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Thoracic Endovascular Aortic Repair for Retrograde Type A Aortic Dissection with an Entry Tear in the Descending Aorta
CLINICAL STUDY
Thoracic Endovascular Aortic Repair for Retrograde Type A Aortic Dissection with an Entry Tear in the Descending Aorta Chang Shu, MD, PhD, Tun Wang, MD, PhD, Quan-ming Li, MD, PhD, Ming Li, MD, PhD, Xiao-hua Jiang, MD, Ming-yao Luo, MD, PhD, and Xin Li, MD, PhD
ABSTRACT Purpose: To report the immediate and follow-up outcome of thoracic endovascular aortic repair (TEVAR) in highly selected patients with retrograde type A aortic dissection (RAAD) and an entry tear in the descending aorta. Materials and Methods: TEVAR was performed in 17 patients with RAAD and an entry tear in the descending aorta. None of the patients had severe aortic regurgitation, cardiac tamponade, coronary artery involvement, or brain ischemia. The false lumen in the ascending aorta was patent in nine patients. Two patients had acute malperfusion of the branched artery. Computed tomography (CT) was performed 14 days, 3 months, and 6 months after the intervention and annually thereafter. Results: All procedures were technically successful, with complete coverage of the entry tear and complete thrombosis of the false lumen in the ascending aorta. All patients survived through the follow-up period (25.7 months ⫾ 17.2). TEVAR resulted in thrombosis of the false lumen, reabsorption of the false lumen thrombus, and enlargement of the true lumen. The mean maximal diameter of the ascending aorta and the false lumen in the ascending aorta significantly decreased after TEVAR. At the distal edge of the stent graft, the mean diameter of the descending aorta and the false lumen markedly decreased after TEVAR. Complete thrombosis of the false lumen was observed at the distal edge of the stent graft in 16 (94.1%) patients and at the diaphragmatic level in 9 (52.9%) patients. Conclusions: TEVAR for RAAD with an entry tear in the descending aorta is a safe and effective technique in highly selected patients.
ABBREVIATIONS DSA ⫽ digital subtraction angiography, RAAD ⫽ retrograde type A aortic dissection, TEVAR ⫽ thoracic endovascular aortic repair
Retrograde type A aortic dissection (RAAD) with an entry tear in the descending aorta is a special subset of aortic dissection. RAAD may extend retrograde into the ascending aorta or even the aortic root and antegrade into the abdominal aorta simultaneously (1,2). Patients with RAAD
From the Department of Vascular Surgery, The 2nd Xiang-ya Hospital of Central-south University, Changsha, Hunan, China. Received August 17, 2011; final revision received December 21, 2011; accepted December 26, 2011. Address correspondence to C.S.; E-mail: changshu_vascular@ 163.com Table E1 is available online at www.jvir.org. None of the authors have identified a conflict of interest. © SIR, 2012 J Vasc Interv Radiol 2012; 23:453– 460 DOI: 10.1016/j.jvir.2011.12.023
have an extremely poor prognosis, with the risk of cardiac tamponade, severe aortic regurgitation, an entry tear in the ascending aorta proximal aortic arch, or aortic rupture (2– 4). The treatment strategy considered to be most effective is simultaneously obliterating the blood flow through the entry tear and inducing thrombosis of the false lumen. In recent years, total arch replacement with elephant trunk implantation with a stent has been advocated as a feasible treatment in patients with RAAD. However, this operation is extremely complicated and needs to be performed under hypothermic cardiopulmonary bypass with selective cerebral perfusion through a median sternotomy (3,5–7). Although this improved surgical technique can repair proximal aortic lesions and close the entry tear in a single-stage operation, it is associated with high mortality and morbidity, likely owing to the suboptimal preservation of critical organs and difficulties in hemostasis intraoperatively, especially in patients with poor clinical health status.
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Table 1. Baseline Characteristics and CT Findings of Study Patients
FL Patency Yes No Yes Yes No No
Pleural Effusion Left Bilateral Bilateral Bilateral No Left
Pericardial Effusion No Yes No Yes No Yes
Male Male Male Male
No Yes No No
Bilateral No Left Bilateral
No No No No
RCIA No No No
49 62 59
Female Male Male
Yes Yes No
No No Left
No No Yes
No No No
58 48 39 39
Male Male Male Male
Yes Yes No Yes
Bilateral Bilateral No Right
Yes No No No
No No No No
Patient 1 2 3 4 5 6
Age (y) 62 42 65 43 59 47
7 8 9 10
57 57 71 69
11 12 13 14 15 16 17
Gender Male Male Male Male Male Male
Malperfusion* No Right renal artery No No No No
Preoperative Comorbidities HTN HTN HTN HTN HTN HTN, DM, sleep apnea syndrome, obesity HTN HTN HTN, DM HTN, gastric ulcer, Legionella pneumonia HTN HTN HTN, DM, gout, angina pectoris Refractory HTN, DM HTN HTN, hepatitis B HTN
DM ⫽ diabetes mellitus, FL ⫽ false lumen in ascending aorta, HTN ⫽ hypertension, RCIA ⫽ the right common iliac artery. * Malperfusion means the branched artery of the aorta was totally compressed.
Endovascular stent graft placement is emerging as a less invasive alternative to surgical procedures for patients with aortic dissection or aneurysm. The efficacy and safety of this approach have been reported for the treatment of infrarenal abdominal aortic aneurysm and DeBakey III aortic dissection with entry tears distal from the orifice of the left subclavian artery (8 –10). More recently, thoracic endovascular aortic repair (TEVAR) was attempted for the treatment of RAAD in highly selected patients (9,11,12). However, there is no consensus on the safety and efficiency of TEVAR in patients with RAAD. We report our experiences using TEVAR to close the entry tear and induce thrombosis of the false lumen of RAADs, including immediate clinical outcome and follow-up examination.
MATERIALS AND METHODS Patients The hospital’s review committee approved this retrospective study, and written informed consent was obtained from all patients or their relatives. From April 2006 to January 2011, 31 consecutive patients with RAAD were admitted to our hospital and underwent computed tomography (CT) scanning with contrast enhancement and three-dimensional reconstruction. Patients who met the following criteria were considered to be good candidates for TEVAR: (a) no signs of cardiac tamponade or severe aortic regurgitation (grade III or better), (b) no involvement of the coronary artery by
aortic dissection, (c) no signs of cerebral ischemia, (d) anatomically adequate femoral and iliac arteries, and (e) no entry tear in the ascending aorta and proximal aortic arch. TEVAR was performed in 17 (54.8%) patients. The baseline characteristics and CT angiography findings of the patients included in this study are summarized in Table 1. There were 16 men and 1 woman with an average age of 54.5 years ⫾ 10.2 (range 39 –71 y). These patients were referred to our hospital 5 days ⫾ 2 after the onset of symptoms (range 1–10 d). All patients had a history of hypertension for 8 years ⫾ 2 (range 1–10 y) and presented with precordial or back pain at symptom onset. The false lumen of the ascending aorta was patent in nine patients (Fig 1a2 and 1b2). The false lumen of the ascending aorta was thrombosed in the remaining eight patients. Two patients (patients 2 and 7) had acute ischemia of the right renal artery (patient 2) (Fig 2a1 and 2a2) and the right common iliac artery (patient 7). TEVAR was performed under emergency conditions in these two patients. Both of the ischemic arteries originated from the true lumens, which were completely compressed by the false lumens. There were 12 patients with pleural effusions; 7 of these patients (patients 2, 3, 4, 7, 10, 14, and 15) had bilateral pleural effusions. A small amount of pericardial effusion was found in five patients (patients 2, 4, 6, 13, and 14). None of these patients experienced cardiac tamponade. Only one patient (patient 10) had a high fever and cough with a little yellow sputum at hospital admission. A chest
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Figure 1. CT images obtained at three different times: on admission (a), after conservative treatment for 2 weeks and before surgery (b), and 13 months after TEVAR (c). RAAD involved the brachiocephalic artery and left subclavian artery (1 in a1). After conservative treatment for 2 weeks, the false lumen of the brachiocephalic artery thrombosed and reabsorbed (2 in b1), and the blood flow in the false lumen of the ascending aorta decreased (compare 4 in b3 with 3 in a3). Acceptable aortic remodeling was obtained at follow-up (c).
CT scan showed little bilateral pleural effusion, and Legionella pneumophila antibody was found in the blood serum.
Images and Stent Grafts Patients underwent emergent CT angiography on admission and digital subtraction angiography (DSA) at the beginning of TEVAR. The measurements were obtained from CT angiography and DSA. The maximal diameter of the as-
cending aorta on admission was 44 mm ⫾ 4 (range 38 –50 mm). The distance between the left subclavian artery and the primary entry tear were 2.8 mm ⫾ 2.2 (range 0.5–10.0 mm) (Table E1; available online at www.jvir.org). The bilateral carotid artery, vertebral arteries, and circle of Willis were evaluated to determine their blood supply by CT angiography before TEVAR. The selected diameter size of the stent graft was 10%–15% greater than the diameter of
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Figure 2. CT images obtained at three different times (patient 2) with acute malformation of the right renal artery: on admission (a), 3 months after TEVAR (b), and 40 months after TEVAR (c). The right renal artery originated from the totally compressed true lumen (a1), and the left renal artery was coming from the false lumen (a2). At 3 months after TEVAR, the true lumen was reopened, and blood perfusion was recovered in the right renal artery (b1); blood flow was still delayed in the left renal artery (b2). At 40 months after TEVAR, the right renal artery was perfused well (c1), but the left renal artery was perfused by the false lumen, and the left kidney atrophied (c2).
the aorta approximately 2 cm proximal to the entry tear, not exceeding the diameter of the ascending aorta. Three types of devices were implanted in the 17 patients, including 10 Hercules stent grafts (MicroPort Medical [Shanghai] Co, Ltd, Shanghai, China), 5 Zenith stent grafts (Cook, Inc, Bloomington, Indiana), and 2 Valiant stent grafts (Medtronic, Inc, Minneapolis, Minnesota). The mean proximal and distal diameters of stent grafts were 33.4 mm ⫾ 2.1 (range 28 –36 mm) and 30.9 mm ⫾ 2.5 (range, 28 –36 mm) (Table E1; available online at www. jvir.org). The mean length of stent grafts was 143 mm ⫾ 22.4 (range 80 –160 mm) (Table E1; available online at www.jvir.org).
Thoracic Endovascular Aortic Repair Antihypertensive drugs and beta blockers was initiated for lowering arterial wall tension immediately after RAAD was diagnosed. All procedures were performed in a hybrid unit with fluoroscopic and angiographic guidance. General anesthesia with tracheal intubation was administered in 13 patients, and local anesthesia was administered in 4 patients (patients 7, 9, 12, and 13). A 5-F sheath was inserted into the left brachial artery, and a 5-F calibrated angiographic pigtail catheter was advanced into the ascending aorta to perform arteriography and permit arteriographic evaluation of the distance between the left subclavian artery and the primary entry tear. Arteriotomy was performed on the femoral artery originating from the true lumen. A 5-F pigtail catheter and a 0.035-inch guide wire were advanced into the true lumen via this arteriotomy site until reaching the ascending aorta.
A Lunderquist Extra Stiff Wire Guide (Cook, Inc) was advanced into the ascending aorta using the catheter exchange technique. After DSA was performed to confirm that the catheter was in the true lumen and measurement was made of the relative data of the aortic lesion again (Fig 3a), the position of the proximal landing zone was marked on the screen. After intravenous administration of heparin sodium (0.5 mg/kg), the stent graft delivery system was advanced over the Lunderquist Extra Stiff Wire Guide under fluoroscopy and placed within the true lumen (Fig 3b). When the proper position was reached, the systolic pressure was decreased to less than 80 –90 mm Hg to ensure precise stent graft positioning. The stent graft was deployed by pulling back the sheath with the mandrel pusher firmly fixed. Coverage of the primary entry tear was achieved by stent graft, and the left subclavian artery was intentionally occluded in four patients (patients 4, 11, 15, and 17). Angiography was performed immediately after deployment to confirm coverage of the entry tear, sealing of the aortic dissection, and blood flow of the aortic lumen and branch vessels (Fig 3c). After the removal of the large sheath, the arteriotomy was repaired.
Follow-up Examination CT images were acquired at 14 days, 3 months, and 6 months after the intervention and annually thereafter. Diameters of the ascending aorta, the false lumen in the ascending aorta, the descending aorta, and the false lumen at the distal end of the stent graft were measured by CT before and after stent graft placement in all patients. At all
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Figure 3. DSA performed during TEVAR. The false lumen progressed retrograde to the ascending aorta (arrow), and the patent false lumen extended to the aortic arch reaching the orifice of the brachiocephalic artery (a). The stent graft delivery system was advanced into the true lumen through the femoral artery (b). Angiography performed after deployment of the stent graft confirmed the sealing of the aortic dissection and blood flow through the aortic lumen and branch vessels. The left subclavian artery was intentionally occluded (c).
levels, the diameter of the aorta and false lumen were measured along a line perpendicular to the intimal flap.
Statistical Analysis All values are expressed as mean ⫾ standard deviation. The diameters of the aortae and false lumens were compared with Student paired t test. P ⬍ .05 was considered statistically significant.
RESULTS Immediate Outcome After initial conservative treatment with antihypertensive drugs and beta blockers, the symptoms of precordial and back pain were significantly relieved and clinical health status markedly improved in all patients. The acute aortic dissection became relatively stable and recovered to some extent. One patient had involvement of the brachiocephalic artery and left subclavian artery on admission (Fig 1a1). At 2 weeks after conservative therapy, the thrombosis of the false lumen and the absorption of the false lumen thrombosis were observed in the brachiocephalic artery (Fig 1b1). TEVAR was successfully performed in all patients. The mean time interval between the onset of symptoms and TEVAR was 15.8 days ⫾ 6.7 (range 2–30 d) (Table E1; available online at www.jvir.org). Two patients (patients 2 and 7) underwent TEVAR in the acute phase 2 days (patient 2) and 4 days (patient 7) after the onset of symptoms. The remaining 15 patients underwent TEVAR in the chronic phase more than 14 days after symptom onset. The mean operative time was 82.1 minutes ⫾ 16.9 (range 50 –110 min) (Table E1; available online at www.jvir.org). The stent grafts were placed in the true lumen of the proximal
descending aorta in 16 patients and in the middle descending aorta in 1 patient (patient 9). Complete coverage of the entry tear was accomplished after deployment of the stent graft in all patients. DSA performed after the intervention showed no residual flow of blood contrast medium into the false lumen of the ascending aorta. No aorta-related complications, including endoleak, malperfusion of aortic branches, or aneurysmal degeneration, were observed in any of the patients. Complete thrombosis of the false lumen in the ascending aorta and partial reabsorption of thrombosis were observed on CT scan after TEVAR in all patients. The blood flow of the fully compressed right renal artery (patient 2) (Fig 2b1 and 2b2) and right common iliac artery (patient 7) recovered immediately after emergency TEVAR. In patient 2, angiography after TEVAR showed that the left renal artery originating from the false lumen was perfused as well as before TEVAR. Because the distance between the left subclavian artery and primary entry tear was ⬍ 1.5 cm and the left vertebral artery did not play a dominant role according to CT angiography performed before TEVAR, the left subclavian artery was intentionally covered in 4 (23.5%; patients 4, 11, 15, and 17) of 17 patients (Table E1; available online at www.jvir.org). No related complications from intentional coverage of the left subclavian artery, including type II endoleak, ischemia, or steal syndrome, were observed in these four patients. The pleural or pericardial effusions were not severe before TEVAR in nine patients, and drainage of the effusions was not performed. Chest radiography and echocardiography showed that effusion progressively decreased after TEVAR and faded away 7– 42 days later. Preexisting L. pneumophila was treated with intravenous injection of sensitive antibiotics in patient 10, and this patient recovered from TEVAR uneventfully. There were no instances of progression of the dissection, formation of new entry
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Figure 4. Individual aortic remodeling after TEVAR. Measurement on CT at follow-up found that the maximal diameter of the ascending aorta (a) and the false lumen in the ascending aorta (b) significantly decreased compared with measurements on admission. At the level of the distal edge of the stent graft, the diameter of the descending aorta (c) and the false lumen (d) was also markedly reduced compared with the CT measurement between admission and follow-up. Mean values ⫾ standard deviation are shown in the full lines with bars.
tears, aortic rupture, ischemia of aortic branches, paraplegia, cardiac tamponade, severe aortic regurgitation (grade III or greater), or death in any of the patients during their hospital stay.
Follow-up Outcome Patients received antihypertensive treatment after discharge from the hospital. The mean duration of follow-up was 25.7 months ⫾ 17.2 (range 4 – 60 mo), and median duration was 22 months. All patients survived through follow-up. The shrinkage of enlarged aortae and reabsorption of false lumen thromboses at the level of the ascending and descending aortae distal to the stent grafts was evident in all 17 patients on CT scans performed after TEVAR (Fig 1c1, 1c2, and 1c3). The mean maximal diameter of the ascending aorta decreased from 44.1 mm ⫾ 4.3 before TEVAR to 37.7 mm ⫾ 3.9 on the latest available CT images after TEVAR (P ⬍ .001) (Fig 4a). The mean diameter of the false lumen in the ascending aorta decreased from 14.8 mm ⫾ 5.6 before TEVAR to 0.6 mm ⫾ 1.8 on the latest follow-up CT images (P ⬍ .001) (Fig 4b). At the level of
the distal edge of the stent graft, the mean diameter of the descending aorta decreased from 34.1 mm ⫾ 8.1 before TEVAR to 28.4 mm ⫾ 3.3 on the latest CT images (P ⫽ .007) (Fig 4c). The mean diameter of the false lumen decreased from 22.7 mm ⫾ 9.3 before TEVAR to 2.8 mm ⫾ 4.8 on the latest CT images (P ⬍ .001) (Fig 4d). Complete thrombosis of the false lumen was observed at the distal edge of the stent graft in 16 (94.1%) patients and at the diaphragmatic level in 7 (41.2%) patients. There were patent false lumens in the distal portion of the descending aorta, abdominal aorta, or both in 10 (58.8%) patients. The reentry tear was present in the distal portion of the descending aorta in two (11.7%) patients including patient 15, in the abdominal aorta in seven (41.1%) patients, and in the common iliac artery in one (5.8%) patient. The false lumen below the reentry tear remained patent but did not enlarge during follow-up in these patients because little blood flow infused into the false lumen through the reentry tear below the stent graft. In patient 2, blood flow of the right renal artery recovered well, and the patient lived without any discomfort during the 40-month follow-up
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period, although the left renal artery supported by the false lumen was poorly perfused with left kidney atrophy (Fig 2c1 and 2c2). At 3 months after TEVAR, patient 15 complained of recurrent dull back pain. CT angiography detected that a new entry tear was located in the distal edge of the stent graft, and considerable blood flow infused into the false lumen through the new entry tear 4 months after TEVAR. The preoperative cross-sectional diameters were 15 mm and 35 mm in the short axis and long axis of the true lumen at the level of the entry tear that subsequently occurred 3 months after TEVAR. An additional stent graft was suggested to cover the new entry tear after the first TEVAR, but the patient did not consent to the second endovascular treatment because of financial reasons. After conservative therapy, all symptoms were relieved; however the new entry tear persisted.
DISCUSSION Retrograde aortic dissection occurs more frequently than is generally realized; the incidence ranges from 5%–25% among type A aortic dissections and 10%–27% among type III aortic dissections (1–3,9,13,14). Appropriate management of RAAD is controversial. Medical therapy has been recommended in patients without severe complications. In unstable RAAD, aggressive surgical treatment should be considered after initial medical therapy. Kaji et al (2) reported that RAAD with a thrombosed false lumen in the ascending aorta could be treated medically with timed surgical repair. Surgery is commonly performed for RAAD to avoid lethal complications such as cardiac tamponade, severe aortic regurgitation, aortic rupture, and ischemia of supraaortic branches and coronary arteries. The replacement of the ascending aorta or total arch has been performed previously, but in these studies the false lumen and distal dissection remained untreated (1,4,5). Erbel et al (15) reported that the replacement of the ascending aorta in RAAD was associated with a false lumen patency rate of 83%; mortality in patients with a patent false lumen was as high as 43%. These authors concluded that a surgical procedure that could not eliminate blood flow into the false lumen was responsible for the poor prognosis of RAAD (15). Similarly, other institutions reported that a persistent patent distal false lumen correlated closely with various late complications (14,16). Arch replacement might be performed in patients with proximal aortic lesions through a median sternotomy, and placement of the descending aorta with resection of the entry tear was simultaneously carried out through lateral thoracotomy, but this combined technique was complicated and had many complications. Kazui et al (4) recommended total replacement of the ascending aorta and aortic arch associated with the resection of an entry tear in RAAD, but the descending aortic dissection was still unresolved. More recently, total arch replacement with antegrade elephant
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trunk implantation with a stent into the proximal descending aorta was proposed to repair proximal aortic lesions and induce thrombosis of the distal false lumen (3,5–7). Sun et al (3) reported surgical mortality of 6.06% in 33 patients with RAAD. As reported in many institutions, postoperative complications include paraparesis, stroke, spinal core injury, renal failure, and reexploration for bleeding (3,5–7). TEVAR of aortic dissection plays a curative role by covering the primary entry tear and release of true lumen collapse and concomitantly promoting thrombosis of the false lumen. TEVAR offers an attractive alternative to surgical procedures in aortic dissection, and critical design modifications such as fenestrated or branched stent grafts increase the number of patients who may benefit from TEVAR (8 –10). Because TEVAR is much less invasive and simpler than surgical procedures, this technique results in enhanced postoperative recovery and reduction in mortality and morbidity. In recent years, a few attempts have been made to use TEVAR for the treatment of RAAD with an entry tear in the descending aorta (9,11,12). Dake et al (9) reported that TEVAR was technically successful in four patients with RAAD and patent false lumens, there was a significant reduction in the diameters of the proximal ascending aortae after TEVAR, and four patients survived without any morbidities during follow-up ranging from 5–18 months. Kato et al (11) reported the closure of entry tears and thrombosis of false lumens achieved by TEVAR in 10 patients. No aortic rupture or aneurysm formation was observed during a mean follow-up period of 20 months. In our study, TEVAR was successfully performed in 17 highly selected patients with RAAD, and no procedure-related complications occurred. Shrinkage of the enlarged aortae and reabsorption of false lumen thromboses were observed in all patients on CT images obtained after TEVAR. It is reasonable to pursue the use of TEVAR more aggressively to avoid the potential risks associated with RAAD. Evaluating patient suitability and planning the intervention at pretreatment is crucial for the success of TEVAR. The following points should be taken into serious consideration: (i) Patients with RAAD whose entry tear is in the descending aorta and who are without severe aortic regurgitation, cardiac tamponade, coronary artery involvement, or correlated cerebral ischemia are good candidates for TEVAR. (ii) For most RAAD cases in the acute phase (within 2 weeks after the onset of symptoms), it is suggested that TEVAR be delayed so that intensive medical therapy may be initiated first to obtain stable clinical status and prevent progression of the dissection. TEVAR performed during the subacute phase (2 months after the acute phase) is usually associated with a great recovery and excellent aortic remodeling. (iii) Emergency TEVAR should be performed if patients have acute end-organ ischemia (including paraplegia and paralysis caused by spinal cord ischemia); any signs of impending rupture including refractory or recurrent pain, increased pleural effusion, and refractory hypertension; or any signs
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of retrograde progression of the dissection confirmed by contrast-enhanced CT and echocardiography. Although preliminary studies have shown the effectiveness of TEVAR for treatment of acute and chronic RAAD, the optimal timing for the procedure is controversial (17–19). Several clinical investigations showed a trend toward a better outcome in patients with chronic aortic dissection undergoing endovascular repair. Eggebrecht et al (18) showed that in-hospital mortality after stent graft placement was significantly higher in patients with acute type B aortic dissection than in patients with chronic aortic dissection. Kato et al (19) also found that the morbidity and mortality after TEVAR in patients with acute type B dissections were significantly higher than in patients with chronic dissections. The arterial wall and dissected flap, which are extremely fragile in the acute phase, become more stable and fibrotic in the chronic phase. These morphologic changes significantly improve the tolerance of the arterial wall toward the edge of the stent graft and the hemodynamic changes associated with its deployment (19). It is recommended that TEVAR should be delayed in patients with acute aortic dissection. During the follow-up ranging from 4 – 60 months, no severe late complications or late death occurred in this study population. TEVAR might be associated with a potential longterm fatal risk, including recurrent ascending aortic dissection. Further studies with long-term follow-up and clinical outcomes of a large cohort of patients are required to clarify the efficacy and safety of TEVAR in treatment of RAAD. In conclusion, before performing TEVAR, we strictly selected patients with RAAD with the entry tear in the descending aorta who did not have severe aortic regurgitation, cardiac regurgitation, coronary artery involvement, an entry tear in the ascending aorta and proximal aortic arch, or correlated cerebral ischemia. In all selected patients, TEVAR was successfully performed with complete coverage of the primary entry tear. Shrinkage of the enlarged aorta and reabsorption of false lumen thrombosis was observed after TEVAR in all patients. All patients survived during follow-up. Only one patient had a new entry tear, located in the distal edge of the stent graft. A second TEVAR procedure was necessary for this patient 4 months after the first procedure. TEVAR is an effective treatment for RAAD with the entry tear in the descending aorta, and simultaneous coverage of the primary entry tear and thrombosis of the false lumen can be achieved.
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REFERENCES 1. Reul GJ, Cooley DA, Hallman GL, Reddy SB, Kyger ER 3rd, Wukasch DC. Dissecting aneurysm of the descending aorta: improved surgical results in 91 patients. Arch Surg 1975; 110:632– 640. 2. Kaji S, Akasaka T, Katayama M, et al. Prognosis of retrograde dissection from the descending to the ascending aorta. Circulation 2003; 108 (Suppl 1):II-300 –II-306. 3. Sun L, Qi R, Chang Q, et al. Surgery for acute type A dissection with the tear in the descending aorta using a stented elephant trunk procedure. Ann Thorac Surg 2009; 87:1177–1180. 4. Kazui T, Tamiya Y, Tanaka T, Komatsu S. Extended aortic replacement for acute type A dissection with the tear in the descending aorta. J Thorac Cardiovasc Surg 1996; 112:973–978. 5. Uchida N, Shibamura H, Katayama A, et al. Operative strategy for acute type A aortic dissection: ascending aortic or hemiarch versus total arch replacement with frozen elephant trunk. Ann Thorac Surg 2009; 87:773–777. 6. Jakob H, Tsagakis K, Tossios P, et al. Combining classic surgery with descending stent grafting for acute DeBakey type I dissection. Ann Thorac Surg 2008; 86:95–101. 7. Uchida N, Katayama A, Tamura K, Sutoh M, Kuraoka M, Ishihara H. Frozen elephant trunk technique and partial remodeling for acute type A aortic dissection. Eur J Cardiothorac Surg 2011; 40:1066 –1071. 8. Shu C, He H, Li QM, Li M, Jiang XH, Luo MY. Endovascular repair of complicated acute type-B aortic dissection with stentgraft: early and mid-term results. Eur J Vasc Endovasc Surg 2011; 42:448 – 453. 9. Dake MD, Kato N, Mitchell RS, et al. Endovascular stent-graft placement for the treatment of acute aortic dissection. N Engl J Med 1999; 340:1546 –1552. 10. Bakoyiannis CN, Economopoulos KP, Georgopoulos S, et al. Fenestrated and branched endografts for the treatment of thoracoabdominal aortic aneurysms: a systematic review. J Endovasc Ther 2010; 17:201–209. 11. Kato N, Shimono T, Hirano T, Ishida M, Yada I, Takeda K. Transluminal placement of endovascular stent-grafts for the treatment of type A aortic dissection with an entry tear in the descending thoracic aorta. J Vasc Surg 2001; 34:1023–1028. 12. Jiang J, Ding X, Zhang G, Hu S, Su Q, Li F. Endovascular stent-graft placement for retrograde type A aortic dissection. J Vasc Interv Radiol 2011; 22:415– 417. 13. Lansman SL, McCullough JN, Nguyen KH, et al. Subtypes of acute aortic dissection. Ann Thorac Surg 1999; 67:1975–1980. 14. Haverich A, Miller DC, Scott WC, et al. Acute and chronic aortic dissections— determinants of long-term outcome for operative survivors. Circulation 1985; 72: II-22–II-34. 15. Erbel R, Oelert H, Meyer J, et al. Effect of medical and surgical therapy on aortic dissection evaluated by transesophageal echocardiography: implications for prognosis and therapy. The European Cooperative Study Group on Echocardiography. Circulation 1993; 87:1604 –1615. 16. Ergin MA, Phillips RA, Galla JD, et al. Significance of distal false lumen after type A dissection repair. Ann Thorac Surg 1994; 57:820 – 825. 17. Akin I, Kische S, Ince H, Nienaber CA. Indication, timing and results of endovascular treatment of type B dissection. Eur J Vasc Endovasc Surg 2009; 37:289 –296. 18. Eggebrecht H, Herold U, Kuhnt O, et al. Endovascular stent-graft treatment of aortic dissection: determinants of post-interventional outcome. Eur Heart J 2005; 26:489 – 497. 19. Kato N, Shimono T, Hirano T, et al. Midterm results of stent-graft repair of acute and chronic aortic dissection with descending tear: the complication-specific approach. J Thorac Cardiovasc Surg 2002; 124:306 –312.
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Table E1. Details of TEVAR Size of Stent Graft
Patient 1 2 3 4 5 6 7 8 9 10 11 12
Interval between Symptom Onset and TEVAR (d) 14 2 14 21 14 15 4 14 15 30 19 17
Distance between LSA and Entry Tear (cm) 2.5 2.5 2.0 0.5 2.5 3.0 4.0 2.0 10.0 2.0 1.0 4.5
Stent Graft Oversizing (%) 10 10 10 10 10 15 10 10 15 10 10 10
Proximal 34 36 32 34 34 32 34 34 28 34 34 34
Distal 34 36 32 34 32 30 32 30 28 30 30 30
Length (mm) 160 130 120 120 120 160 140 157 80 157 160 160
Coverage of LSA No No No Yes No No No No No No Yes No
Operative Time (min) 105 95 90 95 110 60 55 95 90 70 80 80
13 14 15 16 17
14 22 25 14 14
5.0 1.5 1.0 3.0 1.0
10 10 10 15 10
32 34 38 32 32
28 30 34 28 28
160 160 152 150 150
No No Yes No Yes
80 90 50 70 80
Diameter (mm)
LSA ⫽ left subclavian artery; TEVAR ⫽ thoracic endovascular aortic repair.
Thoracic Endovascular Aortic Repair for Retrograde Type A Aortic Dissection with an Entry Tear in the Descending Aorta Chang Shu, MD, PhD, Tun Wang, MD, PhD, Quan-ming Li, MD, PhD, Ming Li, MD, PhD, Xiao-hua Jiang, MD, Ming-yao Luo, MD, PhD, and Xin Li, MD, PhD
ABSTRACT Purpose: To report the immediate and follow-up outcome of thoracic endovascular aortic repair (TEVAR) in highly selected patients with retrograde type A aortic dissection (RAAD) and an entry tear in the descending aorta. Materials and Methods: TEVAR was performed in 17 patients with RAAD and an entry tear in the descending aorta. None of the patients had severe aortic regurgitation, cardiac tamponade, coronary artery involvement, or brain ischemia. The false lumen in the ascending aorta was patent in nine patients. Two patients had acute malperfusion of the branched artery. Computed tomography (CT) was performed 14 days, 3 months, and 6 months after the intervention and annually thereafter. Results: All procedures were technically successful, with complete coverage of the entry tear and complete thrombosis of the false lumen in the ascending aorta. All patients survived through the follow-up period (25.7 months ⫾ 17.2). TEVAR resulted in thrombosis of the false lumen, reabsorption of the false lumen thrombus, and enlargement of the true lumen. The mean maximal diameter of the ascending aorta and the false lumen in the ascending aorta significantly decreased after TEVAR. At the distal edge of the stent graft, the mean diameter of the descending aorta and the false lumen markedly decreased after TEVAR. Complete thrombosis of the false lumen was observed at the distal edge of the stent graft in 16 (94.1%) patients and at the diaphragmatic level in 9 (52.9%) patients. Conclusions: TEVAR for RAAD with an entry tear in the descending aorta is a safe and effective technique in highly selected patients.
ABBREVIATIONS DSA ⫽ digital subtraction angiography, RAAD ⫽ retrograde type A aortic dissection, TEVAR ⫽ thoracic endovascular aortic repair
Retrograde type A aortic dissection (RAAD) with an entry tear in the descending aorta is a special subset of aortic dissection. RAAD may extend retrograde into the ascending aorta or even the aortic root and antegrade into the abdominal aorta simultaneously (1,2). Patients with RAAD
From the Department of Vascular Surgery, The 2nd Xiang-ya Hospital of Central-south University, Changsha, Hunan, China. Received August 17, 2011; final revision received December 21, 2011; accepted December 26, 2011. Address correspondence to C.S.; E-mail: changshu_vascular@ 163.com Table E1 is available online at www.jvir.org. None of the authors have identified a conflict of interest. © SIR, 2012 J Vasc Interv Radiol 2012; 23:453– 460 DOI: 10.1016/j.jvir.2011.12.023
have an extremely poor prognosis, with the risk of cardiac tamponade, severe aortic regurgitation, an entry tear in the ascending aorta proximal aortic arch, or aortic rupture (2– 4). The treatment strategy considered to be most effective is simultaneously obliterating the blood flow through the entry tear and inducing thrombosis of the false lumen. In recent years, total arch replacement with elephant trunk implantation with a stent has been advocated as a feasible treatment in patients with RAAD. However, this operation is extremely complicated and needs to be performed under hypothermic cardiopulmonary bypass with selective cerebral perfusion through a median sternotomy (3,5–7). Although this improved surgical technique can repair proximal aortic lesions and close the entry tear in a single-stage operation, it is associated with high mortality and morbidity, likely owing to the suboptimal preservation of critical organs and difficulties in hemostasis intraoperatively, especially in patients with poor clinical health status.
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Table 1. Baseline Characteristics and CT Findings of Study Patients
FL Patency Yes No Yes Yes No No
Pleural Effusion Left Bilateral Bilateral Bilateral No Left
Pericardial Effusion No Yes No Yes No Yes
Male Male Male Male
No Yes No No
Bilateral No Left Bilateral
No No No No
RCIA No No No
49 62 59
Female Male Male
Yes Yes No
No No Left
No No Yes
No No No
58 48 39 39
Male Male Male Male
Yes Yes No Yes
Bilateral Bilateral No Right
Yes No No No
No No No No
Patient 1 2 3 4 5 6
Age (y) 62 42 65 43 59 47
7 8 9 10
57 57 71 69
11 12 13 14 15 16 17
Gender Male Male Male Male Male Male
Malperfusion* No Right renal artery No No No No
Preoperative Comorbidities HTN HTN HTN HTN HTN HTN, DM, sleep apnea syndrome, obesity HTN HTN HTN, DM HTN, gastric ulcer, Legionella pneumonia HTN HTN HTN, DM, gout, angina pectoris Refractory HTN, DM HTN HTN, hepatitis B HTN
DM ⫽ diabetes mellitus, FL ⫽ false lumen in ascending aorta, HTN ⫽ hypertension, RCIA ⫽ the right common iliac artery. * Malperfusion means the branched artery of the aorta was totally compressed.
Endovascular stent graft placement is emerging as a less invasive alternative to surgical procedures for patients with aortic dissection or aneurysm. The efficacy and safety of this approach have been reported for the treatment of infrarenal abdominal aortic aneurysm and DeBakey III aortic dissection with entry tears distal from the orifice of the left subclavian artery (8 –10). More recently, thoracic endovascular aortic repair (TEVAR) was attempted for the treatment of RAAD in highly selected patients (9,11,12). However, there is no consensus on the safety and efficiency of TEVAR in patients with RAAD. We report our experiences using TEVAR to close the entry tear and induce thrombosis of the false lumen of RAADs, including immediate clinical outcome and follow-up examination.
MATERIALS AND METHODS Patients The hospital’s review committee approved this retrospective study, and written informed consent was obtained from all patients or their relatives. From April 2006 to January 2011, 31 consecutive patients with RAAD were admitted to our hospital and underwent computed tomography (CT) scanning with contrast enhancement and three-dimensional reconstruction. Patients who met the following criteria were considered to be good candidates for TEVAR: (a) no signs of cardiac tamponade or severe aortic regurgitation (grade III or better), (b) no involvement of the coronary artery by
aortic dissection, (c) no signs of cerebral ischemia, (d) anatomically adequate femoral and iliac arteries, and (e) no entry tear in the ascending aorta and proximal aortic arch. TEVAR was performed in 17 (54.8%) patients. The baseline characteristics and CT angiography findings of the patients included in this study are summarized in Table 1. There were 16 men and 1 woman with an average age of 54.5 years ⫾ 10.2 (range 39 –71 y). These patients were referred to our hospital 5 days ⫾ 2 after the onset of symptoms (range 1–10 d). All patients had a history of hypertension for 8 years ⫾ 2 (range 1–10 y) and presented with precordial or back pain at symptom onset. The false lumen of the ascending aorta was patent in nine patients (Fig 1a2 and 1b2). The false lumen of the ascending aorta was thrombosed in the remaining eight patients. Two patients (patients 2 and 7) had acute ischemia of the right renal artery (patient 2) (Fig 2a1 and 2a2) and the right common iliac artery (patient 7). TEVAR was performed under emergency conditions in these two patients. Both of the ischemic arteries originated from the true lumens, which were completely compressed by the false lumens. There were 12 patients with pleural effusions; 7 of these patients (patients 2, 3, 4, 7, 10, 14, and 15) had bilateral pleural effusions. A small amount of pericardial effusion was found in five patients (patients 2, 4, 6, 13, and 14). None of these patients experienced cardiac tamponade. Only one patient (patient 10) had a high fever and cough with a little yellow sputum at hospital admission. A chest
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Figure 1. CT images obtained at three different times: on admission (a), after conservative treatment for 2 weeks and before surgery (b), and 13 months after TEVAR (c). RAAD involved the brachiocephalic artery and left subclavian artery (1 in a1). After conservative treatment for 2 weeks, the false lumen of the brachiocephalic artery thrombosed and reabsorbed (2 in b1), and the blood flow in the false lumen of the ascending aorta decreased (compare 4 in b3 with 3 in a3). Acceptable aortic remodeling was obtained at follow-up (c).
CT scan showed little bilateral pleural effusion, and Legionella pneumophila antibody was found in the blood serum.
Images and Stent Grafts Patients underwent emergent CT angiography on admission and digital subtraction angiography (DSA) at the beginning of TEVAR. The measurements were obtained from CT angiography and DSA. The maximal diameter of the as-
cending aorta on admission was 44 mm ⫾ 4 (range 38 –50 mm). The distance between the left subclavian artery and the primary entry tear were 2.8 mm ⫾ 2.2 (range 0.5–10.0 mm) (Table E1; available online at www.jvir.org). The bilateral carotid artery, vertebral arteries, and circle of Willis were evaluated to determine their blood supply by CT angiography before TEVAR. The selected diameter size of the stent graft was 10%–15% greater than the diameter of
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Figure 2. CT images obtained at three different times (patient 2) with acute malformation of the right renal artery: on admission (a), 3 months after TEVAR (b), and 40 months after TEVAR (c). The right renal artery originated from the totally compressed true lumen (a1), and the left renal artery was coming from the false lumen (a2). At 3 months after TEVAR, the true lumen was reopened, and blood perfusion was recovered in the right renal artery (b1); blood flow was still delayed in the left renal artery (b2). At 40 months after TEVAR, the right renal artery was perfused well (c1), but the left renal artery was perfused by the false lumen, and the left kidney atrophied (c2).
the aorta approximately 2 cm proximal to the entry tear, not exceeding the diameter of the ascending aorta. Three types of devices were implanted in the 17 patients, including 10 Hercules stent grafts (MicroPort Medical [Shanghai] Co, Ltd, Shanghai, China), 5 Zenith stent grafts (Cook, Inc, Bloomington, Indiana), and 2 Valiant stent grafts (Medtronic, Inc, Minneapolis, Minnesota). The mean proximal and distal diameters of stent grafts were 33.4 mm ⫾ 2.1 (range 28 –36 mm) and 30.9 mm ⫾ 2.5 (range, 28 –36 mm) (Table E1; available online at www. jvir.org). The mean length of stent grafts was 143 mm ⫾ 22.4 (range 80 –160 mm) (Table E1; available online at www.jvir.org).
Thoracic Endovascular Aortic Repair Antihypertensive drugs and beta blockers was initiated for lowering arterial wall tension immediately after RAAD was diagnosed. All procedures were performed in a hybrid unit with fluoroscopic and angiographic guidance. General anesthesia with tracheal intubation was administered in 13 patients, and local anesthesia was administered in 4 patients (patients 7, 9, 12, and 13). A 5-F sheath was inserted into the left brachial artery, and a 5-F calibrated angiographic pigtail catheter was advanced into the ascending aorta to perform arteriography and permit arteriographic evaluation of the distance between the left subclavian artery and the primary entry tear. Arteriotomy was performed on the femoral artery originating from the true lumen. A 5-F pigtail catheter and a 0.035-inch guide wire were advanced into the true lumen via this arteriotomy site until reaching the ascending aorta.
A Lunderquist Extra Stiff Wire Guide (Cook, Inc) was advanced into the ascending aorta using the catheter exchange technique. After DSA was performed to confirm that the catheter was in the true lumen and measurement was made of the relative data of the aortic lesion again (Fig 3a), the position of the proximal landing zone was marked on the screen. After intravenous administration of heparin sodium (0.5 mg/kg), the stent graft delivery system was advanced over the Lunderquist Extra Stiff Wire Guide under fluoroscopy and placed within the true lumen (Fig 3b). When the proper position was reached, the systolic pressure was decreased to less than 80 –90 mm Hg to ensure precise stent graft positioning. The stent graft was deployed by pulling back the sheath with the mandrel pusher firmly fixed. Coverage of the primary entry tear was achieved by stent graft, and the left subclavian artery was intentionally occluded in four patients (patients 4, 11, 15, and 17). Angiography was performed immediately after deployment to confirm coverage of the entry tear, sealing of the aortic dissection, and blood flow of the aortic lumen and branch vessels (Fig 3c). After the removal of the large sheath, the arteriotomy was repaired.
Follow-up Examination CT images were acquired at 14 days, 3 months, and 6 months after the intervention and annually thereafter. Diameters of the ascending aorta, the false lumen in the ascending aorta, the descending aorta, and the false lumen at the distal end of the stent graft were measured by CT before and after stent graft placement in all patients. At all
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Figure 3. DSA performed during TEVAR. The false lumen progressed retrograde to the ascending aorta (arrow), and the patent false lumen extended to the aortic arch reaching the orifice of the brachiocephalic artery (a). The stent graft delivery system was advanced into the true lumen through the femoral artery (b). Angiography performed after deployment of the stent graft confirmed the sealing of the aortic dissection and blood flow through the aortic lumen and branch vessels. The left subclavian artery was intentionally occluded (c).
levels, the diameter of the aorta and false lumen were measured along a line perpendicular to the intimal flap.
Statistical Analysis All values are expressed as mean ⫾ standard deviation. The diameters of the aortae and false lumens were compared with Student paired t test. P ⬍ .05 was considered statistically significant.
RESULTS Immediate Outcome After initial conservative treatment with antihypertensive drugs and beta blockers, the symptoms of precordial and back pain were significantly relieved and clinical health status markedly improved in all patients. The acute aortic dissection became relatively stable and recovered to some extent. One patient had involvement of the brachiocephalic artery and left subclavian artery on admission (Fig 1a1). At 2 weeks after conservative therapy, the thrombosis of the false lumen and the absorption of the false lumen thrombosis were observed in the brachiocephalic artery (Fig 1b1). TEVAR was successfully performed in all patients. The mean time interval between the onset of symptoms and TEVAR was 15.8 days ⫾ 6.7 (range 2–30 d) (Table E1; available online at www.jvir.org). Two patients (patients 2 and 7) underwent TEVAR in the acute phase 2 days (patient 2) and 4 days (patient 7) after the onset of symptoms. The remaining 15 patients underwent TEVAR in the chronic phase more than 14 days after symptom onset. The mean operative time was 82.1 minutes ⫾ 16.9 (range 50 –110 min) (Table E1; available online at www.jvir.org). The stent grafts were placed in the true lumen of the proximal
descending aorta in 16 patients and in the middle descending aorta in 1 patient (patient 9). Complete coverage of the entry tear was accomplished after deployment of the stent graft in all patients. DSA performed after the intervention showed no residual flow of blood contrast medium into the false lumen of the ascending aorta. No aorta-related complications, including endoleak, malperfusion of aortic branches, or aneurysmal degeneration, were observed in any of the patients. Complete thrombosis of the false lumen in the ascending aorta and partial reabsorption of thrombosis were observed on CT scan after TEVAR in all patients. The blood flow of the fully compressed right renal artery (patient 2) (Fig 2b1 and 2b2) and right common iliac artery (patient 7) recovered immediately after emergency TEVAR. In patient 2, angiography after TEVAR showed that the left renal artery originating from the false lumen was perfused as well as before TEVAR. Because the distance between the left subclavian artery and primary entry tear was ⬍ 1.5 cm and the left vertebral artery did not play a dominant role according to CT angiography performed before TEVAR, the left subclavian artery was intentionally covered in 4 (23.5%; patients 4, 11, 15, and 17) of 17 patients (Table E1; available online at www.jvir.org). No related complications from intentional coverage of the left subclavian artery, including type II endoleak, ischemia, or steal syndrome, were observed in these four patients. The pleural or pericardial effusions were not severe before TEVAR in nine patients, and drainage of the effusions was not performed. Chest radiography and echocardiography showed that effusion progressively decreased after TEVAR and faded away 7– 42 days later. Preexisting L. pneumophila was treated with intravenous injection of sensitive antibiotics in patient 10, and this patient recovered from TEVAR uneventfully. There were no instances of progression of the dissection, formation of new entry
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Figure 4. Individual aortic remodeling after TEVAR. Measurement on CT at follow-up found that the maximal diameter of the ascending aorta (a) and the false lumen in the ascending aorta (b) significantly decreased compared with measurements on admission. At the level of the distal edge of the stent graft, the diameter of the descending aorta (c) and the false lumen (d) was also markedly reduced compared with the CT measurement between admission and follow-up. Mean values ⫾ standard deviation are shown in the full lines with bars.
tears, aortic rupture, ischemia of aortic branches, paraplegia, cardiac tamponade, severe aortic regurgitation (grade III or greater), or death in any of the patients during their hospital stay.
Follow-up Outcome Patients received antihypertensive treatment after discharge from the hospital. The mean duration of follow-up was 25.7 months ⫾ 17.2 (range 4 – 60 mo), and median duration was 22 months. All patients survived through follow-up. The shrinkage of enlarged aortae and reabsorption of false lumen thromboses at the level of the ascending and descending aortae distal to the stent grafts was evident in all 17 patients on CT scans performed after TEVAR (Fig 1c1, 1c2, and 1c3). The mean maximal diameter of the ascending aorta decreased from 44.1 mm ⫾ 4.3 before TEVAR to 37.7 mm ⫾ 3.9 on the latest available CT images after TEVAR (P ⬍ .001) (Fig 4a). The mean diameter of the false lumen in the ascending aorta decreased from 14.8 mm ⫾ 5.6 before TEVAR to 0.6 mm ⫾ 1.8 on the latest follow-up CT images (P ⬍ .001) (Fig 4b). At the level of
the distal edge of the stent graft, the mean diameter of the descending aorta decreased from 34.1 mm ⫾ 8.1 before TEVAR to 28.4 mm ⫾ 3.3 on the latest CT images (P ⫽ .007) (Fig 4c). The mean diameter of the false lumen decreased from 22.7 mm ⫾ 9.3 before TEVAR to 2.8 mm ⫾ 4.8 on the latest CT images (P ⬍ .001) (Fig 4d). Complete thrombosis of the false lumen was observed at the distal edge of the stent graft in 16 (94.1%) patients and at the diaphragmatic level in 7 (41.2%) patients. There were patent false lumens in the distal portion of the descending aorta, abdominal aorta, or both in 10 (58.8%) patients. The reentry tear was present in the distal portion of the descending aorta in two (11.7%) patients including patient 15, in the abdominal aorta in seven (41.1%) patients, and in the common iliac artery in one (5.8%) patient. The false lumen below the reentry tear remained patent but did not enlarge during follow-up in these patients because little blood flow infused into the false lumen through the reentry tear below the stent graft. In patient 2, blood flow of the right renal artery recovered well, and the patient lived without any discomfort during the 40-month follow-up
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period, although the left renal artery supported by the false lumen was poorly perfused with left kidney atrophy (Fig 2c1 and 2c2). At 3 months after TEVAR, patient 15 complained of recurrent dull back pain. CT angiography detected that a new entry tear was located in the distal edge of the stent graft, and considerable blood flow infused into the false lumen through the new entry tear 4 months after TEVAR. The preoperative cross-sectional diameters were 15 mm and 35 mm in the short axis and long axis of the true lumen at the level of the entry tear that subsequently occurred 3 months after TEVAR. An additional stent graft was suggested to cover the new entry tear after the first TEVAR, but the patient did not consent to the second endovascular treatment because of financial reasons. After conservative therapy, all symptoms were relieved; however the new entry tear persisted.
DISCUSSION Retrograde aortic dissection occurs more frequently than is generally realized; the incidence ranges from 5%–25% among type A aortic dissections and 10%–27% among type III aortic dissections (1–3,9,13,14). Appropriate management of RAAD is controversial. Medical therapy has been recommended in patients without severe complications. In unstable RAAD, aggressive surgical treatment should be considered after initial medical therapy. Kaji et al (2) reported that RAAD with a thrombosed false lumen in the ascending aorta could be treated medically with timed surgical repair. Surgery is commonly performed for RAAD to avoid lethal complications such as cardiac tamponade, severe aortic regurgitation, aortic rupture, and ischemia of supraaortic branches and coronary arteries. The replacement of the ascending aorta or total arch has been performed previously, but in these studies the false lumen and distal dissection remained untreated (1,4,5). Erbel et al (15) reported that the replacement of the ascending aorta in RAAD was associated with a false lumen patency rate of 83%; mortality in patients with a patent false lumen was as high as 43%. These authors concluded that a surgical procedure that could not eliminate blood flow into the false lumen was responsible for the poor prognosis of RAAD (15). Similarly, other institutions reported that a persistent patent distal false lumen correlated closely with various late complications (14,16). Arch replacement might be performed in patients with proximal aortic lesions through a median sternotomy, and placement of the descending aorta with resection of the entry tear was simultaneously carried out through lateral thoracotomy, but this combined technique was complicated and had many complications. Kazui et al (4) recommended total replacement of the ascending aorta and aortic arch associated with the resection of an entry tear in RAAD, but the descending aortic dissection was still unresolved. More recently, total arch replacement with antegrade elephant
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trunk implantation with a stent into the proximal descending aorta was proposed to repair proximal aortic lesions and induce thrombosis of the distal false lumen (3,5–7). Sun et al (3) reported surgical mortality of 6.06% in 33 patients with RAAD. As reported in many institutions, postoperative complications include paraparesis, stroke, spinal core injury, renal failure, and reexploration for bleeding (3,5–7). TEVAR of aortic dissection plays a curative role by covering the primary entry tear and release of true lumen collapse and concomitantly promoting thrombosis of the false lumen. TEVAR offers an attractive alternative to surgical procedures in aortic dissection, and critical design modifications such as fenestrated or branched stent grafts increase the number of patients who may benefit from TEVAR (8 –10). Because TEVAR is much less invasive and simpler than surgical procedures, this technique results in enhanced postoperative recovery and reduction in mortality and morbidity. In recent years, a few attempts have been made to use TEVAR for the treatment of RAAD with an entry tear in the descending aorta (9,11,12). Dake et al (9) reported that TEVAR was technically successful in four patients with RAAD and patent false lumens, there was a significant reduction in the diameters of the proximal ascending aortae after TEVAR, and four patients survived without any morbidities during follow-up ranging from 5–18 months. Kato et al (11) reported the closure of entry tears and thrombosis of false lumens achieved by TEVAR in 10 patients. No aortic rupture or aneurysm formation was observed during a mean follow-up period of 20 months. In our study, TEVAR was successfully performed in 17 highly selected patients with RAAD, and no procedure-related complications occurred. Shrinkage of the enlarged aortae and reabsorption of false lumen thromboses were observed in all patients on CT images obtained after TEVAR. It is reasonable to pursue the use of TEVAR more aggressively to avoid the potential risks associated with RAAD. Evaluating patient suitability and planning the intervention at pretreatment is crucial for the success of TEVAR. The following points should be taken into serious consideration: (i) Patients with RAAD whose entry tear is in the descending aorta and who are without severe aortic regurgitation, cardiac tamponade, coronary artery involvement, or correlated cerebral ischemia are good candidates for TEVAR. (ii) For most RAAD cases in the acute phase (within 2 weeks after the onset of symptoms), it is suggested that TEVAR be delayed so that intensive medical therapy may be initiated first to obtain stable clinical status and prevent progression of the dissection. TEVAR performed during the subacute phase (2 months after the acute phase) is usually associated with a great recovery and excellent aortic remodeling. (iii) Emergency TEVAR should be performed if patients have acute end-organ ischemia (including paraplegia and paralysis caused by spinal cord ischemia); any signs of impending rupture including refractory or recurrent pain, increased pleural effusion, and refractory hypertension; or any signs
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of retrograde progression of the dissection confirmed by contrast-enhanced CT and echocardiography. Although preliminary studies have shown the effectiveness of TEVAR for treatment of acute and chronic RAAD, the optimal timing for the procedure is controversial (17–19). Several clinical investigations showed a trend toward a better outcome in patients with chronic aortic dissection undergoing endovascular repair. Eggebrecht et al (18) showed that in-hospital mortality after stent graft placement was significantly higher in patients with acute type B aortic dissection than in patients with chronic aortic dissection. Kato et al (19) also found that the morbidity and mortality after TEVAR in patients with acute type B dissections were significantly higher than in patients with chronic dissections. The arterial wall and dissected flap, which are extremely fragile in the acute phase, become more stable and fibrotic in the chronic phase. These morphologic changes significantly improve the tolerance of the arterial wall toward the edge of the stent graft and the hemodynamic changes associated with its deployment (19). It is recommended that TEVAR should be delayed in patients with acute aortic dissection. During the follow-up ranging from 4 – 60 months, no severe late complications or late death occurred in this study population. TEVAR might be associated with a potential longterm fatal risk, including recurrent ascending aortic dissection. Further studies with long-term follow-up and clinical outcomes of a large cohort of patients are required to clarify the efficacy and safety of TEVAR in treatment of RAAD. In conclusion, before performing TEVAR, we strictly selected patients with RAAD with the entry tear in the descending aorta who did not have severe aortic regurgitation, cardiac regurgitation, coronary artery involvement, an entry tear in the ascending aorta and proximal aortic arch, or correlated cerebral ischemia. In all selected patients, TEVAR was successfully performed with complete coverage of the primary entry tear. Shrinkage of the enlarged aorta and reabsorption of false lumen thrombosis was observed after TEVAR in all patients. All patients survived during follow-up. Only one patient had a new entry tear, located in the distal edge of the stent graft. A second TEVAR procedure was necessary for this patient 4 months after the first procedure. TEVAR is an effective treatment for RAAD with the entry tear in the descending aorta, and simultaneous coverage of the primary entry tear and thrombosis of the false lumen can be achieved.
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REFERENCES 1. Reul GJ, Cooley DA, Hallman GL, Reddy SB, Kyger ER 3rd, Wukasch DC. Dissecting aneurysm of the descending aorta: improved surgical results in 91 patients. Arch Surg 1975; 110:632– 640. 2. Kaji S, Akasaka T, Katayama M, et al. Prognosis of retrograde dissection from the descending to the ascending aorta. Circulation 2003; 108 (Suppl 1):II-300 –II-306. 3. Sun L, Qi R, Chang Q, et al. Surgery for acute type A dissection with the tear in the descending aorta using a stented elephant trunk procedure. Ann Thorac Surg 2009; 87:1177–1180. 4. Kazui T, Tamiya Y, Tanaka T, Komatsu S. Extended aortic replacement for acute type A dissection with the tear in the descending aorta. J Thorac Cardiovasc Surg 1996; 112:973–978. 5. Uchida N, Shibamura H, Katayama A, et al. Operative strategy for acute type A aortic dissection: ascending aortic or hemiarch versus total arch replacement with frozen elephant trunk. Ann Thorac Surg 2009; 87:773–777. 6. Jakob H, Tsagakis K, Tossios P, et al. Combining classic surgery with descending stent grafting for acute DeBakey type I dissection. Ann Thorac Surg 2008; 86:95–101. 7. Uchida N, Katayama A, Tamura K, Sutoh M, Kuraoka M, Ishihara H. Frozen elephant trunk technique and partial remodeling for acute type A aortic dissection. Eur J Cardiothorac Surg 2011; 40:1066 –1071. 8. Shu C, He H, Li QM, Li M, Jiang XH, Luo MY. Endovascular repair of complicated acute type-B aortic dissection with stentgraft: early and mid-term results. Eur J Vasc Endovasc Surg 2011; 42:448 – 453. 9. Dake MD, Kato N, Mitchell RS, et al. Endovascular stent-graft placement for the treatment of acute aortic dissection. N Engl J Med 1999; 340:1546 –1552. 10. Bakoyiannis CN, Economopoulos KP, Georgopoulos S, et al. Fenestrated and branched endografts for the treatment of thoracoabdominal aortic aneurysms: a systematic review. J Endovasc Ther 2010; 17:201–209. 11. Kato N, Shimono T, Hirano T, Ishida M, Yada I, Takeda K. Transluminal placement of endovascular stent-grafts for the treatment of type A aortic dissection with an entry tear in the descending thoracic aorta. J Vasc Surg 2001; 34:1023–1028. 12. Jiang J, Ding X, Zhang G, Hu S, Su Q, Li F. Endovascular stent-graft placement for retrograde type A aortic dissection. J Vasc Interv Radiol 2011; 22:415– 417. 13. Lansman SL, McCullough JN, Nguyen KH, et al. Subtypes of acute aortic dissection. Ann Thorac Surg 1999; 67:1975–1980. 14. Haverich A, Miller DC, Scott WC, et al. Acute and chronic aortic dissections— determinants of long-term outcome for operative survivors. Circulation 1985; 72: II-22–II-34. 15. Erbel R, Oelert H, Meyer J, et al. Effect of medical and surgical therapy on aortic dissection evaluated by transesophageal echocardiography: implications for prognosis and therapy. The European Cooperative Study Group on Echocardiography. Circulation 1993; 87:1604 –1615. 16. Ergin MA, Phillips RA, Galla JD, et al. Significance of distal false lumen after type A dissection repair. Ann Thorac Surg 1994; 57:820 – 825. 17. Akin I, Kische S, Ince H, Nienaber CA. Indication, timing and results of endovascular treatment of type B dissection. Eur J Vasc Endovasc Surg 2009; 37:289 –296. 18. Eggebrecht H, Herold U, Kuhnt O, et al. Endovascular stent-graft treatment of aortic dissection: determinants of post-interventional outcome. Eur Heart J 2005; 26:489 – 497. 19. Kato N, Shimono T, Hirano T, et al. Midterm results of stent-graft repair of acute and chronic aortic dissection with descending tear: the complication-specific approach. J Thorac Cardiovasc Surg 2002; 124:306 –312.
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Table E1. Details of TEVAR Size of Stent Graft
Patient 1 2 3 4 5 6 7 8 9 10 11 12
Interval between Symptom Onset and TEVAR (d) 14 2 14 21 14 15 4 14 15 30 19 17
Distance between LSA and Entry Tear (cm) 2.5 2.5 2.0 0.5 2.5 3.0 4.0 2.0 10.0 2.0 1.0 4.5
Stent Graft Oversizing (%) 10 10 10 10 10 15 10 10 15 10 10 10
Proximal 34 36 32 34 34 32 34 34 28 34 34 34
Distal 34 36 32 34 32 30 32 30 28 30 30 30
Length (mm) 160 130 120 120 120 160 140 157 80 157 160 160
Coverage of LSA No No No Yes No No No No No No Yes No
Operative Time (min) 105 95 90 95 110 60 55 95 90 70 80 80
13 14 15 16 17
14 22 25 14 14
5.0 1.5 1.0 3.0 1.0
10 10 10 15 10
32 34 38 32 32
28 30 34 28 28
160 160 152 150 150
No No Yes No Yes
80 90 50 70 80
Diameter (mm)
LSA ⫽ left subclavian artery; TEVAR ⫽ thoracic endovascular aortic repair.