous exposure of the visceral segment is desirable in surgical treatment of malperfusion syndrome, we prefer left flank approaches for this procedure.

Depending on body habitus, a 9th or 10th interspace thoracoabdominal approach is used to allow for complete infradiaphragmatic aortic exposure and transperitoneal inspection of the viscera and palpation of the superior mesenteric artery pulse caudal to the mesocolon. At a median follow-up of 19 months, no significant aortic dilatation occurred with such aortic tailoring as a surgical technique.40 Advocates of surgical fenestration for malperfusion syndromes have asserted that the surgical morbidity and mortality rates quoted to support endovascular therapies are outdated and strongly influenced by delays in diagnosis and treatment.

Elefteriades et al41 reported in 1992 their experience using a “complication-specific” approach to acute aortic dissection. Of the 14 patients in the series treated by fenestration, their actuarial survival was 77%, 77%, and 53% at 1, 3, and 5 years, respectively. None of the aortic diameters of the surgically fenestrated patients had expanded on follow-up. Surgical fenestration was performed in the infrarenal aorta and resulted in relief of ischemia in 13 (93%) of 14 patients. The authors concluded that the relative simplicity of surgical fenestration allows subsequent survival almost uniformly, unless the patient’s preoperative overall status has been severely compromised.41

Our cumulative experience affords a perspective over a 35-year period involving 187 patients with acute aortic dissection treated during the 1990s and partly clarifies the role of open surgical fenestration and peripheral endovascular intervention in patients with malperfusion syndromes.10 Nearly a third of the patients had evidence of branch occlusion, and 17 (32%) of these 53 patients underwent peripheral vascular intervention to restore circulation. Surgical fenestration was used in nine patients with mesenteric or renal malperfusion syndromes. Restoration of flow was successful in all patients and all survived, whereas two deaths occurred in patients with mesenteric ischemia managed with percutaneous fenestration.

Open aortic fenestration is an excellent method of restoring circulation to vascular territories affected by malperfusion syndromes, especially when mesenteric and renal beds are involved, and affords the opportunity to assess bowel viability and plan second-look procedures. Treatment priority should be assigned to the most life-threatening condition in patients with acute aortic dissection. The presence of mesenteric ischemia assumes such priority in virtually all patients and constitutes an exception to prompt central aortic repair in those with type A dissections (Fig 7).18

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  • Fig 7. 

    Surgical fenestration of the infrarenal aorta. The septum is excised up to the clamp (dashed line), and proximal anastomosis to a short tube graft is carried out with interrupted pledgetted fine sutures (because part of the anastomosis circumference is carried out to the adventitial layer alone). The distal aortic suture line (inset) is carried out to an aorta-felt composite after aortic layers have been approximated.

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Stent-graft repair of aortic dissection entry site 

Technical considerations 

Stent-graft repair at the aortic entry tear may ultimately provide the means to accomplish the intuitively logical short- and long-term goals of central aortic repair while obviating the substantial morbidity of conventional open surgical repair. In 1999, the endovascular treatment of acute type B dissections with stent-graft technology was described in two seminal reports.42 Such an approach, said these reports, will effectively treat malperfusion syndromes (at least those caused by dynamic obstruction) and at least theoretically reduce late aortic-related complications by minimizing the incidence of aneurysmal degeneration of the outer wall of the false lumen.

In the natural history of medically managed type B dissections, continued patency of the false lumen is an independent risk factor for progression of chronic dissections to aneurysmal dilatation.43 During the first 4 to 7 years after acute aortic dissection, an aneurysm of the false lumen in the thoracic aorta may develop in 14% to 40% of patients treated with medical therapy alone.3 The concept of inducing false lumen thrombosis by sealing the aortic tear with an aortic endograft has the potential to both reduce early and late complications of type B dissection (Fig 8, Fig 9).

  • View full-size image.
  • Fig 8. 

    Stent-graft deployment to cover the proximal entry tear in the hopes of inducing false lumen thrombosis and true lumen re-expansion. The latter should also alleviate “downstream” branch compromise caused by dynamic obstruction mechanisms. False lumen thrombosis in the thoracic aorta should, in theory, minimize subsequent aneurysmal expansion of the outer wall of the false lumen.

  • View full-size image.
  • Fig 9. 

    Thoracic aortic stent-graft designed specifically for treatment of dissection. This particular polyester-over-Z-stent construct has bare metal proximal fixation stents (desirable to minimize risk of retrograde dissection) but is augmented with multiple uncovered distal stents to insure true lumen expansion.

Placing uncovered stents over the entry tear within the proximal true aortic lumen is ill advised and can result in perforation of the fragile intima media in the normal aorta proximal to the entry tear. This, in turn, can precipitate fatal retrograde dissection (ie, the conversion of a distal to a proximal dissection). The ability of an uncovered stent to direct flow away from the false lumen relies on sheer radial force, and the tolerance of the acutely dissected intimal flap to accommodate aggressive oversizing in an effort to compress the false lumen, is unknown. In addition, the eccentricity of the true and false lumen geometry may also place demands on radial force distribution, resulting in over-distention of the true lumen in tortuous portions of the aorta. By these two mechanisms, deployment of uncovered stents may cause aortic rupture.

The location of the entry tear and proper recognition of the proximal fixation zone are fundamental to the successful performance of the stent-graft repair. The goals of therapy are to remodel the descending thoracic aorta by sealing the proximal entry tear(s), thus redirecting flow into the true lumen and promoting depressurization and thrombosis of the false lumen. Reconstruction of the collapsed true lumen will, in theory, result in re-establishment of side branch flow, at least in dynamic obstruction. Dake et al42 reported that some 80% of compromised branch vessels were reperfused after proximal entry tear stent-grafting.

Preprocedure device measurement involves a combination of axial and reconstructed images. The proximal landing zone neck diameter (ie, normal undissected aorta) is used for device sizing. A minimum distance of 2 cm proximal from the site of entry tear is considered an adequate neck length. The left subclavian often will be covered to achieve adequate neck length. The goal for device length is to have at least 10 cm of coverage distal to the primary entry tear. Adequate iliac and femoral access is essential for larger profile devices, and an iliac conduit may be required for device placement (Fig 10).

Once the device is selected, stent-graft repair of acute aortic dissection should be performed in an operating room with adequate fluoroscopic imaging. True lumen access should be obtained from either brachial or femoral approach; typically, since the tear in type B dissection is distal to the left subclavian artery, rapid true lumen access is easily obtained through a transbrachial approach. Once definitive true and false lumen access is achieved, the specific location of the entry tear and any branch vessel compromise should be documented with a combination of intravascular ultrasound (IVUS) and angiography. It is important that the operator has definitive knowledge of the three-dimensional aortic topography displayed on the preintervention CT scan.

The induction of hypotension or bradycardia by pharmacologic means may increase the accuracy of entry tear sealing during deployment. Furthermore, the use of compliant, large diameter (33 to 40 mm) aortic occlusion balloons may be needed to ensure adequate apposition of the device to the aortic wall; however, most authorities do not recommend aggressive balloon overinflation in aortic dissection cases.44

Clinical series 

The EUROSTAR/United Kingdom registry report is the largest compendium of patients treated with thoracic aortic stent-grafts to date. In the combined registry, 131 patients with aortic dissection (5% proximal, 81% distal, 14% not classified) were treated with stent-grafts, and 57% had symptoms of rupture, aortic expansion, or side branch occlusion. Although no meaningful long-term data are available, primary technical success was achieved in 89%, and 30-day mortality was 8.4%.45 Paraplegia occurred in 0.8% of those treated, and survival at 1 year after treatment was reported in 90% of 67 patients who had such follow-up.

Experience at the Arizona Heart Institute, with 40 patients (23 acute, 17 chronic) treated with a thoracic endograft for complicated distal aortic dissection, revealed technical success in 95%. There was one perioperative death due to iliac rupture and one patient developed paraplegia. 15 patients (38%) experienced post-operative complications, mostly renal and pulmonary. One-year survival was 85%. Of the patients available for follow up CT scan, 97% (30 of 31 patients) exhibited a stable or decreasing aortic diameter. There were no ruptures in any of the patients during the study period. The authors concluded that thoracic aortic stent grafting stabilized the aorta and might decrease the incidence of late aortic expansion and rupture.46

White et al. treated 24 high-risk distal aortic dessection patients (16 acute, 8 chronic). Peri-procedural mortality was 13% (3 of 24) due to rupture with associated endoleak in one patient and retrograde dissection and tamponade in the other two. Another patient survived open conversion due to retrograde dissection. The three cases of retrograde dissection were all associated with an open wire stent graft design deployed within the thoracic arch. Overall, 2-year mortality was 17% in this emergent and high-risk patient population.47 Bartone et al. reported on 43 patients with complicated distal aortic dissection (24 acute, 19 chronic). Three patients in their series developed abrupt retrograde dissection following stent graft deployment (open stent design) leading to cardiac tamponade and death. No cases of spinal cord ischemia were noted. Two patients died during follow up secondary to progression of the dissection despite stent grafting of the entry tear. In the remaining 38 patients (mean follow up of 20 months), all survived and developed thrombosis of the false lumen.48

The INvestigation of STEnt grafts in patients with type B Aortic Dissection (INSTEAD) trial, currently recruiting patients in Europe with an expected completion in 2006, is the first randomized trial investigating the role of stent-graft treatment of uncomplicated type B aortic dissection compared with best medical therapy alone. Inclusion criteria are patients with distal chronic (2 to 52 weeks from the onset of symptoms) dissections without evidence of malperfusion syndrome. Thus, the INSTEAD trial will address whether patients with chronic, uncomplicated, distal aortic dissection treated with an endovascular stent-graft have an improved initial outcome and freedom from late dissection complications. In designing the trial, 80 patients treated by the primary author with stent-graft repair of type B aortic dissection were retrospectively compared with 80 patients managed medically. Two-year survival was 67.5% in the medically treated group and 94.9% in the group managed with endovascular stent-graft treatment.46

Currently in the United States, no thoracic endograft devices are specifically approved for the treatment of aortic dissection; however, such devices are being used off label for this purpose in many centers. Several device companies have plans for upcoming trials in the United States for the endovascular stent-graft treatment of complicated aortic pathologies.

Although preliminary data suggest that stent-graft repair may ultimately become the treatment of choice for most patients with distal dissections, the available evidence to date does not justify indiscriminate use of this technology in patients currently managed with medical therapy alone. Comparative clinical trials are clearly needed to clarify the role of stent-graft repair in acute distal dissections.

Endovascular approach to malperfusion syndrome 

Malperfusion syndromes may complicate the initial presentation of acute aortic dissection in 25% to 40% of patients. Operative mortality for open repair has been reported to be >20% in most contemporary series.41 Endovascular therapy for malperfusion syndrome, which is rooted in the concepts of surgical fenestration, has been performed in an attempt to decrease the substantial morbidity and mortality associated with open repair, but definitive data on this treatment modality are lacking.19

In the initial arteriographic evaluation of the patient with an acute aortic dissection complicated by malperfusion, true and false lumen access must be obtained. The confirmation of position within the true or false lumen is facilitated by IVUS scans. Angiography should be performed in the proximal, undissected aorta to fully appreciate intimal flap mobility and any dynamic aortic obstruction, and may be assured by brachial artery cannulation in most cases. As noted earlier, power injection in the true lumen of the dissected aorta may give the false impression of adequate perfusion to branch vessels compromised by dynamic obstruction. All aortic branches should be visualized before intervention, as changes in flap mobility owing to relief of obstruction in any single vessel may alter perfusion in other aortic side branches.

If compromise of any aortic branch vessel is identified by the dissection, wire access into the distal true lumen of the vessel should be secured. In general, placement of self-expanding stents in a potentially compromised aortic branch should precede aortic fenestration, as the latter may unpredictably alter aortic flow and make it extremely difficult to regain endovascular access to compromised vessels.47

Fenestration of the intimal flap may be performed by several techniques using the combination of IVUS scans and fluoroscopy. The goal of fenestration of the dissected intima is decompression of the false lumen, allowing for unrestricted flow in both the true and false lumens. Fenestration is most commonly performed from the smaller (usually true lumen) to the larger false lumen. One technique uses an endovascular puncture needle to access the false lumen. After contrast injection confirms placement in the opposite lumen, an angioplasty balloon of at least 12 to 15 mm in diameter and 20 to 40 mm in length is used to create a fenestration tear. Alternative techniques of fenestration include the “scissors” technique and snare wire techniques that are described elsewhere. In light of the dramatic and unpredictable alterations in intimal flap anatomy and flow dynamics incurred by overly aggressive fenestration in the visceral aorta, those investigators with the largest series of patients currently recommend that percutaneous fenestration be limited to the distal aorta (Fig 11).48

  • View full-size image.
  • Fig 11. 

    Endovascular balloon fenestration from the true to the false lumen. This causes decompression of the false lumen and allows perfusion of side branches originating from the true lumen and compromised by dynamic obstruction (see text). In this particular example, note also static obstruction of the left renal artery, which will require stenting from the true lumen.

The largest reported series of percutaneous balloon fenestration and endovascular stenting for peripheral ischemic complications in the setting of acute aortic dissection was reported by the Stanford group.48 In their series of 40 patients with malperfusion syndromes, 14 patients underwent combined stenting and balloon fenestration, 24 underwent stenting alone, and 2 fenestration alone. Overall, flow was restored to the ischemic territories in 37 (93%) of 40 patients. Thirty-day mortality was 25% (10 of 40). The variables found to be significant predictors of death on multivariate analysis were ischemia of three vascular beds, which carries a nearly fourfold increase in risk, and advanced age.

The role of stent-graft therapy in the treatment of acute distal dissection with malperfusion syndrome or aortic rupture was studied by Greenberg et al.49 The indication for treatment in their series of 31 patients was malperfusion syndrome (77%) or aortic rupture (23%). Of the 31 patients, 29 were treated by stent-graft therapy alone and two by fenestrations when definitive true lumen access could not be established. When true lumen compression resulted in visceral vessel malperfusion, the authors established definitive true lumen access to a minimum of at least two visceral vessels (typically the superior mesenteric artery and a renal artery).

Early mortality was 29% in these critically ill patients, compared with a historically documented mortality in the 80% range.11 Four of the deaths occurred immediately after stent-grafting because of massive reperfusion injuries with hyperkalemic cardiac arrest. Overall, mesenteric infarction accounted for 44% of the early deaths. The authors concluded that morbidity and mortality associated with a stent-graft approach to acute distal aortic dissection with end organ ischemia may be lower than conventional surgical approaches but still carries a significant risk.49

Clearly, a delay in diagnosis and appropriate referral will materially influence treatment results. Contemporary surgical series have demonstrated substantially improved operative mortality, even for those patients with mesenteric compromise.10 Thus, it is worth emphasizing that mortality in such patients is more often referable to delayed diagnosis than to the intervention itself.

Finally, endovascular and conventional surgical approaches should be viewed in a complimentary, rather than competitive fashion, particularly in the circumstances of mesenteric ischemia, where our approach has typically been to proceed directly to surgery. This speaks to the clinical trap of apparently adequate percutaneous mesenteric revascularization followed by the evolution of ischemic bowel to frank infarction, which was responsible for several deaths in the endovascular fenestration series.10

The effect of fenestration on long-term outcome of false lumen expansion in patients with distal dissections remains in question, since the false lumen remains pressurized and at risk for continued progression to aneurysm. Available data from our series of patients treated with open surgical fenestration, as well as others,50 suggest that the incidence of aortic intervention at the site of previous open surgical fenestration is low (0 of 9 patients at 33 months follow-up) and that the presumed risk of late aneurysm formation may be overestimated.31

Selection of the initial mode of intervention is straightforward for those patients with type B dissections who present with malperfusion syndromes. Because morbid events related to the entry tear itself are uncommon, such patients heretofore have been managed with directed peripheral vascular intervention (either surgical or endovascular), a “complication-specific” approach. As reviewed earlier, stent-graft repair at the aortic entry tear site has become an additional “revascularization” modality likely to be effective in most patients with dynamic aortic obstruction mechanisms.

More complex is the treatment algorithm in patients with type A dissections complicated by malperfusion syndromes. Involvement of the mesenteric circulation constitutes one of the exceptions to prompt central aortic repair for type A dissection. Deeb et al18 found that the likelihood of death was 33 times greater in patients with acute type A dissections associated with malperfusion syndrome who first underwent immediate ascending aortic surgery as opposed to endovascular peripheral revascularization.

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Natural history and follow-up 

The primary late complication of aortic dissection is aneurysmal dilatation of the outer wall of the false lumen; of patients surviving acute dissection, 25% to 40% will progress to have aneurysmal dilation of the dissected aorta despite medical management.15, 16 In most clinical series of thoracoabdominal aneurysms, some 20% of cases are the sequelae of chronic dissection, for which conventional open repair is typically the only treatment option in contemporary practice.51 Factors that appear to have a significant impact on chronic aneurysm development after dissection include poorly controlled hypertension, maximal aortic diameter of at least 4 cm in the acute phase, and continued patency of the false lumen. Furthermore, some 10% to 20% of those with dissection will subsequently experience late rupture of the aneurysm,14 and conventional surgical repair of such lesions is considerably more complex than with degenerative aneurysms (Fig 12).52

  • View full-size image.
  • Fig 12. 

    Thoracoabdominal aneurysm of chronic dissection etiology 22 years after short graft repair of type B dissection entry tear (large arrow). Note large aneurysmal dilatation of the outer wall false lumen and narrowed compressed true lumen (3 arrows), from which multiple patent intercostals vessels emanate. Open surgical thoracoabdominal resection was curative.

Similar to “hybrid” procedures for degenerative thoracoabdominal aortic aneurysm repair (TAAA), elaborate stent-graft repair of such extensive TAAAs has recently been reported. Mossop et al52 from Australia described their experience in 25 patients with a staged thoracoabdominal and branch vessel endoluminal repair. The initial treatment involved endograft closure of the proximal entry tear and bare metal, self-expanding Z-stenting of the true lumen, thereby supporting the true lumen and stabilizing the dissection flap. At the 1-week follow-up, secondary re-entry tears were then sealed by a variety of endovascular approaches, including placement of branch vessel covered stents, short-segment covered aortic endografts, and coil embolization of the false lumen. In their series over 4 years, they reported no Z-stent migration or stent-related intimal trauma resulting in rupture. Induction of false lumen thrombosis was achieved in 85%. Survival at mean follow-up of 2.5 years was 100%.

Aneurysms that are the sequelae of chronic dissection tend to be more extensive and occur in younger patients compared with degenerative aneurysms. Treatment with effective β-blockade is an essential feature of long-term therapy and follow-up. The rationale of such therapy is based on the recognition that patients with aortic dissection have a systemic illness that places their entire aorta at risk for further dissection, aneurysm, or rupture. Guidelines recommend progressive upward titration of β-blockade to achieve a blood pressure <125/80 mm Hg in usual patients and <120 in those with Marfan syndrome. In addition, aggressive β-blockade has been shown to retard the growth of the aortic root in these patients and may have a similar effect on the thoracoabdominal aorta.53

Serial imaging is the cornerstone of long-term follow up, and axial imaging modalities should encompass the entire aorta. Branched stent-graft technologies are in the developmental stages at present and will likely have an important role in the future management of patients with aneurysms of chronic dissection etiology.

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 Competition of interest: none.

PII: S0741-5214(05)01867-7

doi:10.1016/j.jvs.2005.10.052

Journal of Vascular Surgery
Volume 43, Issue 2, Supplement , Pages A30-A43, February 2006

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