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Ann Thorac Surg 2008;85:465-469. doi:10.1016/j.athoracsur.2007.10.017
© 2008 The Society of Thoracic Surgeons
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Original Articles: Cardiovascular

Antegrade Cerebral Perfusion for Acute Type A Aortic Dissection in 120 Consecutive Patients

Farhad Bakhtiary, MD*, Selami Dogan, MD, PhD, Andreas Zierer, MD, Omer Dzemali, MD, Feyzan Oezaslan, MD, Panagiotis Therapidis, MD, Faisal Detho, MD, Thomas Wittlinger, MD, PhD, Sven Martens, MD, PhD, Peter Kleine, MD, PhD, Anton Moritz, MD, PhD, Tayfun Aybek, MD, PhD

Department of Thoracic and Cardiovascular Surgery, Johann Wolfgang Goethe University Hospital, Frankfurt/Main, Germany

Accepted for publication October 3, 2007.

* Address correspondence to Dr Bakhtiary, Department of Thoracic and Cardiovascular Surgery, Johann Wolfgang Geothe University Hospital, Theodor-Stern-Kai 7, Frankfurt/Main, 60596, Germany (Email: farhad{at}bakhtiary.de).


   Abstract
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 Abstract
Introduction
 Material and Methods
 Results
 Comment
 References
 
Background: Treatment of acute type A aortic dissection remains a surgical challenge because of prolonged operative times, bleeding complications, and a considerable risk of neurologic morbidity and mortality. The following study investigates clinical results after modification of perfusion technique for cardiopulmonary bypass as well as temperature management.

Methods: Between January 2000 and August 2006, 120 consecutive patients underwent repair of acute type A dissection. Selective antegrade cerebral perfusion through the right subclavian artery combined with mild systemic hypothermia (30°C) was used in all patients.

Results: Mean cardiopulmonary bypass time was 144 ± 53 minutes, and mean myocardial ischemic time was 98 ± 49 minutes. Isolated cerebral perfusion was performed for 25 ± 12 minutes. Mean core temperature amounted to 30.1° ± 2.2°C. Chest tube drainage during the first 24 hours was 525 ± 220 mL. Mean ventilation time was 54 ± 22 hours. Elevation of serum lactate levels at 1, 12, and 24 hours postoperatively rose to 22 ± 14, 18 ± 11, and 19 ± 8 mg/dL respectively. We observed new postoperative permanent neurologic deficits in 5 patients (4.2%) and TND in 3 patients (2.5%). The 30-day mortality rate was 5% (n = 6). After a mean follow-up period of 2.8 years, 104 patients (87%) were still alive.

Conclusions: Antegrade cerebral perfusion in combination with mild hypothermia offered sufficient neurologic protection in our patient cohort, provided adequate distal organ protection, and reduced perioperative complications in surgery for type A dissection. This perfusion strategy may help in reducing perioperative complications in this particular patient population.


   Introduction
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 Abstract
 Introduction
Material and Methods
 Results
 Comment
 References
 
Surgical treatment of acute type A dissection is considered to be high-risk surgery because of the potential for neurologic injury, prolonged operative times, and bleeding complications [1]. The optimal brain protection strategy during surgical repair of acute type A dissection is a primary concern and still remains controversial [2, 3]. For surgery of thoracic aneurysms, potential advantages of antegrade cerebral perfusion (ACP) versus deep hypothermic circulatory arrest or retrograde cerebral perfusion techniques have been described before, including improved cerebral protection and reduced overall mortality [4–7]. However, this technical modification has not yet gained widespread acceptance for treatment of acute type A dissections.

Our goal was to simplify the surgical procedure using a standardized ACP technique and moderate hypothermia. This paper describes the concept and the single-center experience regarding clinical outcome.


   Material and Methods
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 Abstract
 Introduction
 Material and Methods
Results
 Comment
 References
 
Between January 2000 and August 2006, 120 consecutive adult patients presenting with Stanford type A aortic dissection underwent emergency operative treatment at our unit with a standardized concept of selective ACP through the right subclavian artery combined with mild systemic hypothermia. The study was approved by the Johann Wolfgang Goethe University ethic committee; individual consent for the study was waived. Survived patients were followed yearly in our outpatient department or by phone calls to assess their clinical status (96.6% completed).

Operative Technique
All patients had intravenous anesthesia with propofol (Astra Zeneca, Wedel, Germany), sufentanil (Janssen Cilag, Neuss, Germany), and cisatracurium (GlaxoSmithKline, Munich, Germany). The left radial artery was cannulated for continuous blood pressure monitoring. A transesophageal echocardiographic probe was placed and used for confirmation of the diagnosis and assessment of the aortic valve function. Temperature probes were placed for esophagopharyngeal and rectal temperature monitoring. The patient was positioned on the operating table in a supine position.

After systemic heparinization (300 IU/kg), the right subclavian artery was directly cannulated (18F to 22F flexible arterial cannula, Edwards Lifescience, Irvine, CA). The right atrium was cannulated with double-stage venous cannula (Edwards Lifescience, Irvine, CA). Our standard cardiopulmonary bypass (CPB) circuit included a membrane oxygenator (Avant Physio, Dideco Stöckert, Munich, Germany) and heat exchanger (Jostra AG, Hirrlingen, Germany). The circuit was primed with blood-free solution including 500 mL of hydroxyethylstarch 10% (Fresenius, Bad Homburg, Germany), 250 mL of mannitol (Köhler Pharma, Alsbach-Hähnlein, Germany), 2 mL of heparin (10,000 IU), 500 mL of Ringer’s lactate solution. The protocol for aprotinin (Bayer, Leverkusen, Germany) usage was the "Hammersmith dose." This consisted of administering 2 million kallikrein inhibitor units of aprotinin as a loading dose, with an additional 2 million kallikrein inhibitor units added to the CPB circuit prime solution immediately after anesthetic induction and a continuous infusion of 500,000 kallikrein inhibitor units during the operation. Acid-base balance was maintained with the alpha-stat method. Cardiopulmonary bypass was started, and the heart was arrested with intermittent retrograde and selective antegrade cold-blood cardioplegia. Cooling was limited to 30°C rectal temperature. The innominate artery, the left carotid artery, and the left subclavian artery were snared with silicone elastomer loops and occluded at the time of initiation of the ACP. Antegrade cerebral perfusion was conducted, targeting a core temperature of 30°C, and flow to the brain was controlled in a pressure-controlled manner. Perfusion pressure was kept at 75 mm Hg, which allowed for a mean flow of 1,320 ± 160 mL/min. At this point, the arch resection or repair was performed. If preserved in part, the inner and outer layers of the arch wall were dried carefully and glued with a two-component glue. The glue was made up of an adhesive (gelatin and resorcinol) provided in a tube, and a polymerizing agent (formaldehyde and glutaraldehyde) provided in an amber glass vial (Colle Chirurgicale, Cardial, Saint-Etienne, France). The distal anastomosis with the collagen-coated woven polyester vascular graft (InterVascular, La Ciotal Cedex, France) was completed in a continuous fashion with Prolene 4-0 (Ethicon Ltd, Norderstedt, Germany) and, if necessary, reinforced with polytetrafluoroethylene (Teflon) felts. Once distal repair was completed, the patient was placed in a head-down position, the loops around the arch vessels were released, and removal of air from the vessels was completed. Finally the prosthetic graft was clamped just proximal to the innominate artery and the arterial flow was returned to full body perfusion via the right subclavian artery. Proximal repair followed during the rewarming period. The decision regarding the strategy of proximal aortic repair was mainly based on the surgical inspection of the involvement of the aortic root, including the aortic valve leaflets as well as the coronary ostia. Associated coronary artery grafting procedures, if necessary, were conducted after the aortic repair. Cerebral monitoring was not used routinely in our center during the study period.

Study end points were neurologic morbidity, operative mortality, and long-term survival. The following definitions were used in this study. Temporary neurologic dysfunction (TND) was defined as presence of reversible postoperative motoric deficit, confusion, agitation, or transient delirium. The computed tomography scan had to be normal and all the symptoms resolved before discharge. Permanent neurologic deficit (PND) was defined as the presence of either new focal (stroke) or global (coma) permanent neurologic dysfunction. Operative mortality was defined as death during the first 30 days after the operation.

Statistical Analysis
All data were collected in a FileMaker-based database (FileMaker 7.0, Inc, Santa Clara, CA). Data were presented as mean ± standard deviation. Actuarial survival curves were estimated with the standard nonparametric Kaplan–Meier method. All statistical analyses were performed with StatView (version 5.0) for Windows software (SAS Institute, Inc, Cary, NC). A probability value of less than 0.05 was defined as statistically significant.


   Results
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 Abstract
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 Material and Methods
 Results
Comment
 References
 
Patient demographics and profiles are summarized in Table 1. Hypertension was the most common etiologic comorbidity. Preoperative neurologic deficit was present in 4 patients (3.3%). Two of these patients were admitted to the operating room in coma in unstable hemodynamic condition with continuous cardiopulmonary resuscitation. Both patients died in the hospital. The third patient became somnolent just before induction of anesthesia. Postoperatively, he presented a PND with right hemiplegia. The computed tomographic scan of the brain showed no new specific regional ischemia. The fourth patient was admitted to our unit with convulsions as well as motor aphasia before surgery. Postoperatively, the computed tomographic scan of the brain showed ischemia of the left hemisphere. The symptoms were completely reversible in the postoperative course.


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  		Table 1 Patient Characteristics
 
The mean CPB time was 144 ± 53 minutes, and the mean myocardial ischemic time was 98 ± 49 minutes. Isolated cerebral perfusion time was 25 ± 12 minutes. Mean core temperature was 30.1° ± 2.2°C. Mean chest tube drainage within first 24 hours was 525 ± 220 mL. Total replacement of the aortic arch was performed in 12 patients (10%). Hemiarch replacement was performed in 92 patients (77%). The aortic valve was resuspended in 47 patients (39%) and replaced in 37 patients (31%). Coronary artery bypass grafting was necessary in 19 patients (16%). Additionally 2 patients required mitral valve repair, and 1 patient required tricuspid valve repair (Table 2).


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  		Table 2 Perioperative Results and Surgical Procedures
 
Mean ventilation time was 54 ± 22 hours. Renal failure requiring continuous venovenous hemofiltration occurred in 18 patients (15%). Rethoracotomy for bleeding or tamponade had to be performed in 8 patients (7%). With regard to direct cannulation of the subclavian artery, there was no case of malperfusion or compartment syndrome of the arm in our patient cohort. One patient suffered from an iatrogenic nerve lesion of the pectoralis nerve. New postoperative neurologic complications as PND occurred in 4.2% of patients, and TND occurred in 2.5%. Most of the TNDs in this series were temporary motor deficits isolated to the right arm or delirium. All of these TNDs resolved completely at discharge from the hospital.

Elevation of serum lactate levels at 1, 12, and 24 hours postoperatively were 22 ± 14, 18 ± 11, 1and 9 ± 8 mg/dL. The 30-day mortality rate was 5% (6 patients). Table 3 contains causes of in-hospital death of the patients. Figure 1 shows the Kaplan–Meier survival curve. After a follow-up period of up to 6 years, 104 patients (87%) were still alive (mean, 2.8 years; 96.6% complete follow-up).


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  		Table 3 Causes of In-Hospital Death
 

Figure 1
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  		Fig 1. Kaplan–Meier survival curve of all patients with surgical treatment of acute type A dissection and the number of patients at risk.

 

   Comment
Top
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
References
 
Operations for acute Stanford type A aortic dissections are still associated with a high perioperative risk. The reported mortality rate varies between 5% and 25%, and the rate of PND ranges between 5% and 20% [1–4, 8]. These complication rates depend on numerous factors such as the preoperative hemodynamic and neurologic status of the patient, perfusion technique for CPB, type of cerebral protection strategy, required extent of distal and proximal aortic repair, and operative times.

Historically, reconstruction of the aortic arch has been exclusively performed with the adjunct of deep hypothermia with or without antegrade or retrograde brain perfusion [1, 2, 9, 10]. The extensive cooling and rewarming periods not only added to the already long CPB and operative times but also increased CPB-related negative side effects and could therefore negatively influence postoperative outcomes. Besides disturbance of the coagulation system, temperature-related systemic vasoconstriction causes diminished organ perfusion leading to lactate acidosis [11] and resulted in impairment of cerebral autoregulation [12–14]. Furthermore, CPB-related alterations in the blood–brain barrier and potential leukocyte activation caused brain edema. The long rewarming period on CPB leads to a secondary vasodilation with increased flow into the brain and even more interstitial edema and reperfusion injury [14]. For many years deep hypothermic circulatory arrest was the only surgical method to correct aortic disease with involvement of the arch. To overcome some of the disadvantages of deep hypothermic circulatory arrest, retrograde cerebral perfusion was implemented as an adjunct to improve brain protection. Although this technique was studied in animal models, it failed to demonstrate sufficient cerebral blood flow [15, 16].

The advent of ACP has brought a new concept of cerebral protection during aortic arch surgery [6, 9, 17–19].

It has recently been shown that brain oxygen consumption drops down to 50% of baseline value with moderate hypothermia (28°C). Further cooling below 28°C does not decrease brain oxygen consumption effectively [11]. At the same time, regional cerebral blood flow under ACP conditions is decreased when combined with temperatures below 28°C [16]. The combination of reduced brain oxygen consumption with adequate regional blood flow at 30°C systemic temperature should allow for effective cerebral protection during aortic arch surgery. To study this theoretical concept, we combined the technique of ACP with a temperature management aiming at 30°C core temperature.

The technique of ACP through the right subclavian artery under mild hypothermic conditions carries the potential drawback of left hemispheric ischemia [20]. In fact, when a patient presents with neurologic symptoms preoperatively, an additional antegrade perfusion route through the left internal carotid artery should be considered [21]. We observed a low in-hospital mortality of 5% and a mean long-term survival of 87% in our study cohort, which is fairly low compared with the literature [22]. This can be explained by the potential advantages of ACP with mild hypothermia. Encouraging initial results have been reported in clinical studies [23, 24] and led to an increasing acceptance of this strategy.

Most importantly, we observed a low rate of TND and PND. This supports our hypothesis that cerebral protection is more effective under mild hypothermic conditions combined with ACP. The rate of PND was 4.2%. This is at the lower normal level when compared with previous reports [1–4, 8, 22, 25]. A limitation of our study is that we did not routinely use any cerebral monitoring. The pressure-controlled perfusion through the right subclavian artery provided blood flow to the brain in almost physiologic ranges [13, 16]. If 20% to 25% of the cardiac output is required for the normothermic brain, than a mean of 1,320 ± 160 mL/min should meet the brain oxygen demands at mild hypothermic temperature.

Historically, we have started to use 30°C moderate systemic hypothermia together with ACP for operations of aortic arch aneurysms [6, 7]. The aim of this technique in combination with mild hypothermia was to decrease CPB side effects during cooling and rewarming while providing protection for the rest of the body. This report demonstrates safety and reproducibility of ACP with mild hypothermia in patients with acute type A dissections of different causes.

In summary, selective ACP with mild systemic hypothermia appears to be a safe and sufficient concept for brain protection during surgical repair of the ascending aorta or aortic arch, even if an acute dissection is present. This technique may help to reduce CPB time and hypothermia-related side effects.


   References
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 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 References
 

  1. Ergin MA, Galla JD, Lansman SL, Quintana C, Bodian C, Griepp RB. Hypothermic circulatory arrest on operations on the thoracic aorta: determinants of operative mortality and neurologic outcome J Thorac Cardiovasc Surg 1994;107:788-797.[Abstract/Free Full Text]
  2. Griepp RB, Stinson EB, Hollingsworth JF, Buehler D. Prosthetic replacement of aortic arch J Thorac Cardiovasc Surg 1975;70:1051-1053.[Abstract]
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