ICVTS Click here for other ICVTS advertising opportunities
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Interact CardioVasc Thorac Surg 2009;9:426-430. doi:10.1510/icvts.2009.203976
© 2009 European Association of Cardio-Thoracic Surgery
This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to Personal Folders
Right arrow Download to citation manager
Right arrow Author home page(s):
Alberto Forteza
Enrique Pérez
Right arrow Permission Requests
Google Scholar
Right arrow Articles by Forteza, A.
Right arrow Articles by Cortina, J.
PubMed
Right arrow PubMed Citation
Right arrow Articles by Forteza, A.
Right arrow Articles by Cortina, J.

Institutional report - Vascular thoracic

Acute type A aortic dissection: 18 years of experience in one center (Hospital 12 de Octubre){star}

Alberto Fortezaa,*, Carlos Martína, Jorge Centenoa, María Jesús Lópeza, Enrique Péreza, Javier de Diegoa, Violeta Sánchezb and José Cortinaa

a Department of Cardiac Surgery, Hospital Universitario 12 de Octubre, Madrid, Spain
b Department of Cardiology, Hospital Universitario 12 de Octubre, Madrid, Spain

Received 3 February 2009; received in revised form 19 April 2009; accepted 20 April 2009

{star} Special mention to Dr. J.J. Rufilanchas (Chief Division of Cardiac Surgery from 1988–2005).

*Corresponding author. C/Agastia n° 45 3° C, 28041, Madrid, Spain. Tel.: +34 91636275497; fax: +34 913908396.

E-mail address: apforteza{at}yahoo.es (A. Forteza).


   Abstract
Top
 Abstract
1. Introduction
 2. Materials and methods
 3. Results
 4. Reoperation
 5. Discussion
 6. Conclusions
 References
 
Here, we review our experience in acute type A aortic dissection analyzing the role of antegrade brain protection. A total of 105 patients underwent surgery for acute type A aortic dissection between March 1990 and October 2008. An open technique with deep hypothermia was used in 81 patients. Deep hypothermia alone was induced in 32 patients; in combination with retrograde cerebral perfusion in 26 patients and in combination with antegrade cerebral perfusion (ACP) in the final 23 patients. The overall hospital mortality rate was 15%. Hospital mortality risk factors were age ≥70 years and preoperative shock (P<0.05). Hospital mortality was reduced to 9% in the last 23 consecutive patients in whom ACP was accomplished (P=0.05). Survival rate after 1, 5, 10 and 15 years of follow-up was 97.6±1.7%, 84.3±4.4%, 60.7±7.5% and 57.1±7.8%, respectively. The only late death risk predictor was the non-use of ACP (P<0.05). Surgery for acute aortic dissection provides excellent results. ACP via the axillary artery improves the prognosis for these patients and should be the brain protection method of choice.

Key Words: Aorta; Aortic dissection; Cerebral protection; Surgery complication; Neurologic injury


   1. Introduction
Top
 Abstract
 1. Introduction
2. Materials and methods
 3. Results
 4. Reoperation
 5. Discussion
 6. Conclusions
 References
 
Despite new advances, acute type A aortic dissection is still associated with high morbidity and mortality rates. At present, hospital mortality is reported between 15% and 35%, with 5-year survival rate of 65–75% [1–4].

The high incidence (10–20%) of postoperative neurological complications in these patients has been associated with inadequate brain protection during circulatory arrest, embolic accidents and/or cerebral malperfusion due to preferential flow to the false lumen during perfusion. In recent years, the introduction of new brain protection techniques, such as antegrade cerebral perfusion (ACP) and cannulation of axillary artery, has considerably reduced the incidence of this complication [5–8].

The aim of this retrospective study is to consider our experience in acute type A aortic dissection in terms of hospital mortality, reoperation and long-term survival.


   2. Materials and methods
Top
 Abstract
 1. Introduction
 2. Materials and methods
3. Results
 4. Reoperation
 5. Discussion
 6. Conclusions
 References
 
A total of patients (85 men and 20 women) underwent surgery in our hospital for acute type A aortic dissection from March 1990 to October 2008.

The mean age was 59±8 years. The diagnosis was confirmed using aortography in the initial experience (17%) and transthoracic echocardiography (77%), transesophageal echocardiography (67%) and/or thoracoabdominal scan (66%) later on.

A total of 98 patients (93%) underwent emergency surgery (<24 h) and the remainder underwent urgent surgery (within 72 h of diagnosis).

Imaging tests showed aortic regurgitation in 87 patients (52% severe). The preoperative clinical and demographic characteristics of the patients are given in Table 1.


View this table:
[in this window]
[in a new window]

  		Table 1 Preoperative characteristics of patients (n=105)

 
2.1. Surgical technique

Initially, the inclusion method was used with simple aortic cross-clamping. Open distal anastomosis was introduced in 1994 and this is currently the method of choice.

Arterial cannulation was performed on femoral artery (76%), axillary artery (20%) or aortic arch (4%), and venous drainage on the right atrium (86%) or femoral vein (14%). The ascending aorta was clamped and cardioplegic solution (5–10 ml/kg) was infused into the coronary sinus at a pressure around 40 mmHg. A longitudinal opening was made in the ascending aorta with a supracoronary circumferential transection; the rupture of the intima was located and the morphology and functionality of the aortic valve was examined. The esophageal and bladder temperatures were monitored and cooling was interrupted when the bladder temperature reached 18 °C. The pathological segment of aorta was resected and replaced with Hemashield Dacron graft (Boston Scientific, Natick, MA, USA), reinforcing the native aorta with gelatine-resorcine-formaldehyde (Laboratories Cardial, Saint-Etienne, France). Isolated ascending aortic replacement was performed in 66 patients, involving the hemiarch in 26 and the whole aortic arch in 13. Elephant trunk technique was added in six patients. The aortic valve was preserved in 64 patients and it was replaced in 38. A proximal rupture was located in 88 patients. The mean CPB duration was 183±56 min. The mean aortic clamp time was 113±38 min and the mean circulatory arrest time was 37±23 min. During circulatory arrest, the brain protection method used was deep hypothermia. It was combined with retrograde cerebral perfusion in 26 patients (100–600 ml/min) and with ACP via the right axillary artery in the last 23 patients (10–15 ml/kg/min).

2.2. Follow-up

All the surviving patients were required to have serial computed tomography (CT) to assess the distal aorta. Clinical data were obtained by means of personal and/or telephone interviews with patients, their family and primary care physicians. These data included information on postoperative morbidity/mortality and any reoperations performed. A total of 85 patients were available for follow-up.

2.3. Statistical analysis

The SPSS statistical package (version 15.00 for Windows SPSS, Chicago, IL, USA) was used for all analyses. Univariate analysis was carried out on the perioperative variables to determine the statistically significant risk factors (P<0.05) for hospital mortality, reoperation and mortality during follow-up. Univariate analysis was followed by logistic regression or Cox regression analysis to determine the independent risk factors. Kaplan–Meier survival curves were developed to estimate patients free of reoperation and survival in terms of time.


   3. Results
Top
 Abstract
 1. Introduction
 2. Materials and methods
 3. Results
4. Reoperation
 5. Discussion
 6. Conclusions
 References
 
3.1. Hospital mortality

Hospital mortality was 15% (16/105). Six patients died as a result of intraoperative hemorrhage, four due to low cardiac output, two from neurological damage, two from sepsis and two from postoperative multiple organ failure. The complications observed during the postoperative period are shown in Table 2.


View this table:
[in this window]
[in a new window]

  		Table 2 Postoperative complications

 
Univariate analysis showed advanced age (≥70 years), left ventricular dysfunction, preoperative cardiogenic shock, CPB time >200 min, clamp time >130 min and postoperative stroke as risk factors for hospital mortality.

Multivariate analysis identified advanced age (≥70 years) and preoperative cardiogenic shock as risk factors for hospital mortality (P=0.043; RR=2.77 and P=0.025; RR=2.6, respectively).

3.2. Neurological complications

Patients were grouped according to whether or not circulatory arrest was introduced and those who had received it were classified to the different methods of brain protection used. Mortality and postoperative neurological complications were calculated in each of these groups. No statistical significance was observed (Table 3).


View this table:
[in this window]
[in a new window]

  		Table 3 Neurological complications and mortality with the different brain protective methods used

 
3.3. Follow-up

Postoperative follow-up was possible in 95% of the patients (median 67 months, range 1–204 months). After discharge from hospital, 70% of the patients (62/89) had at least one CT scan. Of the 27 surviving patients who did not undergo CT, 17 declined to have the imaging test, four were lost to follow-up and six patients died during the follow-up period.

Tomographic analysis showed a false lumen in the distal aorta remaining permeable in 71% of the patients, although progressive dilation of the thoracic and or abdominal aorta was observed in only 17%.


   4. Reoperation
Top
 Abstract
 1. Introduction
 2. Materials and methods
 3. Results
 4. Reoperation
5. Discussion
 6. Conclusions
 References
 
Reoperation was not required after 1, 5, 10 and 15 years in 98.4±16%, 92.8±3.5%, 81.8±6% and 42.7±13.3% of the patients, respectively (Fig. 1). Cox regression analysis pointed to severe preoperative aortic regurgitation and preservation of the aortic valve as independent reoperation risk factors (P=0.043; RR=2.8 and P=0.037; RR=4.1, respectively). Determinant factors in univariate analysis are shown in Table 4.


Figure 1
View larger version (10K):
[in this window]
[in a new window]

  		Fig. 1. Freedom from reoperation curve.

 

View this table:
[in this window]
[in a new window]

  		Table 4 Univariate analysis in hospital survival patients (determinant factors)

 
During follow-up period, 13 patients (14.6%) were reoperated for the following reasons: severe aortic insufficiency and dilation of the ascending aorta in five patients, severe aortic insufficiency and redissection of the ascending aorta in three, isolated severe aortic insufficiency in one, severe aortic and mitral insufficiency in one, mitroaortic endocarditis in one, aortobronchial false aneurysm in one and fistula between ascending aorta and the right atrium in one patient. No patient was reoperated for pathology in descending thoracic aorta. The hospital mortality rate was 23% (3/13 patients).

4.1. Long-term survival

Mortality rate was 25% (22/89). The actuarial survival rate was 97.6±1.7%, 84.3±4.4%, 60.7±7.5% and 57.1±7.8% after 1, 5, 10 and 15 years, respectively (Fig. 2). Ten patients died as a result of cardiac disease, two due to intraoperative hemorrhage, two due to neurological damage, two from neoplasia, two from sudden rupture of thoracic aorta and four from an unknown cause.


Figure 2
View larger version (11K):
[in this window]
[in a new window]

  		Fig. 2. Survival during follow-up curve.

 
Determinants factors of follow-up mortality are shown in Table 5.


View this table:
[in this window]
[in a new window]

  		Table 5 Follow-up mortality. Univariate analysis (determinant factors)

 
Multivariate analysis showed the non-use of antegrade brain protection to be the only significant independent mortality predictor during the follow-up period (Cox regression) (P=0.02; RR=3.2).


   5. Discussion
Top
 Abstract
 1. Introduction
 2. Materials and methods
 3. Results
 4. Reoperation
 5. Discussion
6. Conclusions
 References
 
Acute type A aortic dissection is a critical situation requiring emergency surgical intervention in the majority of cases.

Siegal [9] estimated that mortality risk in untreated patients increases by 1% per hour during the first 48 h, reaching 70% after a week. According to data provided by the International Registry of Acute Aortic Dissection (IRAD), mortality rate for patients treated conservatively is 58%, the compared to a global surgical mortality of 24% [1, 10, 11].

Although recent years have brought important advances in diagnostic and surgical techniques, there are marked variations in hospital mortality, with a range between 15% and 30% [1, 10–12].

Predictor factors of hospital mortality in acute type A aortic dissection are similar in the majority of the articles published [2, 12]. According to IRAD data [1], independent mortality factors are advanced age, hypotension/shock, previous cardiopathy and preoperative renal, mesenteric or myocardial ischemia. In our experience, the only independent hospital mortality predictors were advanced age (≥70 years) and preoperative cardiogenic shock.

Postoperative neurological complications are a frequent cause of morbidity/mortality in aortic dissection, the estimated incidence being between 10% and 20% [3]. Ergin et al. [5] suggest that postoperative stroke is caused mainly by embolic incidents related possibly to retrograde perfusion from the femoral artery, and not directly to the method of brain protection used, while temporary neurological dysfunction (TND) could be linked to inadequate brain protection. ACP has been associated with a significant reduction in TND in various recent reviews [6, 13], although its role is not so apparent in the reduction of stroke. Neurological damage in aortic dissection is multifactorial and may be caused by prolonged circulatory arrest, embolic incidents and/or by a syndrome of cerebral malperfusion due to preferential flow to the false lumen.

Cannulation of the axillary reduces the risk of malperfusion and it also reduces the embolization of thrombi from the abdominal and thoracic aorta [7, 8]. In our experience, ACP via the axillary artery reduced the incidence of TND to 8.6% and the incidence of hospital mortality to 9% in the last 23 patients, suggesting its protective role against neurological complications and associated morbidity/mortality.

Acute preoperative aortic regurgitation and preservation of the aortic valve were the determining factors for late aortic reoperation. According to these data and supported by other reports, an aggressive approach on the aortic root in the initial surgery (Bentall procedure) could be justified [4]. Estrera et al. [14], on the other hand, observed an acceptable durability of the aortic valve after preservation, indicating that potential reoperation should not dictate the initial procedure. On discharge from hospital, only 8 (13%) of the 62 surviving patients who had undergone CT during the follow-up period showed progressive dilation in other areas of the aorta requiring surgery – one patient with aortobronchial false aneurysm, one with fistula between ascending aorta and the right atrium, two patients with abdominal aortic aneurysm, two with thoraco-abdominal aneurysm and two with descending thoracic aorta aneurysm. Two of these patients were operated, two declined reintervention and the remainder presented high comorbidity which made the procedure non-indicated.

This low rate of reoperation of the distal aorta is probably due to the high percentage of primary ruptures of the intima identified during the intervention. Thus, various authors report that not resecting the area of rupture in the initial surgery is the principal factor for late reoperation due to dilation of the thoracic or abdominal aorta [4, 14].

Actuarial survival curve after discharge from hospital shows similar shape than those described by other authors [3, 4]. Non-use of antegrade brain protection was found to be a predictor of late mortality, showing that although antegrade perfusion did not significantly alter the initial postoperative results, it is of major importance with regard to late survival. This finding shows that maintaining correct cerebral and neurological function has a direct effect on survival. Pompilio et al. [15] determined the effect of perioperative neurological incidents on late mortality, i.e., the patients who survived neurological damage while in hospital, presented a lower long-term survival rate. This could be explained by these patients' high-risk of contracting bronchopneumonia, new neurological incidents and other complications associated with their limited functional capacity [2].

5.1. Limitations

This article is subject to all the limitations of a non-randomized retrospective study. The low incidence of this pathology entails a small number of patients operated, limiting the statistical power of these findings.

Only 70% of the patients had a follow-up CT scan, probably because our hospital supports a high marginal population. Because the review covered a long period (18 years), the three methods of brain protection were not in use at the same time, with the statistical significance of this issue being unknown.


   6. Conclusions
Top
 Abstract
 1. Introduction
 2. Materials and methods
 3. Results
 4. Reoperation
 5. Discussion
 6. Conclusions
References
 
Short- and long-term results of acute aortic dissection are acceptable. ACP via the axillary artery has modified the concept of circulatory arrest and seems to improve long-term prognosis of these patients. We feel it should be the method of choice for brain protection in acute aortic dissection when the supra-aortic vessels are not affected.


   References
Top
 Abstract
 1. Introduction
 2. Materials and methods
 3. Results
 4. Reoperation
 5. Discussion
 6. Conclusions
 References
 

  1. Rampoldi V, Trimarchi S, Eagle KA, Nienaberc CA, Oh JK, Bossone E, Myrmel T, Sangiorgia GM, De Vincentiis C, Cooper JV, Fang J, Smith D, Tsai T, Raghupathy A, Fattori R, Sechtem U, Deeb MG, Sundt TM III, Isselbacher EM. Simple risk models to predict surgical mortality in acute type A aortic dissection: The International Registry of Acute Aortic Dissection Score. Ann Thorac Surg 2007;83:55–61.[Abstract/Free Full Text]
  2. Halstead J, Meier M, Etz C, Spielvogel D, Bodian C, Wurm M, Shahani R, Griepp R. The fate of the distal aorta after repair of acute type A aortic dissection. J Thorac Cardiovasc Surg 2007;133:127–135.[Abstract/Free Full Text]
  3. Ehrlich MP, Ergin AM, McCullough JN, Lansman SL, Galla JD, Bodian CA, Apaydin A, Griepp RB. Results of immediate surgical treatment of all acute type A dissections. Circulation 2000;102(Suppl_3):248–252.
  4. Kazui T, Washiyama N, Bashar AH, Terada H, Suzuki T, Ohkura K, Yamashita K. Surgical outcome of acute type A aortic dissection: analysis of risk factors. Ann Thorac Surg 2002;74:75–81; discussion 81–82.[Abstract/Free Full Text]
  5. Ergin A, Uysal S, Reich DL, Apaydin A, Lansman SL, McCullough JN, Griepp RBl. Temporary neurological dysfunction after deep hypothermic circulatory arrest: a clinical marker of long-term functional deficit. Ann Thorac Surg 1999;67:1887–1890.[Abstract/Free Full Text]
  6. Yamashita K, Kazui T, Terada H, Washiyama N, Suzuki K, Bashar AH. Cerebral oxygenation monitoring for total arch, replacement using selective cerebral perfusion. Ann Thorac Surg 2001;72:503–508.[Abstract/Free Full Text]
  7. Sabik JF, Lytle BW, McCarthy PM, Cosgrove DM. Axillary artery an alternative site of arterial cannulation for patients with extensive aortic and peripheral vascular disease. J Thorac Cardiovasc Surg 1995;109:885–890.[Abstract]
  8. Moizumi Y, Motoyoshi N, Sakuma K, Yoshida S. Axillary artery cannulation improves operative results for acute type A aortic dissection. Ann Thorac Surg 2005;80:77–83.[Abstract/Free Full Text]
  9. Siegal EM. Acute aortic dissection. J Hosp Med 2006;1:94–105.[Medline]
  10. Evangelista A. Avances en el síndrome aórtico agudo. Rev Esp Cardiol 2007;60:428–439.[CrossRef][Medline]
  11. Hagan PG, Nienaber CA, Isselbacher EM, Bruckman D, Karavite DJ, Russman PL, Evangelista A, Fattori R, Suzuki T, Oh JK, Moore AG, Malouf JF, Pape LA, Gaca C, Sechtem U, Lenferink S, Deutsch HJ, Diedrichs H, Marcos y Robles J, Llovet A, Gilon D, Das SK, Armstrong WF, Deeb GM, Eagle KA. The International Registry of Acute Aortic Dissection (IRAD): new insights into an old disease. J Am Med Assoc 2000;283:897–903.[Abstract/Free Full Text]
  12. Mehta RH, Suzuki T, Hagan PG, Bossone E, Gilon D, Llovet A, Maroto LC, Cooper JV, Smith DE, Armstrong WF, Nienaber CA, Eagle KA. Predicting death in patients with acute type A aortic dissection. Circulation 2002, 15;105:200–206.[Abstract/Free Full Text]
  13. Okita Y, Minatoya K, Tagusari O, Ando M, Nagatsuka K, Kitamura S. Prospective comparative study of brain protection in total aortic arch replacement: deep hypothermic circulatory arrest with retrograde cerebral perfusion or selective anterograde cerebral perfusion. Ann Thorac Surg 2001;72:72–79.[Abstract/Free Full Text]
  14. Estrera A, Miller C, Villa A, Lee TY, Meada R, Irani A, Azizzadeh A, Coogan S, Safi HJ. Proximal reoperations after repaired acute type A aortic dissection. Ann Thorac Surg 2007;83:1603–1608; discussion 1608–1609.[Abstract/Free Full Text]
  15. Pompilio G, Spirito R, Alamanni Fl. Determinants of early and late outcome after surgery for type A aortic dissection. World J Surg 2001;25:1500–1506.[Medline]




This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to Personal Folders
Right arrow Download to citation manager
Right arrow Author home page(s):
Alberto Forteza
Enrique Pérez
Right arrow Permission Requests
Google Scholar
Right arrow Articles by Forteza, A.
Right arrow Articles by Cortina, J.
PubMed
Right arrow PubMed Citation
Right arrow Articles by Forteza, A.
Right arrow Articles by Cortina, J.

HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
ANN THORAC SURG ASIAN CARDIOVASC THORAC ANN EUR J CARDIOTHORAC SURG
J THORAC CARDIOVASC SURG ICVTS ALL CTSNet JOURNALS