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Eur J Cardiothorac Surg 2000;17:462-467
© 2000 Elsevier Science NL

Bilateral antegrade selective cerebral perfusion during surgery on the proximal thoracic aorta

Karl M. Dosschea, Wim J. Morshuisa, Marc A. Schepensa, Frans G. Waandersb

a Department of Cardiopulmonary Surgery, St. Antonius Hospital, Koekoekslaan 1, 3435 CM Nieuwegein, The Netherlands
b Department of Clinical Perfusion, St. Antonius Hospital, 3435 CM Nieuwegein, The Netherlands

Corresponding author. Tel.: +31-30-609-2047; fax: +31-30-609-2120
e-mail: dossche{at}planet.nl


    Abstract
 Top
 Abstract
 1. Introduction
 2. Materials and methods
 3. Results
 4. Discussion
 Appendix A. Conference...
 References
 
Objective: To assess risk factors for hospital death and neurologic outcome after surgery on the proximal thoracic aorta using moderate hypothermic circulatory arrest and bilateral antegrade selective cerebral perfusion. Methods: From October 1995 through June 1999, 163 patients with a mean age of 63±11 years underwent surgery using bilateral antegrade selective cerebral perfusion. Degenerative aneurysms (55%) and acute type A dissection (28%) were the predominant indications for operation. Forty-six (28%) operations were considered as emergency procedure. Twenty-four (15%) procedures were reoperations. Results: Mean ASCP time was 48±20 min. Hospital mortality was 8.6% (n=14; 70% confidence limit (CL): 6.4–10.8%). Univariate risk factors for hospital mortality were acute type A dissection (P=0.003), central neurologic damage <24 h before the operation (P=0.000), preoperative hemodynamic instability (P=0.034), and rethoracotomy for any cause (P=0.036). Logistic regression analysis identified central neurologic damage <24 h (P=0.006, odds ratio 14) as an independent risk factor. Temporary neurologic damage occurred in 3.8% (n=6; 70% CL: 2.3–5.3%) of patients. Logistic regression analysis indicated preoperative hemodynamic instability (P=0.003, odds ratio 13) as an independent risk factor. Perioperative permanent central neurologic damage was reported in another 3.8% (n=6; 70% CL: 2.3–5.3%) patients. Acute type A dissection (P=0.018, odds ratio 8) and the non-use of a midline sternotomy (P=0.049, odds ratio 8) were retained as independent risk factors. Conclusion: Hospital mortality and perioperative neurologic complications are not significantly influenced by the duration of antegrade selective cerebral perfusion. Overall complication rate is low.

Key Words: Antegrade selective cerebral perfusion • Proximal thoracic aorta • Risk factors • Mortality • Morbidity


    1. Introduction
 Top
 Abstract
 1. Introduction
 2. Materials and methods
 3. Results
 4. Discussion
 Appendix A. Conference...
 References
 
Various techniques including deep hypothermic circulatory arrest [13], partial or bilateral antegrade selective cerebral perfusion (ASCP) [46], and retrograde cerebral perfusion through the superior vena cava [79] have been proposed as means to protect the central nervous system from ischemia during surgery on the ascending aorta or aortic arch. All methods have both advantages and disadvantages.

Since 1989, we have been using ASCP – first partial, later bilateral – as an adjunct to extend the safe period of circulatory arrest in operations on the proximal thoracic aorta, in which a circulatory arrest period of more than 30 min is anticipated. Our experience with ASCP has been described before [6]. This study is an update on our continuing experience with bilateral ASCP in combination with moderate hypothermic circulatory arrest.


    2. Materials and methods
 Top
 Abstract
 1. Introduction
 2. Materials and methods
 3. Results
 4. Discussion
 Appendix A. Conference...
 References
 
From October 1995 through June 1999, 163 patients underwent operations on the various portions of the thoracic aorta, using bilateral ASCP. There were 94 men and 69 women, mean age 63±11 years (range 21–85 years). Indications for operation were an atherosclerotic or degenerative aneurysm in 90 (55%) patients, a chronic postdissection aneurysm in 24 (15%) patients, acute type A dissection in 45 (28%) patients, aneurysm of an aberrant right subclavian artery in two (1%) patients and miscellaneous in another two (1%) patients. Sixteen patients with acute type A dissection and 1 patient with a frank aneurysmal rupture presented with preoperative hemodynamic instability (resulting from cardiac tamponade, shock, superior vena cava compression or myocardial ischemia). Forty-six (28%) operations were considered as emergency procedures (within 24 h after onset of symptoms). Eight (5%) patients had a history of a recent central neurologic deficit (paresis, paralysis or loss of consciousness <24 h before surgery). Other pertinent data relating to patients and operation are given in Table 1.


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Table 1. Overview of disease- and operation-related variables included in univariate analysis (n=163)

 
Preoperative evaluation in all electively operated patients included Doppler ultrasound of the extracranial vessels, digital subtraction angiography of the ascending aorta, aortic arch, extracranial vessels and intracranial circulation, and carotid compression test with monitoring by electroencephalogram.

2.1. Operative technique
A median sternotomy was used in 152 (93%) patients, a left posterolateral thoracotomy in 10 (6%) patients, and a clamshell incision in one (1%) patient. Table 2 summarizes the operative procedures. Details of our cannulation techniques were described elsewhere [6].


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Table 2. Overview of operative procedures (n=163)

 
The technique of bilateral ASCP was described by Kazui and coworkers in 1994 [4,5]. In short, the technique consisted in the following. Patients were cooled down to nasopharyngeal temperatures between 22 and 25°C. Systemic circulation was then arrested and the aorta was opened in continuity with the aneurysm. Under direct visual control, and with the patient in Trendelenburg position, the innominate artery and the left common carotid artery were both cannulated, usually with a 15-F retrograde coronary sinus perfusion cannula with manual-inflating cuff and silicone body (Medtronic DLP, Grand Rapids, MI, USA). Subsequently, the left subclavian artery was either clamped or occluded with a Fogarty catheter (Baxter Health Care, Irvine, CA). Blood was then perfused into both arteries at a flow rate of 10 ml/kg per min using a single roller pump, separated from the systemic circulation. The cerebral perfusion pressure was adjusted to maintain a right radial pressure of 40–70 mmHg. During the period of body circulation arrest, nasopharyngeal temperatures were kept at 25°C. If available, transcranial Doppler (TCD) measurements of blood velocity of the middle cerebral artery (MCA) confirmed the proper placement and function of both cannulas. The introduction of the cerebral perfusion catheters usually took less than 1 min, even in patients with aortic dissection extending into the aortic arch vessels.

Details of the operative procedures are listed in Table 2. In general, all diseased aortic tissue was resected in every patient; there were no patients in whom the aortic graft prosthesis was covered by the native aortic wall. If aortic dissection was present, the proximal and distal aortic cuffs were supported by a rim of Teflon felt to reinforce these aortic segments. In the case of aortic arch replacement, the aortic vessels were reimplanted through a single cuff in 29 patients, or separately in 40 patients.

2.2. Statistical methods
The continuous data are expressed as mean±standard deviation. A number of patient-, disease- and operation-related variables (Table 1) were first analyzed using univariate analysis (chi-square or Fisher's exact test) to determine whether any single variable influenced early mortality and perioperative neurologic complications. A variable with a P-value of less than 0.05 was found to be significant. The same variables were then analyzed using backward logistic regression analysis; a multiple logistic regression model was used to determine the independent predictability of the retained variables in influencing early mortality and postoperative central neurologic complications. All computations were performed with the aid of SPSS (SPSS for Windows, version 7.5; SPSS Inc., Chicago, IL, USA) statistical software packages.


    3. Results
 Top
 Abstract
 1. Introduction
 2. Materials and methods
 3. Results
 4. Discussion
 Appendix A. Conference...
 References
 
3.1. Hospital mortality
The overall hospital mortality was 8.6% (n=14; 70% confidence limit (CL): 6.4–10.8%). This includes one intraoperative death due to exsanguination and two patients who died within 24 h after surgery on the intensive care unit due to low cardiac output. Five patients with an otherwise uneventful postoperative course died of rupture of a residual distal aneurysm or dissected aorta; four patients died of multi-organ failure; one patient died of low cardiac output. Severe operation-related neurologic damage was a contributing factor in one death. On univariate analysis, several factors proved to have significant influence on the overall mortality. Acute type A dissection (P=0.003), central neurologic damage <24 h before the operation (P=0.000), preoperative hemodynamic instability (P=0.034), and rethoracotomy for any cause (P=0.036) were found to be statistically significant predictors of hospital mortality. Duration of cardiopulmonary bypass, prolonged ASCP time and extent of the replacement had no significant influence on hospital mortality. One factor was retained as an independent predictor of hospital mortality with significant relative risk calculated by logistic regression analysis: the presence of a central neurologic deficit <24 h before surgery (P=0.006, odds ratio 14).

3.2. Hospital morbidity
All but three patients regained consciousness postoperatively, and were included for neurologic examination. Excluded from the analysis are the patient who died of exsanguination in the operating room, and two patients who died within 24 h after surgery. Of these patients, 69% (n=112) were awake and alert within 24 h; 88% (n=143) within 48 h. Temporary neurologic dysfunction (TND) including mental confusion, lethargy, and weakness, associated with negative computed tomographic scanning and complete resolution of symptoms before discharge was reported in six (3.8%; 70% CL: 2.3–5.3%) patients. These temporary disturbances were excluded from the definition of postoperative permanent neurologic damage. On univariate analysis, preoperative hemodynamic instability (P=0.009), emergency operation (P=0.034) and acute type A dissection (P=0.031) emerged as dominant determinants predicting temporary neurologic dysfunction (TND). By multiple logistic regression, the only independent predictor of temporary neurologic dysfunction was preoperative hemodynamic instability (P=0.003, odds ratio 13).

Postoperative permanent central neurologic injury was reported in 11 (6.9%; 70%CL: 4.9–8.9%) patients, although five of them presented with a recent (<24 h) central neurologic deficit before the operation. Thus, only six (3.8%; 70% CL: 2.3–5.3%) patients sustained perioperative permanent central neurologic damage (defined as any lateralizing deficit that was present immediately postoperatively, i.e. without free interval, but not preoperatively). One patient who developed a delayed stroke (5 days after the intervention), but was not considered as a neurologic problem caused by the ASCP technique. The neurologic damage consisted of hemiplegia in three patients, multiple cerebral infarction in another two patients, and paraparesis in one patient. These patients were further analyzed statistically. On multivariate analysis, acute type A dissection (P=0.019, odds ratio 8) and the non-use of a midline sternotomy – left posterolateral thoracotomy or clamshell incision – (P=0.049, odds ratio 8) were found to be independent predictors of postoperative permanent neurologic damage (Table 3). Again, the duration of ASCP did not significantly influence the incidence of permanent neurologic damage.


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Table 3. Multivariate prediction (stepwise logistic regression analysis) of perioperative permanent central neurologic damage

 
Thirty-one patients underwent an early reoperation. Fifteen (9.2%; 70% CL: 6.9–11.5%) of them underwent an early (<24 h after the initial operation) reintervention for excessive bleeding or cardiac tamponade; in another 12 (7.5%; 70% CL: 5.5–9.5%) patients with diffuse bleeding from various anastomotic sites, compresses were left in place for 24 h, after which they were removed. In four patients, a salvage rethoracotomy was performed on the postoperative ward because of acute severe hemodynamic complications.

Perioperative myocardial infarction (serum CPK>500 IU/l with a CPK-MB fraction >3%) occurred in 7 (4.3%; 70% CL: 2.7–5.9%) patients. Three of these patients presented with acute type A dissection and did not undergo preoperative coronary angiography. Postoperative coronary angiography revealed three-vessel coronary disease in one of them, requiring PTCA of the target lesion.

Stable elevated serum creatinine levels (>200 µmol/l) were present in seven (4.3%; 70% CL: 2.7–5.9%) patients; one of them already had elevated serum creatinine levels preoperatively. Temporary hemodialysis was necessary in four (2.5%; 70% CL: 1.3–3.8%) patients; two of them died subsequently, the other two recovered completely.

3.3. Extracorporeal circulation data
The data concerning extracorporeal circulation in the 162 patients who left the operation theatre alive were as follows: total pump time (ECC) ranged from 96 to 431 min (mean 216±62 min), myocardial ischemic time (CC) ranged from 28 to 267 min (mean 123±45 min), and ASCP time ranged from 16 to 119 min (mean 48±20 min) (defined as the time period during which only the brain is perfused); 48% of patients had an ASCP time >45 min.


    4. Discussion
 Top
 Abstract
 1. Introduction
 2. Materials and methods
 3. Results
 4. Discussion
 Appendix A. Conference...
 References
 
Since there are currently three main methods of brain protection used during aortic arch exclusion, it seems relevant to ask which one is best, and in particular whether antegrade selective cerebral perfusion is superior to DHCA alone or in combination with RCP [10]. As our study is retrospective and non-randomized, it is not possible to make any statement on the superiority of either technique. However, when we compare our overall results with ASCP as an adjunct with those of reports using the two other techniques, some conclusions can be made. Deep hypothermia alone, provided it is carried out properly, is efficient in protecting the central nervous system when circulatory arrest lasts less than 45 min [1,2]. Recent data suggest that the protective effect of hypothermia at 15°C may even be shorter, i.e. ±29 min [11]. In about 50% of our patients, ASCP time required to perform an adequate repair exceeded 45 min. The overall incidence of TND was 3.8%, which is considerably lower than 19–28% reported by the group of Ergin [1,12]. Although we did not perform the extensive psychological testing as did the group of Ergin – which might underestimate our true incidence of TND – the difference is striking. They found a significant correlation between the incidence of TND and the duration of DHCA, as well as with patient age. In our series, there was no significant relationship between TND and ASCP time; the only independent risk factor for TND was preoperative hemodynamic instability, which confirms our findings in a previous study [6]. It is supposed that this clinical syndrome is a manifestation of subtle brain injury due to inadequate cerebral protection. Further comparison of the influence of various protective methods on the incidence of TND is difficult; there are few data in the literature since this complication goes unmentioned by many investigators. We have never been in favor of RCP as an adjunct to extend the safe duration of DHCA because of the many unresolved issues regarding this technique. Okita and associates report an incidence of severe TND of 25% in 148 patients who underwent operations on the aortic arch involving DHCA and RCP [13]. So far, it is the only series in literature that contains an analysis of the incidence of TND after RCP. Griepp and colleagues found experimentally significant brain edema and increased cellular injury in situations in which prolonged and effective RCP was used [14]. This should raise a caution flag for all who believe that RCP gives one the luxury of time that one would not have with DHCA alone.

Perioperative permanent central neurologic damage was encountered is 3.8% of patients in our series. This compares favorably with other reports using the same technique for ASCP [4,5] or DHCA [1,2]. We did not encounter a significant increase in stroke rate beyond 40 min of ASCP as was the case in an important contribution of Svensson and colleagues on the use of DHCA [2]. Okita and associates found no correlation between the technique for brain protection and the incidence of postoperative stroke [13,15]. This is in agreement with findings of the group of Ergin et al. [1]. It is now assumed that perioperative stroke or central neurologic damage is largely due to embolization of atheromatous material. Multiple regression analysis identified acute type A dissection and the non-use of a midline sternotomy as risk factors for perioperative central neurologic damage in our series. The isolation of the aortic arch vessels and installation of our ASCP catheters through a posterolateral thoracotomy requires more manipulation of the aortic arch or descending aorta than through a midline sternotomy. We think that this may enhance the risk of embolization of atheromatous debris from these usually atheromatous aortic segments into the arch vessels. In one patient, central neurologic complications occurred due to inadequate deairing of the ASCP catheters. Throughout the series, we did not encounter problems in isolating the aortic arch vessels or in introducing the catheters into the arch vessels.

We do not feel that ASCP results in a more complex and time-consuming procedure. The preparation and introduction of the ASCP catheters usually takes less than 1 min in experienced hands. As the perfusion catheters are flexible, they can be placed towards the patient's head; therefore, they do not obscure the operation field. Most of our elective operations are now performed with continuous bilateral TCD monitoring of the MCA. We found that the embolic event rate during manipulation of the arch vessels was absent or low in most of our procedures. We do not use routinely the bilateral TCD in situations where a posterolateral thoracotomy is used, because of the patient's position. TCD flow monitoring has the additional advantage that it provides the surgical team with ‘on-line’ information on the proper functioning of the ASCP system. Especially in situations of acute type A dissection or postdissection aneurysm with involvement of the arch vessels, it may be difficult to identify the true lumen. Malpositioning is easily and immediately recognized during TCD flow monitoring. We do not feel that the TCD monitoring system makes a complex operation even more complex. The installation of the system takes only a few minutes.

The number of reoperations for bleeding was high in our series, compared to data of other studies. We used the open technique in every patients, i.e. the native diseased aorta was not wrapped around the vascular graft in any of the patients. In addition, we did not use aprotinin or other hemostatic agents in any of these patients. This may be an explanation for this high number of reoperations. Whether or not damage to the various blood components, induced by prolonged perfusion of the brain using small 15-F catheters, may be an additional factor, is unclear.

We conclude that the use of bilateral ASCP in operations on the proximal thoracic aorta, where it is necessary to interrupt the blood circulation to the brain, allows these operations to be performed with a low hospital mortality and few neurologic complications. The duration of ASCP was not a significant predictor of hospital mortality or perioperative neurologic damage in our series. The ASCP system is easy to set up and does not create additional difficulties to the surgeon. Considering the low incidence of postoperative TND, ASCP seems to be an effective adjunct in prevention of ischemic damage to the brain.


    Footnotes
 
Presented at the 13th Annual Meeting of the European Association for Cardio-thoracic Surgery, Glasgow, Scotland, UK, September 5–8, 1999.


    Appendix A. Conference discussion
 Top
 Abstract
 1. Introduction
 2. Materials and methods
 3. Results
 4. Discussion
 Appendix A. Conference...
 References
 
Dr C. Minale (Genova, Italy): I would address your attention to one issue, that is, to the acute antegrade dissection of the aorta, where very often you encounter also a dissection of the arch vessels and many times you have also a re-entry along these vessels. How would you proceed in such cases?

Dr Dossche: I must say in all our cases of type A dissection we encircled the arch vessels, and this has never been a problem with regard to damage of those vessels. Then, after opening the aorta, we always had a nice view of where the true lumen was. There have been cases in which initially the cannula was not in the proper position, but thanks to our transcranial Doppler measurement, you immediately see whether the flow is adequate or not. That's why we don't rely on one monitoring system. We usually try to have three monitoring systems available, just to avoid the occurrence of malperfusion of one of the extracranial vessels.

Dr Minale: Sometimes we encounter a partial thrombosis along the false lumen of the arch vessels. With introduction of a cannula in those vessels there is the potential risk of mobilizing forward thrombotic material. Should this be the case, perhaps you would discover a malperfusion by your monitoring system, but at the same time it would mean that an embolization has already occurred.

Dr Dossche: Could you please repeat the question?

Dr Minale: If you have a thrombosis of the false lumen and you control the perfusion of cerebral vessels with your Doppler, then it could be too late, because you could have already caused embolization of the cerebral vessels.

In such cases we have done something different, that is, we prepared directly the common carotid artery at the bifurcation, we implanted a vascular graft to the bifurcation and ligated the carotid below to avoid embolization or malperfusion. Then we put the perfusion cannula directly into the graft just to avoid this accidental embolization. What is your opinion about this solution?

Dr Dossche: It's difficult to answer the question, because we really did not encounter that problem. I must say we have no experience with that.

Dr E. Jansen (Utrecht, The Netherlands): I noticed in your series that you have a very high percentage of early awakening thanks to antegrade perfusion, so that is a very positive point; but also I noticed that you have 25% in your series of type A dissections. So my concern is that antegrade perfusion of a dissected anonymous artery is rather dangerous. What is your policy? Do you first glue the anomalous trunk and then perfuse it, so you take a few minutes before you perfuse it, or are you going directly with your cannula into the dissected anomalous trunk?

Dr Dossche: Thanks to the antegrade cerebral perfusion, we are rather aggressive in, let's say, also, dissections including the arch vessels. But to answer your question, we open the aorta and we immediately insert a cannula. So we don't do any procedure before we insert the cannula. And as I told you, when we opened up the aorta, in nearly all operations, we had a nice view of where one had to put the cannula. So we just start by inserting the cannula and then we have a good look at the pathology.

Dr Y. Okita (Osaka, Japan): I agree with you regarding the patient who is a total arch replacement, a complex arch procedure, in terms of using antegrade cerebral perfusion, especially a procedure that requires over 40 or 50 min. But in patients with ascending aorta only or a hemiarch repair, we found no problem with the deep hypothermic circulatory arrest. In selective antegrade cerebral perfusion, sometimes it requires two cannulations and a cumbersome operative field and sometimes causes thrombosis. What is the advantage in such a sick patient or subset of patients? And my second question is what is the percentage of patients who are total arch replacement in this series?

Dr Dossche: To answer your first question, we initially had the same drawbacks regarding the use of the technique in, let's say, when you only have to do an open distal anastomosis. But with our growing experience, we found it very simple to insert these cannulas. And the alternative in our hospital was the use of deep hypothermic circulatory arrest, but there have been some recent reports by a group of Dr Griepp stating that probably the safe duration of deep hypothermic circulatory arrest may be less than 30 min. So considering that, we found it no problem using these antegrade cannulas also for open distal anastomosis. With regard to your second question, I think about half of the patients underwent a complete arch replacement.


    References
 Top
 Abstract
 1. Introduction
 2. Materials and methods
 3. Results
 4. Discussion
 Appendix A. Conference...
 References
 

  1. Ergin M.A., Galla J.D., Lansman S.L., Quintana C., Bodian C., Griepp R.B. Hypothermic circulatory arrest in operations on the thoracic aorta. Determinants of operative mortality and neurologic outcome. J Thorac Cardiovasc Surg 1994;107:788-799.[Abstract/Free Full Text]
  2. Svensson L.G., Crawford E.S., Hess K.R., Coselli J.S., Raskin S., Shenag S.A., Safi H.J. Deep hypothermia with circulatory arrest. Determinants of stroke and early mortality in 656 patients. J Thorac Cardiovasc Surg 1993;106:19-31.[Abstract]
  3. Griepp R.B., Ergin M.A., Lansman S.L., Galla J.D., Dogo G. The physiology of hypothermic circulatory arrest. Semin Thorac Cardiovasc Surg 1991;3:188-193.[Medline]
  4. Kazui T., Kimura N., Yamada O., Komatsu S. Surgical outcome of aortic arch aneurysms using selective cerebral perfusion. Ann Thorac Surg 1994;57:904-911.[Abstract]
  5. Kazui T., Kimura N., Komatsu S. Surgical treatment of aortic arch aneurysms using selective cerebral perfusion. Eur J Cardio-thorac Surg 1995;9:491-495.[Abstract]
  6. Dossche K.M., Schepens M.A., Morshuis W.J., Muysoms F.E., Langemeijer J.J., Vermeulen F.E. Antegrade selective cerebral perfusion in operations on the proximal thoracic aorta. Ann Thorac Surg 1999;67:1904-1910.[Abstract/Free Full Text]
  7. Ueda Y., Miki S., Kusuhara K., Okita Y., Tahata T., Yamanaka K. Surgical treatment of aneurysm or dissection involving the ascending aorta and aortic arch utilizing circulatory arrest and retrograde cerebral perfusion. J Cardiovasc Surg 1990;31:553-558.[Medline]
  8. Usui A., Abe T., Murase M. Early clinical results of retrograde cerebral perfusion for aortic arch operations in Japan. Ann Thorac Surg 1996;62:94-104.[Abstract/Free Full Text]
  9. Ueda Y., Okita Y., Aomi S., Koyanagi H., Takamoto S. Retrograde cerebral perfusion for aortic arch surgery: analysis of risk factors. Ann Thorac Surg 1999;67:1879-1882.[Abstract/Free Full Text]
  10. Bachet J., Guilmet D., Goudot B., Dreyfus G., Delentdecker P., Brodaty D., Dubois C. Antegrade cerebral perfusion with cold blood: a 13-year experience. Ann Thorac Surg 1999;67:1974-1978.
  11. McCullough J.N., Zhang N., Reich D.L., Juvonen T.S., Klein J.J., Spielvogel D., Ergin M.A., Griepp R.B. Cerebral metabolic suppression during hypothermic circulatory arrest in humans. Ann Thorac Surg 1999;67:1895-1899.[Abstract/Free Full Text]
  12. Ergin M.A., Uysal S., Reich D.L., Apaydin A., Lansman S.L., McCullough J.N., Griepp R.B. Temporary neurologic 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]
  13. Okita Y., Takamoto S., Ando M., Morata T., Matsukawa R., Kawashima Y. Mortality and cerebral outcome in patients who underwent aortic arch operations using deep hypothermic circulatory arrest with retrograde cerebral perfusion: no relation of early death, stroke and delirium to the duration of circulatory arrest. J Thorac Cardiovasc Surg 1998;115:129-138.[Abstract/Free Full Text]
  14. Griepp R.B., Juvonen T., Griepp E.B., McCullough J.N., Ergin M.A. Is retrograde cerebral perfusion an effective means of neural support during deep hypothermic circulatory arrest?. Ann Thorac Surg 1997;64:913-916.
  15. Okita Y., Takamoto S., Ando M., Morota T., Yamaki F., Kawashuna Y., Nakajuna N. Predictive factors for postoperative cerebral complications in patients with thoracic aortic aneurysms. Eur J Cardio-thorac Surg 1996;10:826-832.[Abstract]
Received September 6, 1999; received in revised form January 19, 2000; accepted February 8, 2000.




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C. Hagl, N. Khaladj, M. Karck, K. Kallenbach, R. Leyh, M. Winterhalter, and A. Haverich
Hypothermic circulatory arrest during ascending and aortic arch surgery: the theoretical impact of different cerebral perfusion techniques and other methods of cerebral protection
Eur. J. Cardiothorac. Surg., September 1, 2003; 24(3): 371 - 378.
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Eur. J. Cardiothorac. Surg.Home page
S. Numata, H. Ogino, H. Sasaki, Y. Hanafusa, M. Hirata, M. Ando, and S. Kitamura
Total arch replacement using antegrade selective cerebral perfusion with right axillary artery perfusion
Eur. J. Cardiothorac. Surg., May 1, 2003; 23(5): 771 - 775.
[Abstract] [Full Text] [PDF]


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J. Thorac. Cardiovasc. Surg.Home page
M. Di Eusanio, R. M. J. Wesselink, W. J. Morshuis, K. M. Dossche, and M. A. A. M. Schepens
Deep hypothermic circulatory arrest and antegrade selective cerebral perfusion during ascending aorta-hemiarch replacement: A retrospective comparative study
J. Thorac. Cardiovasc. Surg., April 1, 2003; 125(4): 849 - 854.
[Abstract] [Full Text] [PDF]


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Ann. Thorac. Surg.Home page
M. Di Eusanio, M. E. S.H. Tan, M. A.A.M. Schepens, K. M. Dossche, R. Di Bartolomeo, A. Pierangeli, and W. J. Morshuis
Surgery for acute type A dissection using antegrade selective cerebral perfusion: experience with 122 patients
Ann. Thorac. Surg., February 1, 2003; 75(2): 514 - 519.
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Card Surg AdultHome page
R. Pretre and M. I. Turina
Deep Hypothermic Circulatory Arrest
Card. Surg. Adult, January 1, 2003; 2(2003): 401 - 412.
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J. Thorac. Cardiovasc. Surg.Home page
M. Di Eusanio, M. A. A. M. Schepens, W. J. Morshuis, R. Di Bartolomeo, A. Pierangeli, and K. M. Dossche
Antegrade selective cerebral perfusion during operations on the thoracic aorta: Factors influencing survival and neurologic outcome in 413 patients
J. Thorac. Cardiovasc. Surg., December 1, 2002; 124(6): 1080 - 1086.
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J. Thorac. Cardiovasc. Surg.Home page
E. Neri, M. Massetti, L. Barabesi, G. Pula, R. Tassi, T. Toscano, E. Tucci, A. Benvenuti, G. Capannini, F. Miraldi, et al.
Extrathoracic cannulation of the left common carotid artery in thoracic aorta operations through a left thoracotomy: Preliminary experience in 26 patients
J. Thorac. Cardiovasc. Surg., May 1, 2002; 123(5): 901 - 910.
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Eur. J. Cardiothorac. Surg.Home page
M. A. Schepens, K. M. Dossche, W. J. Morshuis, P. J. van den Barselaar, R. H. Heijmen, and F. E. Vermeulen
The elephant trunk technique: operative results in 100 consecutive patients
Eur. J. Cardiothorac. Surg., February 1, 2002; 21(2): 276 - 281.
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Eur. J. Cardiothorac. Surg.Home page
R. Di Bartolomeo, M. Di Eusanio, D. Pacini, M. Pagliaro, C. Savini, A. Nocchi, and A. Pierangeli
Antegrade selective cerebral perfusion during surgery of the thoracic aorta: risk analysis
Eur. J. Cardiothorac. Surg., June 1, 2001; 19(6): 765 - 770.
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