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Ann Thorac Surg 2005;80:1297-1302
© 2005 The Society of Thoracic Surgeons


Original article: Cardiovascular

Long-Term Effectiveness of Total Arch Replacement for Type A Aortic Dissection

Yoshie Ochiai, MD a , * , Yutaka Imoto, MD a , Masato Sakamoto, MD a , Yasutaka Ueno, MD b , Tetsuro Sano, MD a , Hironori Baba, MD a , Akira Sese, MD a

a Department of Cardiovascular Surgery, Kyushu Koseinenkin Hospital, Kitakyushu
b Department of Cardiovascular Surgery, Shimonoseki Municipal Hospital, Shimonoseki, Japan

Accepted for publication April 1, 2005.

* Address reprint requests to Dr Ochiai, Department of Cardiovascular Surgery, Kyushu Koseinenkin Hospital, 1-8-1, Kishinoura, Yahatanishi-ku, Kitakyushu, 806-8501, Japan (Email: ochiaiy{at}alto.ocn.ne.jp).


    Abstract
 Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 References
 
BACKGROUND: With recent improvements in cerebral protection during aortic arch repair, total aortic arch replacement has become an accepted surgical method for acute type A aortic dissection involving the aortic arch. Our surgical strategy is to perform total arch replacement with a branched graft using antegrade selective cerebral perfusion for the patients with type A aortic dissection involving the aortic arch. The objective of this study is to evaluate the effectiveness of this strategy on late outcome.

METHODS: From October 1988 to April 2003, 46 patients underwent total arch replacement for acute type A dissection involving the aortic arch. Operations were performed with hypothermic cardiopulmonary bypass, antegrade selective cerebral perfusion during the arch repair, and open distal anastomosis.

RESULTS: Hospital mortality was 6.5% (3 patients), and permanent neurologic dysfunction was observed in 1 patient. During the follow-up period (mean, 5.4 years; range, 13 months to 15.6 years), 2 patients died, but the causes were not related to the aorta or aortic valve. Survival rates at 5 and 10 years postoperatively were 89.6% ± 5.2% and 82.7% ± 8.2%, respectively. Of the 41 survivors, 3 patients underwent successful reoperation for the distal thoracic aorta. Freedom from reoperation was 93.6% ± 4.6% and 88.7% ± 6.5% at 5 and 10 years, respectively. The residual false lumen in the thoracic aorta was frequently thrombosed (76.2%).

CONCLUSIONS: Total arch replacement for acute type A dissection may decrease the risk of late complications related to the false lumen and lead to excellent long-term survival.


    Introduction
 Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 References
 
With recent advances in preoperative recognition, operative technique, and cerebral protection during aortic arch repair, total aortic arch replacement has become an accepted surgical method for acute type A dissection involving the aortic arch [1–6]. During the past 15 years, we have performed a simultaneous replacement of the ascending aorta and aortic arch using a branched graft for type A aortic dissection extending to the aortic arch except for DeBakey type II dissection. Complete resection of intimal tears may contribute to reducing the pressure in the residual false lumen, which would lead to an obliteration of the remaining false lumen and decrease late complications related to the distal false lumen. However, there has been no conclusive evidence whether a persistent patent false lumen in the distal aorta has an adverse influence on long-term event-free survival [7]. In this study, we evaluated the operative results, late survival, reoperation rate, and state of residual false lumen in patients who underwent total arch replacement to elucidate the long-term effectiveness of this surgery.


    Patients and Methods
 Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 References
 
Patients
The subjects were 46 patients who underwent total arch replacement (defined as total arch replacement simultaneously performed with ascending aortic replacement) for acute type A aortic dissection involving the aortic arch from October 1988 to April 2003. During the same period, 10 patients with acute type A dissection underwent graft replacement of the ascending aorta (n = 8) or hemiarch repair (n = 2), and another 14 patients underwent various operations for chronic type A dissection. The patients of the present study were aged 38 to 78 years (mean, 61.8 ± 9.9) and consisted of 24 men and 22 women. Table1 shows patients' preoperative characteristics. Two patients had previous cardiac operations (aortic valve replacement and removal of left atrial myxoma). The preoperative condition related to the aortic dissection included shock, which was defined as a systolic pressure less than 80 mm Hg or preoperative use of the inotropic agent in 11 patients (24%), cardiac tamponade in 25 (54%), aortic rupture in 4 (9%), and transient cerebral ischemia in 9 (20%). The time of initial dissection was defined by the onset of chest or back pain. Acute dissection was defined by an onset of symptoms within 14 days of presentation. A total of 40 patients (87%) had surgery within 24 hours of symptom onset and 6 patients (13%), within 72 hours of symptom onset.


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Table 1. Preoperative Patient Characteristics
 
All patients underwent preoperative computed tomography (CT) with contrast media to diagnose the extent of dissection. By direct intraoperative observation, together with transesophageal echocardiography, the primary intimal tear (entry site) was located in the ascending aorta in 13 patients (28%), aortic arch in 16 (35%), between the ascending aorta and aortic arch (near the origin of the innominate artery) in 1 (2%), and just below the left subclavian artery (within 5 cm from the origin of the left subclavian artery) in 8 (17%). The entry site was not identified in the remaining 8 patients (17%), in whom the entry site might have been located in the more distal descending aorta. Therefore, in our series, 16 patients (35%) had acute type A dissection with the initial intimal tear in the descending aorta, in whom the dissection extended retrogradely to the aortic arch or ascending aorta—so called "retrograde dissection." Resection of the entry site was completed in 38 (76%) of 46 patients.

Surgical Technique
Our surgical strategy is to perform simultaneous replacement of the ascending aorta and aortic arch using a branched graft for type A dissection in which the aortic arch is injured by the dissection, except DeBakey type II dissection. There was a variability of operative techniques used, and the following reflects our actual general operative approach. A median sternotomy was performed in all patients. We determined the arterial cannulation site according to the extent of dissection. As a result, the arterial cannulation sites were the following: the femoral artery in 34 patients, femoral artery and right axillary artery in 7, right axillary artery in 4, and left common carotid artery in 1 patient. Two venous cannulae were directly inserted into the superior vena cava and inferior vena cava.

After cardiopulmonary bypass (CPB) was established, a left ventricular vent was inserted through the right superior pulmonary vein. Systemic cooling was initiated while the ascending aorta, aortic arch vessels, and descending thoracic aorta were exposed. After clamping of the ascending aorta, the aorta was incised and cold crystalloid cardioplegia was infused directly into the both coronary arteries. After the internal surface of the ascending aorta and the aortic valve were examined, the aorta was transected above the commissure. When the false lumen was present within the proximal part, the false lumen was approximated with fibrin glue. Then, the ascending aorta was anastomosed to a short segment of a straight graft (Hemashield Gold; Meadox Medicals, Oakland, New Jersey) by applying the Teflon (Impra, subsidiary of L.R. Bard, Tempe, Arizona) felts to the internal and external surfaces of the aorta for reinforcement.

Systemic cooling progressed until the patient's rectal temperature reached below 25 °C, and the pharmacologic agents (thiamylal sodium, phenytoin, and mannitol) [8] were administered for brain protection in addition to ice packs placed around the head, before circulatory arrest. After circulatory arrest had been instituted, the ascending aorta was unclamped and the aortic arch was opened. The innominate artery, left common carotid artery, and left subclavian artery were cannulated from inside of the aorta using three balloon catheters. Thereafter, antegrade selective cerebral perfusion was started at a perfusion rate of 10 mL· kg-1· min-1 for brain protection. The proximal descending aorta was transected circumferentially just distal to the ostium of the left subclavian artery or distal to the intimal tear in the proximal descending aorta if exposed. The distal false lumen was obliterated by the same method as the proximal false lumen, and an open distal anastomosis (a short segment of a graft and the distal descending aorta) was performed using a modified elephant trunk technique by attaching a Teflon strip to the outside of the aortic wall.

After completion of two graft-to-graft anastomoses (the distal side of a four-branched graft with the straight elephant trunk graft, and the proximal side of the four-branched graft with the proximal ascending aortic graft), the heart was reperfused, and antegrade systemic perfusion was reestablished through a side branch of the arch graft. During rewarming, reconstruction of three arch vessels was subsequently performed and completed the operation. After termination of CPB, the side branch used for antegrade systemic perfusion was closed. For aortic arch reconstruction, en bloc repair technique was used in the first 2 patients. In the remaining 44 patients, the branched graft technique was used. Before 1997, a branched arch graft was constructed in our operating room; since then the graft has been commercially available. The total CPB time, cardiac ischemic time, selective cerebral perfusion time, and lower body ischemic time was 249 ± 69, 120 ± 40, 114 ± 37, and 56 ± 21 minutes, respectively.

Concomitant Procedure
Aortic valve resuspension was performed in 23 patients. In 2 patients, coronary artery bypass grafting (CABG) with saphenous vein graft was performed because of right coronary artery (RCA) disruption. Reimplantation of the RCA was conducted in 1 patient whose RCA was opened to the false lumen. In 1 patient, the Bentall operation using a composite graft containing a mechanical valve was performed with direct reimplantation of the left coronary artery onto the ascending graft and CABG-to-RCA.

Follow-Up
All survivors except for 1 patient underwent body CT before discharge. The state of the residual false lumen was evaluated by CT at least once a year after discharge. The patients were followed up until May 2004 by direct contact with patients or their physicians, or both.

Statistical Methods
Results are reported as percentages or means ± SD, as appropriate. Survival rate was estimated by the Kaplan-Meier method. Statistical analysis was performed with SPSS 10.0.5 statistical software (SPSS, Chicago, Illinois).


    Results
 Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 References
 
Operative Mortality and Morbidity
A total of 3 patients (6.5%) died during hospitalization. The first case was a 69-year-old man who had postoperative cerebral infarction, pneumonia, and acute renal failure. He died of multiple organ failure on the 33rd postoperative day. The second patient, a 67-year-old man, died of myocardial infarction due to coronary malperfusion with RCA disruption. In this case, coronary malperfusion was diagnosed by transesophageal echocardiography after cessation of CPB, and thereafter an emergent CABG-to-RCA using saphenous vein graft was performed. However, the heart did not recover because of massive acute myocardial infarction. The third patient was a 61-year-old man with severe preoperative shock and consciousness disturbance. We performed composite valved graft replacement with reimplantation of the left main coronary trunk and CABG-to-RCA using the saphenous vein graft. This patient died of disseminated intravascular coagulopathy and cerebral damage on the fourth postoperative day.

Reexploration for bleeding was necessary in 6 patients (13%). Respiratory failure requiring the aid of a respirator for more than 3 days was observed in 18 patients (39%). Three patients (7%) had acute renal failure requiring temporary hemodialysis. Regarding neurologic complications, permanent cerebral damage occurred in 1 patient (2%), transient neurologic deficit or seizure in 2 (4%), and prolonged delirium in 3 (7%).

Late Survival and Reoperation
A total of 43 patients who survived the early postoperative period were followed up. Only 1 patient was untraced. Follow-up for survival was 97.7% complete. Until May 2004, follow-up extended beyond 5 years in 53.5%, but beyond 10 years in only 9.3%. Mean follow-up period for survivors was 5.4 ± 3.4 years (range, 13 months to 15.6 years). During the follow-up period, 2 patients died of dissection-unrelated disease: 1 of renal failure and the other of pneumonia after 7.2 and 4.4 years of the total arch replacement, respectively. Survival rates at 5 and 10 years postoperatively were 89.6% ± 5.2% and 82.7% ± 8.2%, respectively, as shown in Figure 1.



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Fig 1. Survival rate for the patients who had type A aortic dissection and underwent total arch replacement.

 
During the study period, none of our patients required reoperation of arch lesions. Reoperation was performed because of the development of lesions in the distal thoracic aorta in 3 patients. In the first patient, dilatation of the false lumen in the distal thoracic aorta developed, and graft replacement of the descending thoracic aorta through left thoracotomy was performed 11 months after total arch replacement. In the second patient, development of a peudoaneurysm at the anastomotic site between the graft and the descending thoracic aorta was highly suspected 4 years after total arch replacement. However, intraoperative finding revealed that it was a not a newly developed lesion but a localized residual false lumen of 5.0 cm in length. Therefore, we just closed the residual false lumen directly with reinforcement of the Teflon felts. The third patient with thrombosed false lumen showed progressive aneurysmal dilatation of the thoracic aorta (5.5 cm) and underwent emergent graft replacement of the descending thoracic aorta for rupture of this lesion 5 years after total arch replacement. All these patients survived the reoperation and were discharged without paraplegia.

We have not encountered any reoperation for the proximal aorta or aortic valve. By transthoracic echocardiography, no patient had more than moderate aortic regurgitation at the latest follow-up. In 2 patients with atherosclerotic infrarenal abdominal aortic aneurysm, graft replacement of the abdominal aorta was performed 2 and 8 years after total arch replacement. Mitral valve replacement due to mitral valve regurgitation was performed in 1 patient 4 years after total arch replacement. Freedom from reoperation was 93.6% ± 4.6% and 88.7% ± 6.5% at 5 and 10 years after total arch replacement, respectively.

State of the Residual False Lumen
We evaluated the fate of the residual false lumen by CT annually according to the preoperative extent of the patent false lumen in 42 patients (Tables 2 and 3). Go In 9 patients who had preoperative false lumen localized in the thoracic aorta (Table 2), false lumen in the thoracic aorta was thrombosed in 7 patients before discharge. In 1 patient, residual false lumen was surgically closed as mentioned above. During the follow-up period (mean, 5.4 ± 1.9 years; range, 3.0 to 7.8 years), residual false lumen in the thoracic aorta was thrombosed in 8 of 9 patients. Regarding 33 patients with preoperative false lumen up to the abdominal aorta (Table 3), 8 patients had no patent residual false lumen; 8 patients had patent residual false lumen in the abdominal aorta only; 1 patient had it in the thoracic aorta only; and 16 had it in the thoracic and abdominal aorta before discharge. During the follow-up period (mean, 4.1 ± 3.4 years; range, 17 months to 13.4 years), thrombosis of the residual false lumen in the thoracic aorta progressed. Thereafter, 16 patients had residual false lumen in the abdominal aorta only, and 8 had it in the thoracic and abdominal aorta at the latest follow-up. Therefore, in 24 of 33 patients (72.7%) with preoperative thoracoabdominal false lumen, residual false lumen in the thoracic aorta was thrombosed. As a whole, false lumen in the thoracic aorta was frequently thrombosed (76.2%; 32 of 42 patients) during the follow-up period (mean, 4.4 ± 3.2 years; range, 7 months to 13.4 years).


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Table 2. State of Postoperative Patent False Lumen (Before Discharge and Late Stage) According to Preoperative Extent of Patent False Lumen Confined to Thoracic Aorta and Up to Abdominal Aorta
 

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Table 3. Univariate Analyses for Determining Thrombosis of the False Lumen in the Thoracic Aorta
 
We tried to identify perioperative factors for thrombosis of the false lumen in the thoracic aorta by analysis of data between patients with patent false lumen in the thoracic aorta (n = 10) and with thrombosed false lumen in the thoracic aorta (n = 32), as shown in Table 3. Resection of entry site, usage of elephant trunk technique, or preoperative extent of the false lumen up to the abdominal aorta did not affect thrombosis of the false lumen in the thoracic aorta.

We compared aortic diameters in the descending thoracic aorta from the latest CT image between patients with patent false lumen (n = 10) and patients with thrombosed false lumen (n = 32). Aortic diameter in the descending thoracic aorta was larger when false lumen in the thoracic aorta was patent (44 ± 7 mm versus 34 ± 7 mm, p < 0.01). Regarding postdissection aneurysmal dilatation, 3 patients showed aneurysmal dilatation in the descending thoracic aorta (>50 mm).

In 2 of 3 patients, false lumen of the descending thoracic aorta was patent. Figure 2 shows dilated descending thoracic aorta with a patent false lumen in a patient who we are monitoring carefully. However, surgical intervention for persistent aortic dissection with dilatation has not been carried out in these 3 patients because the lesion has not become larger during the follow-up period.



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Fig 2. Computed tomography image showing a dilated descending thoracic aorta with a patent false lumen in a 72-year-old patient, 6.3 years after total arch replacement.

 

    Comment
 Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 References
 
In our series, hospital mortality rate was low with 6.5% (3 of 46 patients) compared with recent reports from other institutes (5.9% to 18.6%) [1–6]. All 3 cases were in a preoperative shock state, and coronary malperfusion due to the dissection was associated in 2 of 3 cases. This emphasizes the need for urgent surgical repair in patients with acute type A dissection before the onset of hemodynamic instability if at all possible [9]. As for operative morbidity, there was only 1 patient with permanent cerebral damage. We believe that these favorable early results were attributed to the established antegrade selective cerebral perfusion and branched graft technique [1]. The antegrade selective cerebral perfusion allows unhurried and accurate reconstruction of arch vessels and distal anatomosis with the friable aortic tissue. Using a four-branched graft, we are able to reconstruct the arch vessels after resuming the antegade systemic perfusion from a side branch. For reconstruction of the arch vessels with the branched graft, the anastomotic sutures can be placed more distally on the intact arch vessels to which the dissection does not usually extend, compared with the island technique. We have not experienced any complications related to the antegrade selective cerebral perfusion and branched graft technique or any aortic arch reoperations.

Improvement of long-term prognosis after surgical repair of acute type A dissection is largely dependent on the reduction of complications related to the distal false lumen. To facilitate thrombosis of the distal false lumen, we conducted maximal graft replacement possible through median sternotomy to excise the segment of the aorta containing the intimal tear and used a separate graft with elephant trunk technique for open distal anastomosis. In our series, the false lumen in the descending thoracic aorta was frequently thrombosed (76.2%) at the latest follow-up period. This high rate might be a manifestation of a large number of patients (21%; 9 of 42) with preoperative dissection only of the thoracic aorta. However, this rate is obviously higher than some previous reports (52.7% [10], 59.2% [11]) in which arch replacement was performed confined to selected patients, and is consistent with other reports (54% [3] and 73.5% [4]) in which total arch replacement was done in all patients with acute type A dissection extending to the descending aorta. In this study, resection of entry, usage of the elephant trunk technique, or preoperative extent of the false lumen down to the abdominal aorta did not relate to the thrombosis of the false lumen. Because of a lack of aortic wall histology from all of the patients and no patients with Marfan syndrome, we were not able to detect a potential relationship between the aortic wall histology such as cystic medial degenaration and residual false lumen.

Regarding the effect of thrombosed false lumen on long-term outcome, the aortic diameter in the descending thoracic aorta was smaller when the false lumen in the thoracic aorta was thrombosed (34 ± 7 mm [n = 32] versus 44 ± 7 mm [n = 10]; p < 0.01). Barron and colleagues [12] also reported a connection between a persistent false lumen and increased diameter of the downstream aorta at hiatus. We think that thrombosis of the false lumen might provide the protective effect from postdissection dilatation. However, the number of patients is too small to draw a conclusion whether the thrombosed false lumen has less likelihood of reoperation or rupture or not.

The freedom from reoperation rate (93.6% at 5 years and 88.7% at 10 years) in our series is comparable to other reports (77% at 5 years [1], 93.0% at 7 years [3], 96.3% at 5 years, and 77.0% at 10 years [5]) after total arch replacement, and is higher than other reports (92.5% at 5 years and 77.0% at 10 years [13]) in which arch grafting was performed only in selected patients. As a result, the high rate of freedom from reoperation rate would contribute to our high survival rate (89.6% at 5 years and 82.7% at 10 years).

Of note, there were no reoperations for failure at the proximal repair, such as sinus dilatation, redissection, or aortic regurgitation during the follow-up period. Recently, several recent studies have raised concerns that the use of gelatin-resorcinol-formalin (GRF) glue for reapproximating the layers of the dissected aortic root has associated with aortic wall necrosis, which leads to redissection of the aortic root [14, 15]. We consistently infused the fibrin glue, not GRF glue, into the proximal false lumen and reunited the proximal dissected aortic layers with two Teflon felts. Additional supracoronary aortic valve resuspension demonstrated excellent long-term durability without any significant aortic regurgitation so far. In this regard, there were no patients with Marfan syndrome, which is reported to be an incremental risk factor for reoperation of the aortic root or valve after conservative proximal repair [16].

There still remains discussion whether such an extended arch replacement for acute type A dissection increases the risk of early mortality and subsequently results in less satisfactory outcome compared with surgery limited to the ascending aorta [5]. We think that total arch replacement does not contribute to excessive operative mortality compared with ascending aortic replacement without arch replacement. Because resection of entry site did not influence thrombosis of the false lumen in the descending thoracic aorta, it would be inevitable to encounter some patients who require the subsequent reoperation for the descending thoracic aorta after total arch replacement. To facilitate the proximal anastomosis in the possible subsequent reoperation for the descending thoracic aorta through left thoracotomy, we have to continue to apply the elephant trunk technique at initial total arch replacement. For the reasons stated above, we believe that total arch replacement can be accomplished with a low mortality rate and is an excellent technique in consideration of feasibility of subsequent reoperation through left thoracotomy. In conclusion, our aggressive total arch replacement accelerated thrombosis of the residual false lumen and led to excellent late results in the form of high freedom from reoperation and high survival rate[10].


    References
 Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 References
 

  1. Kazui T, Washiyama N, Muhammad BA, et al. Extended total arch replacement for acute type A aortic dissectionexperience with seventy patients. J Thorac Cardiovasc Surg 2000;119:558-565.[Abstract/Free Full Text]
  2. Hirotani T, Kameda T, Kumamoto T, Shirota S. Results of a total aortic arch replacement for an acute aortic arch dissection J Thorac Cardiovasc Surg 2000;120:686-691.[Abstract/Free Full Text]
  3. Hirotani T, Nakamichi T, Munakata M, Takeuchi S. Routine extended graft replacement for an acute type A aortic dissection and the patency of the residual false channel Ann Thorac Surg 2003;76:1957-1961.[Abstract/Free Full Text]
  4. Takahara Y, Sudo Y, Mogi K, Nakayama M, Sakurai M. Total aortic arch grafting for acute type A dissectionanalysis of residual false lumen. Ann Thorac Surg 2002;73:450-454.[Abstract/Free Full Text]
  5. Tan ME, Dossche KM, Morshuis WJ, Kelder JC, Waanders FG, Schepens MA. Is extended arch replacement for acute type A aortic dissection an additional risk factor for mortality? Ann Thorac Surg 2003;76:1209-1214.[Abstract/Free Full Text]
  6. Urbanski PP, Siebel A, Zacher M, Hacker RW. Is extended aortic replacement in acute type A dissection justifiable? Ann Thorac Surg 2003;75:525-529.[Abstract/Free Full Text]
  7. Myrmel T, Lai DT, Miller DC. Can the principles of evidence-based medicine be applied to the treatment of aortic dissections? Eur J Cardiothorac Surg 2004;25:236-242.[Abstract/Free Full Text]
  8. Hirotani T, Kameda T, Kumamoto T, Shirota S, Yamano M. Protective effect of thiopental against cerebral ischemia during circulatory arrest Thorac Cardiovasc Surg 1999;47:223-228.[Medline]
  9. Long SM, Tribble CG, Raymond DP, et al. Preoperative shock determines outcome for acute type A aortic dissection Ann Thorac Surg 2003;75:520-524.[Abstract/Free Full Text]
  10. 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.[Abstract]
  11. David TE, Armstrong S, Ivanov J, Barnard S. Surgery for acute type A aortic dissection AnnThorac Surg 1999;67:1999-2001.[Abstract/Free Full Text]
  12. Barron DJ, Livesey SA, Brown IW, Delaney DJ, Lamb RK, Monro JL. Twenty-year follow-up of acute type A dissectionthe incidence of extent of distal aortic disease using magnetic resonance imaging. J Card Surg 1997;12:147-159.[Medline]
  13. Kirsch M, Soustelle C, Houel R, Hillion ML, Loisance D. Risk factor analysis for proximal and distal reoperations after surgery for acute type A aortic dissection J Thorac Cardiovasc Surg 2002;123:318-325.[Abstract/Free Full Text]
  14. Kazui T, Washiyama N, Bashar AH, et al. Role of biologic glue repair of proximal aortic dissection in the development of early and midterm redissection of the aortic root Ann Thorac Surg 2001;72:509-514.[Abstract/Free Full Text]
  15. Yoshitatsu M, Nomura F, Katayama A, et al. Pathologic findings of aortic redissection after glue repair of proximal aorta J Thorac Cardiovasc Surg 2004;127:593-595.[Free Full Text]
  16. Casselman FP, Tan ES, Vermeulen FE, Kelder JC, Morshuis WJ, Schepens MA. Durability of aortic valve preservation and root reconstruction in acute type A aortic dissection Ann Thorac Surg 2000;70:1227-1233.[Abstract/Free Full Text]



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