Endovascular Management of Thoracic Dissections
2008; Lippincott Williams & Wilkins; Volume: 117; Issue: 11 Linguagem: Inglês
10.1161/circulationaha.107.690966
ISSN1524-4539
Autores Tópico(s)Cardiac Structural Anomalies and Repair
ResumoHomeCirculationVol. 117, No. 11Endovascular Management of Thoracic Dissections Free AccessResearch ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessResearch ArticlePDF/EPUBEndovascular Management of Thoracic Dissections Warren Swee, MD, MPH and Michael D. Dake, MD Warren SweeWarren Swee From the Department of Radiology, Division of Angiography and Interventional Radiology, University of Virginia Health System, Charlottesville, Va. and Michael D. DakeMichael D. Dake From the Department of Radiology, Division of Angiography and Interventional Radiology, University of Virginia Health System, Charlottesville, Va. Originally published18 Mar 2008https://doi.org/10.1161/CIRCULATIONAHA.107.690966Circulation. 2008;117:1460–1473The first surgical management of aortic dissection was reported in 1935 by Gurin et al,1 who created a distal reentry point in the iliac artery to decompress the false lumen. In 1949, Abbott2 reported the repair of a chronic dissection by wrapping cellophane around the descending aorta to reinforce it. Despite the efforts of these early pioneers and other investigators, it was not until 1955 that a major therapeutic advance was made; this was the year that DeBakey, Cooley, and Creech introduced a revolutionary surgical treatment that involved excision of the intimal tear, obliteration of the false lumen, and either direct reanastomosis or insertion of a prosthetic graft.3 The next great milestone in therapy was introduced by Wheat et al4 in 1965, when they described medical therapy directed toward lowering blood pressure and dP/dt. Since then, investigators have made significant advances in the detection, characterization, and treatment of aortic dissection; however, the morbidity and mortality of this debilitating disease remain alarmingly high, with an overall in-hospital mortality of 27.4% reported by the International Registry of Aortic Dissection (IRAD).5The latest additions to the armamentarium to treat dissection have been based on percutaneous interventional techniques. The minimally invasive nature of these techniques makes them an attractive alternative to open surgical intervention; however, the exact role and long-term durability of these procedures remain to be proven. The earliest endovascular therapies were directed toward the complications of aortic dissections and included angioplasty of an obstructed aorta, stenting of obstructed branch vessels, and fenestration of the dissection flap to relieve mesenteric ischemia.6–8 More recently, the advent of the stent graft has led to a novel endovascular approach aimed at treating the inciting lesion of aortic dissection by obliterating the primary intimal tear.9,10 Since the first reports in 1999, which involved treatment of acute and chronic aortic dissections, investigators have extended the application of stent grafts to treat a variety of related pathologies, such as intramural hematoma (IMH), penetrating atherosclerotic ulcer (PAU), and traumatic dissection.11,12In this report, we begin by reviewing key features of aortic dissection pertinent to endovascular management. We also review the natural history of aortic dissection and conventional medical and surgical management. Then, we introduce the principles and techniques of endovascular management and review the current literature. Specifically, we will discuss the use of stent grafts, fenestration, and branch-vessel stenting in the treatment of aortic dissection and related pathologies.Pertinent FeaturesClassic DissectionThe sine qua non of the classic aortic dissection is a tear in the intima that allows pulsatile blood to penetrate the vessel wall. A cleavage plane develops between the layers of the intima and media and allows a column of blood to form within the intramural space, composing the false lumen. The dissection may propagate in an antegrade or retrograde direction or in both directions. The location of the intimal tear usually occurs in a compromised region of the vessel with underlying mural degeneration. Common causes include long-standing hypertension, connective tissue disorders, and trauma.13It is important to differentiate the primary or entry intimal tear from the secondary or reentry tear(s). Approximately two thirds of primary tears occur in the ascending aorta, with more than half of these located within the first 2 cm of the ascending aorta. The next most common site of the primary tear is the isthmus of the aorta just beyond the ligamentum arteriosum.14 These regions are presumably subjected to the greatest hemodynamic stress, which makes them more susceptible to injury.15 In either location, these tears are 5 times more likely to be transverse in orientation rather than longitudinal. Other sites of primary tears include the descending thoracic aorta, aortic arch, and abdominal aorta, with multiple primary tears seen in ≈8% of cases.14Secondary tears are identified less frequently than primary tears. The secondary tears tend to occur at the ostia of branch vessels, where often circumferential shearing of the intima from the vessel origin has taken place. When present, they allow blood to communicate between the true lumen and the dissecting column.14Whether a reentry tear is present or not, during the acute phase of a dissection, the local environment of the false lumen is highly thrombogenic owing to the exposed adventitial and medial layers. This, in addition to the morphology of the dissection and underlying hemodynamics, may cause the false channel to become completely or partially thrombosed.16Commonly, the true lumen, which is bound by intima, will course along the inferomedial aspect of the distal arch and descending aorta. Typically, the celiac trunk, superior mesenteric artery, and right renal arteries arise from the true lumen, and the left renal artery arises from the false lumen; however, variation in this pattern is frequent. Although branch-vessel obstruction may occur, more commonly, flow to branch vessels remains unobstructed with supply from the true lumen, false lumen, or both the true and false lumens.Related PathologiesRapid advances in imaging technology have led to a greater understanding of aortic dissection variants. In particular, 2 entities (IMH and PAU) have been recognized and, when diagnosed in symptomatic patients, are categorized under the umbrella term "acute aortic syndromes" alongside classic type A and type B dissection.17,18IMH is defined as blood within the intramural space without identification of an intimal disruption. In the purest description, IMH is considered a precursor to dissection, originating from a ruptured vasa vasorum within the medial layer. Subsequent aortic wall weakening or infarction may lead to formation of an intimal tear and result in a classic dissection. However, it is possible that numerous cases of IMH actually represent cases of classic dissection in which the intimal tear is occult on imaging studies.19PAU is defined as focal ulceration of an atherosclerotic plaque that penetrates a variable depth through the intima and may be associated with intramural blood. The hematoma may propagate along the media and lead to aortic rupture or, less frequently, to an aortic dissection with development of a true and false lumen.20,21Malperfusion SyndromeA major complication of aortic dissection is obstruction of flow to the aortic branch vessels. This may involve any aortic branch with 1 or more vascular territories threatened. Critical ischemia of the vascular territory is termed "malperfusion syndrome." It is usually related mechanistically to branch flow obstruction by an intimal flap. Two patterns of branch-vessel involvement are described, dynamic obstruction and static obstruction.22Dynamic obstruction is a term that characterizes the phenomenon of aortic true-lumen collapse or obliteration. Imaging in the setting of dynamic branch-vessel obstruction shows a paper-thin, crescent-shaped true aortic lumen dwarfed by a larger false lumen. The aortic flap has a convex contour that appears to flatten or efface the true lumen. Consequently, flow to all downstream abdominal branches supplied by the true lumen may be compromised. Further obstruction to a particular branch vessel may occur as the dissection flap prolapses over the branch-vessel ostium. Because of the constantly changing position of the intimal flap, particularly in the acute phase, these obstructions can be total or subtotal with persistent or intermittent features and thus are referred to as dynamic obstructions. A clear understanding of the pathophysiology responsible for dynamic obstruction is not apparent; however, large proximal entry tears are frequently observed.22In distinction, static obstruction refers to the effects of direct extension of the dissection process into an individual branch. Typically, flap progression into a branch is tolerated. This occurs when the false lumen within the branch vessel develops a distal reentry tear that allows double-barrelled flow to the vascular bed with both true- and false-lumen contribution. In most cases, biluminal perfusion of the branch-vessel tissue bed is sufficient and is not associated with serious ischemia or the risk of necrosis. However, despite the "reentry" branch configuration described, the physical presence of the flap may cause various degrees of static obstruction depending on the artery involved, the adequacy of flow, and the presence of underlying lesions.22The potential for profound malperfusion exists when the false lumen within the branch does not have a reentry point in the vessel. As a result, the false lumen is a blind cul-de-sac that enlarges and compresses the true lumen. The severity of true lumen obstruction is maximum at the distal margin of false-lumen extension, where a prominent bulbous contour is frequently evident. This "no reentry" branch configuration of static obstruction is often associated with severe ischemia related to the absence of false-lumen flow within the branch and a severely compromised true lumen. Fortunately, static obstruction with no reentry of the false lumen occurs relatively infrequently compared with the more common pattern of false-lumen reentry.22In addition, it is possible for a combination of dynamic and static obstruction with or without branch-vessel reentry to coexist within an individual patient, which creates an interesting "signature" profile depending on the particular branch vessels affected and mechanism(s) of involvement by the process. As we will see, differentiating between a dynamic or static obstruction has significant implications for endovascular management.9,22Classification SystemsThe 2 most common anatomic classifications of aortic dissection are the DeBakey and Stanford classifications. Under the DeBakey system, type I dissection begins in the proximal aorta and involves both the ascending and descending thoracic aorta, type II dissection is confined to the ascending aorta, and type III is confined to the descending aorta. Under the Stanford system, type A dissection involves the ascending aorta, whereas type B dissection does not.The convenience and prognostic value of the Stanford system has resulted in its popular use; however, an important feature that is not distinguished in the Stanford system is the location of the primary tear. In a typical type A dissection, the primary tear is located in the ascending aorta, whereas in a retrograde type A dissection, the tear is located in the descending aorta. This detail has a profound influence on the current feasibility of stent-graft management.Aortic dissections are temporally classified as acute when identified ≤2 weeks from the onset of symptoms and chronic when identified >2 weeks from the onset of symptoms, with the highest morbidity and mortality occurring during the acute phase. Some investigators further classify the acute phase as early (<24 hours) and late (≥24 hours to 2 weeks) from the onset of symptoms.In addition, type B dissections are often classified as complicated or uncomplicated. Complicated cases involve rupture, lesion progression, impending rupture, refractory hypertension, localized large false aneurysm, continued pain, or malperfusion syndrome and are associated with worse outcomes.23,24Natural History and Conventional ManagementConventional treatment of both type A and B dissection involves prompt management of systemic blood pressure and dP/dt to stabilize the extent of dissection, avoid false-lumen dilatation, reduce pain, and decrease risk of rupture. In type A dissection, concomitant emergent surgical graft replacement with or without aortic valve repair or replacement is mandated to reduce the risk of sudden death associated with aortic rupture, aortic regurgitation, pericardial tamponade, coronary artery involvement, and malperfusion of the brain. In uncomplicated type B dissection, surgical therapy has shown no superiority over medical management alone and is reserved for complicated cases.25Acute Type A DissectionAlthough shown to be superior to medical management alone, surgical management is still associated with alarmingly high rates of morbidity and mortality. In a review of 547 type A dissections, IRAD investigators demonstrated a hospital mortality rate of 27% for those patients treated surgically.26 In another IRAD report, surgical repair was associated with in-hospital mortality rates of 10% by 24 hours, 16% by 7 days, and nearly 20% by 14 days.5 Long-term survival for patients treated with surgery who were discharged alive has been shown to be 96% at 1 year and 91% at 3 years.27Patients with retrograde type A dissection (DeBakey type IIId) represent an important subgroup that comprises 4% to 20% of all type A cases.16,23,28,29 In these individuals, the inciting primary tear is typically positioned in the distal arch, with retrograde extension of the dissection process to the ascending aorta. This poses a dilemma for surgical repair that involves either excision of the entry tear with replacement of both the ascending aorta and aortic arch, which is associated with high morbidity and mortality, or graft replacement of the ascending aorta alone without excision of the primary tear, which leaves the patient at risk of postoperative aortic rupture.16,23,28–30 Regardless, conventional therapy mandates immediate surgical repair in this patient subgroup.Acute Type B DissectionOwing to the small risk of aortic rupture and sudden death and the high morbidity and mortality associated with surgical repair of the descending aorta, medical treatment alone is advocated for uncomplicated type B dissection. Surgery is typically reserved for complicated type B dissections. IRAD investigators reviewed 175 patients treated according to this complication-specific approach and identified in-house mortality rates of 11% and 31% for medical and surgical treatment, respectively.5 Patients who undergo surgery also have a high rate of morbidity; in particular, paraplegia has been reported in 1.5% to 19% despite advances in surgical technique.31 IRAD investigators also performed long-term evaluation of outcomes for patients discharged after hospital management of type B dissection. This analysis identified 3-year survival rates of 78% and 83% for patients treated medically and surgically, respectively.32Because medical therapy alone does not stop flow within the false lumen, 20% to 50% of patients who survive the acute phase develop aneurysmal dilatation of the false lumen within 1 to 5 years after onset.15,33,34 In this regard, the majority of late deaths that occur in patients with type B dissection initially managed by medical therapy are due to rupture, extension of dissection, and perioperative mortality of subsequent aortic or vascular surgeries. In fact, the long-term survival of patients with type B dissection remains worse than that of patients with type A dissection.27,32Aortic Dissection Variants (IMH and PAU)Intramural HematomaThe natural history of IMH is not well understood; however, it accounts for 5% to 20% of acute aortic syndrome cases.13,21,35,36 IRAD investigators demonstrated an association between increased hospital mortality and proximity of IMH to the aortic valve, regardless of medical or surgical treatment.18 A meta-analysis of 11 studies identified an overall mortality of 34% for type A IMH, 24% for those treated surgically and 47% for those treated medically.19 Overall mortality for type B IMH was 14%, with little difference between surgical (15%) and medical (13%) groups. Thus, the treatment paradigm for IMH parallels that of classic aortic dissection, with surgical repair favored for type A IMH and medical management preferred for type B IMH.Penetrating Atherosclerotic UlcerAlthough PAU is poorly understood, its prognosis is thought to be much poorer than that of classic aortic dissection.37 Coady et al20 reported the risk of aortic rupture in patients with PAU and acute symptoms to be 40% compared with patients with type A or type B dissection, for whom the rupture risks were 7% and 3.6%, respectively. Although no consensus treatment strategy exists, early surgical graft replacement of the aorta has been advocated in symptomatic patients.38,39Chronic DissectionThose patients who survive the acute stage of aortic dissection, which is associated with the greatest mortality, by definition have chronic dissection. The 30-day survival rate for this population is high at 90%, independent of whether they were managed medically or surgically.40 Medical therapy is therefore recommended for patients with both type A and type B chronic dissection. Surgery is reserved for those who develop an aneurysm, rupture, peripheral branch-vessel compromise, or other complications.41,42Malperfusion SyndromeIt is estimated that branch-vessel involvement complicates approximately one third to one half of all aortic dissections.24,43 With control for both age and gender, branch-vessel involvement presents a nearly 3-fold increased likelihood of in-hospital morality in acute type B dissections.44Primary surgical aortic repair results in successful revascularization in the vast majority of patients with type B dissection; however, the presence of renal or mesenteric ischemia has been correlated with especially high surgical mortality rates of 70% and 87%, respectively.24,43,45,46 For this reason, alternative surgical procedures have been explored to address organ ischemia specifically. In particular, surgical aortic fenestration has been shown to relieve malperfusion syndrome in 93% to 100% of cases, with an in-hospital mortality rate of 0% to 43%.47–49Endovascular ManagementEndovascular management of dissection comprises 3 major treatments: (1) aortic stent-graft placement, (2) dissection flap fenestration, and (3) branch-vessel stenting. Typically, 1 or more of these techniques is used to treat aortic dissection. In some cases, endovascular techniques may obviate the need for surgical management, whereas in other cases, endovascular techniques are complementary to surgical repair.Stent-Graft TechnologyThe development of thoracic aortic stent grafts has largely followed in the footsteps of abdominal aortic stent-graft technology used primarily to treat abdominal aortic aneurysms. The earliest feasibility and safety studies of thoracic stent grafts were performed in 1992 to treat thoracic aortic aneurysms. Since then, the number of applications of this technology has grown rapidly to include the management of aortic dissection and dissection variants. Although treatment of descending thoracic aneurysm with a stent graft (TAG; WL Gore and Associates, Flagstaff, Ariz) is currently approved by the US Food and Drug Administration, the use of stent grafts to treat other indications such as aortic dissection and its related pathologies remains off-label.The first-generation stent grafts were primarily homemade devices that married graft materials such as polyester or polytetrafluoroethylene to modified self-expanding stents such as the Gianturco Z stent. Most delivery systems were large (24F to 27F), relatively rigid, and difficult to deploy smoothly and accurately owing to extensive frictional resistance. Significant improvements were made in the second generation of devices, which are largely manufactured commercially. However, as we will demonstrate, numerous design issues remain. Current devices include the TAG (WL Gore and Associates), Talent (Medtronic Inc, Santa Rosa, Calif), TX-2 (Cook Inc, Bloomington, Ind), Relay (Bolton Medical, Inc, Sunrise, Fla), and Valiant (Medtronic Inc).Principles and Techniques of Endovascular ManagementStent-Graft ManagementThe rationale of stent-graft management is 2-fold. First, in the acute phase, the use of stent grafts may prevent imminent aortic rupture and relieve dynamic branch-vessel obstruction. Second, stent-graft management may promote thrombosis of the thoracic false lumen and decrease the long-term morbidity associated with patency of the false lumen, including aneurysmal dilatation, late aortic rupture, and late mortality.9,16Stent-graft treatment is predicated on the ability to cover the primary intimal tear and create a seal to stop the flow of blood entering the false lumen and prevent the transmission of systemic pressure across the major intimal defect (Figures 1 and 2). If the seal is adequate, cardiac output is redirected into the true lumen and rapid and the false lumen simultaneously decompresses (which relieves dynamic obstruction of branches supplied by a diminutive true lumen). As a result, within seconds, the true lumen diameter typically enlarges, with markedly improved flow. The immediate hemodynamic and morphological alterations may prevent imminent rupture and relieve aortic true-lumen collapse and branch-vessel ischemia.9Download figureDownload PowerPointFigure 1. Right anterior oblique aortogram of a Stanford type B dissection (A and B) demonstrates a jet of contrast (arrows) passing from the true lumen (TL) to the false lumen (FL) that demarcates the primary tear, with contrast opacification of the true lumen preceding that of the false lumen. Left anterior oblique aortogram (C) again demonstrates the true and false lumens. After stent-graft repair of the dissection (D), the primary tear is sealed, with no contrast identified in the false lumen. Computed tomography (CT) images before treatment (E, F, and G) demonstrate the aortic dissection, with greater contrast opacification of the true lumen than of the false lumen. The primary tear (arrow) is well seen as an interruption in the dissection flap (F). A large left pleural effusion is also noted. CT images 4 months after stent-graft treatment (H, I, and J) demonstrate increased diameter of the true lumen, with no change in transaortic diameter, and complete thrombosis of the false lumen. The left pleural effusion is significantly decreased in size.Download figureDownload PowerPointFigure 2. Axial (A and B) and sagittal (C) CT images of a retrograde type A aortic dissection demonstrate the primary tear (B, arrow) to be positioned in the distal thoracic aortic arch just beyond the left subclavian artery. Contrast opacification of the true lumen (TL) and false lumen (FL) is seen distal to the left subclavian artery. Panel A also demonstrates retrograde involvement of the ascending thoracic aorta by intramural thrombus (black arrows) and the development of hemopericardium (white arrowheads). Axial (D and E) and sagittal (F) CT images 6 months after treatment with a stent graft positioned just beyond the left common carotid artery demonstrate successful sealing of the primary tear, with complete resolution of hemopericardium and ascending aortic intramural thrombus, as well as complete obliteration of the false lumen along the descending thoracic aorta. Note the origin of the left subclavian artery (LSA) has been covered by the stent graft, yet it continues to receive retrograde flow through collateral circulation (F).Furthermore, stent-graft management of retrograde type A dissection and type B dissection has been shown to decrease flow in the false lumen and induce false-lumen thrombosis.50,51 Again, this is a critical point, because natural history studies of type B dissection have shown 20% to 50% of patients who receive medical therapy alone and survive the acute phase ultimately develop aneurysmal dilatation of the false lumen within 1 to 5 years.15,33,34 Even if complete thrombosis of the false lumen does not occur, it is likely that partial thrombosis and decreased flow will limit the progression to aneurysmal dilatation.9To obliterate the primary tear, an adequate seal zone is required. One of the anatomic requirements is a proximal landing zone (relative to the primary tear) of at least 15 to 20 mm. The ideal landing zone should be uniform in shape and free of significant disease; however, this ideal is rarely met, because the position of the primary tear and its proximity to branch vessels usually requires device deployment within a dissected segment. A common dilemma is selection of the "correct" device dimension, because the true lumen is generally crescentric or elliptical in shape and a fraction of the overall transaortic diameter. Most operators base their selection on more than 1 measurement, the most compelling of which is the diameter of the nondissected aorta immediately proximal to the entry tear. In the setting of a classic entry location just distal to the left subclavian artery origin, the segment between the left carotid and left subclavian arteries is used. This is the best estimate of the original size of the involved aorta before dissection. This measurement is oversized by ≈10% and used to select the stent-graft diameter. The oversizing factor ensures secure anchoring and a tight circumferential seal.Depending on the type and size of the stent graft, currently available devices will require delivery systems that are 20F to 24F in size. The iliofemoral arteries should be assessed routinely to ensure that an adequate intraluminal diameter to accommodate introduction of the device exists. Access usually involves surgical exposure of the common femoral artery. In the case of small or heavily calcified femoral arteries, surgical exposure of the iliac arteries or aorta with or without placement of a graft conduit may be required. Recently, in select patients, stent-graft procedures have been performed entirely percutaneously, with the puncture sites closed by commercially available suture-mediated access-closure devices.52 The obvious benefits of this approach over surgical exposure are the decreased time to recovery and possible reduced risk of infection, lymphocele, seroma, and postoperative scar.FenestrationFenestration of the intimal flap serves as an alternative endovascular treatment to stent-graft management of aortic dissection (Figure 3). Rather than treating the entry tear, which increases the resistance to false-lumen inflow, fenestration is aimed at artificially creating a distal reentry channel, which decreases the resistance to false-lumen outflow.53 The reentry channel is not dissimilar to spontaneously formed reentry tears that help to balance pressures within the aortic lumens. The equalization of pressure between the true and false lumen alone may relieve dynamic obstruction of the aorta and branch vessels. In addition, strategic positioning of fenestrations may locally redirect a sufficient amount of blood flow to perfuse compromised end organs.8,54–56 Although beneficial in the acute phase, the continued patency of the false lumen potentially predisposes the patient to less salutary long-term outcomes, such as false-lumen dilatation, aneurysm development, and rupture, compared with those after stent-graft placement and thoracic false-lumen thrombosis.16Download figureDownload PowerPointFigure 3. This patient underwent surgical repair for a Stanford type A dissection several years previously and returned complaining of severe lower-extremity claudication. An aortogram (A) demonstrated flow-limiting compression of the true lumen by the false lumen (arrows) between the levels of the celiac trunk and an infrarenal aortic stent as the cause of claudication. The aortic stent seen in panel A was placed soon after surgical repair of the dissection to improve distal flow. With use of an Outback reentry catheter, wire access was obtained from the true lumen to the false lumen (B). Angioplasty alone was insufficient in relieving the obstruction; thus, the fenestration was reinforced with a self-expanding stent (C). The postfenestration aortogram (D) demonstrates improved flow through both the true and false lumens.Because stent-graft treatment generally achieves similar results with a greater likelihood of false-lumen thrombosis, stent-graft management is preferred over fenestration as the primary mode of treatment in patients with malperfusion caused by dynamic obstruction. However, fenestration continues to be a valuable option in poor surgical candidates and in cases in which stent-graft treatment is not available or not feasible owing to anatomic constraints. Fenestration may also serve as a valuable adjunctive treatment in cases in which surgical repair or stent-graft repair inadequately addresses the indications for intervention.Currently, percutaneous balloon fenestration of the flap is most frequently performed distally in the abdominal aorta at the level of the aortic bifurcation, usually to manage unilateral lower-extremity ischemic symptoms. Several approaches to dissection flap fenestration have been described.53–55,57,58 The 2 most commonly detailed techniques involve combined intravascular ultrasound and fluoroscopic guidance or fluoroscopic guidance alo
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