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Ann Thorac Surg 2006;82:1278-1285
© 2006 The Society of Thoracic Surgeons

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Original Articles: Cardiovascular

Complex Neonatal Single Ventricle Palliation Using Antegrade Cerebral Perfusion

Congenital Heart Institute, Miami Children's Hospital, and Arnold Palmer Hospital, Miami and Orlando, Florida

Accepted for publication May 5, 2006.

^_* Address correspondence to Dr Hannan, Division of Cardiovascular Surgery, Miami Children's Hospital, 3200 SW 62nd Court, Suite 102, Miami, FL 33155 (Email: rhannan001{at}aol.com).

Presented at the Forty-second Annual Meeting of The Society of Thoracic Surgeons, Chicago, IL, Jan 30–Feb 1, 2006.

	Abstract

Top Abstract Introduction Material and Methods Results Comment Discussion Acknowledgments References

 
BACKGROUND: The efficacy of antegrade cerebral perfusion (ACP) during complex neonatal single ventricle palliation requiring arch reconstruction is uncertain. We adapted the use of ACP in early 2001 in a programmatic effort to minimize the use of deep hypothermic circulatory arrest (DHCA).

METHODS: We retrospectively analyzed data of 126 consecutive patients operated on between 1995 and 2004, including stage-one palliation of hypoplastic left heart syndrome, stage-one palliation for nonhypoplastic left heart syndrome, and Damus-Kaye-Stansel procedures. Patients were divided into two groups: those repaired with prolonged DHCA only (n = 67) and those with ACP (n = 59) and usually a shorter period of DHCA. Risk was further stratified into high risk (weight 2.5 kg or other cardiac lesion) and usual risk for each group.

RESULTS: Survival at 30 days in the usual-risk groups was 72.0% DHCA and 93.2% ACP (p 0.025), and in the high-risk groups it was 61.5% DHCA and 80% ACP (not significant). One-year survival in the usual-risk groups was 57.4% DHCA and 84.1% ACP (p 0.01), and in the high-risk groups it was 38.5% DHCA and 46.7% ACP (not significant). Overall survival to date is 52.2% DHCA and 71.2% ACP (p 0.5).

CONCLUSIONS: There is a statistically significant survival advantage for usual-risk patients with the use of ACP. Although there is a trend to improved survival in the high-risk groups, it does not reach statistical significance and long-term outcomes in these patients remains disappointing. We continue to use ACP and believe it contributes to an overall survival advantage in our institution.

	Introduction

Top Abstract Introduction Material and Methods Results Comment Discussion Acknowledgments References

 
The role of deep hypothermic circulatory arrest (DHCA) in congenital heart surgery is controversial [1]. The issue has become increasingly controversial because of the introduction of techniques that utilize continuous perfusion techniques to achieve technical results previously thought to be obtainable only with DHCA. This has been especially true in cases requiring complex neonatal arch reconstruction with the introduction of regional perfusion techniques [2–4].

The impact of these alternative techniques on surgical morbidity and mortality are poorly understood. The analysis of the impact of these techniques is difficult because of sparse data as well as a wide variability in the precise execution of either DHCA or continuous perfusion between both surgeons and institutions. The issue is further confounded by other institutional variables such as case volume and details of preoperative and postoperative management in these patients [5].

Our institutional philosophy from 1995 to 2001 was to limit DHCA almost exclusively to patients requiring arch reconstruction. Neither small size nor complexity of repair was viewed as an indication for using DHCA when arch reconstruction was not required. In early 2001, we extended this philosophy to patients requiring arch reconstruction using antegrade cerebral perfusion (ACP) during arch reconstruction with a short period of DHCA for cannula manipulation and atrial septectomy when required. This decision was influenced by laboratory reports of the efficacy of low-flow perfusion in cerebral protection [6], reports of the techniques and efficacy of ACP [2–4] and of the adverse neurodevelopment consequences of DHCA [7], and has been reinforced by studies further demonstrating that the duration of DHCA is an important variable affecting neurodevelopmental outcome [8–10].

We adapted ACP for all patients requiring arch reconstruction. In our institutional experience, the most prolonged use of DHCA was for stage-one palliation of hypoplastic left heart syndrome (HLHS), stage-one palliation of non-HLHS, and Damus–Kaye-Stansel procedures. These procedures are grouped into category 6 of the Risk Assessment in Congenital Heart Surgery classification (RACHS-1), the highest risk group [11]. We hypothesized that ACP might result in a survival advantage as well as decreased morbidity in these complex patients. We retrospectively reviewed our RACHS-1 category 6 patients from 1995 to 2004 in an attempt to determine if our change in institutional philosophy and operative technique may have impacted outcomes in these patients.

	Material and Methods

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For this retrospective study, we obtained an approval from the Institutional Review Board with a waiver for informed consent. Data were obtained through CardioAccess (1995–2005) Web-based charting (i-Rounds, Teges Corp 2001–2005), as well as perfusion databases and chart reviews. All patients were stratified using the RACHS-1 method, receiving a score between 1 and 6. Mean, median, and Mann-Whitney rank sum tests for statistical significance were conducted using SigmaStat 3.1 Advisory Statistics for Scientists Software (Systat software).

We analyzed data of 126 consecutive patients in RACHS-1 category 6 operated on between 1995 and 2004. RACHS-1 category 6 includes stage-one palliation of hypoplastic left heart syndrome (HLHS), stage-one palliation for non-HLHS, and Damus-Kaye-Stansel procedures. Patients were divided into two groups: those repaired with prolonged DHCA only (n = 67) and those repaired with ACP (n = 59) and usually a short period of DHCA. Longer periods of DHCA were employed in a few cases in the ACP group to repair associated total anomalous pulmonary venous connection. DHCA patients were almost all operated on between 1995 and 2001. Each group was further stratified into two subcategories: high risk, which we defined as patients weighing 2.5 kg or less, or patients with other cardiac lesions (Table 1); and usual risk, which describes all other patients. All procedures were performed by two surgeons in one institution (one surgeon 1995 to present, the other 1998 to present). Mortality, initiation of cardiopulmonary support, cardiac arrest requiring cardiopulmonary resuscitation, hospital length of stay, and clinical seizures as well as demographic variables were noted in our analysis. Clinical seizures and cardiopulmonary resuscitation, in particular, were based on prospective data base entries as well as complete chart reviews in all patients. Clinical seizure is defined as any observation of clinical seizure activity in the chart, with or without confirmatory neurologic studies (eg, electroencephalogram) and based on definitions in previous reports [12, 13].

The DHCA patients were cooled to a body core target temperature of 18°C for a minimum of 15 minutes of cooling time (mean, 20 minutes) before circulatory arrest. An alpha-Stat blood gas strategy was utilized during cooling and warming, a minimum hematocrit of 18%, and the pO₂ maintained between 150 and 250 mm Hg during bypass. In 1999, minimum cooling time was increased to 20 minutes.

Starting in 2001, ACP patients were cooled to a target core temperature of 18°C with a minimum 20-minute cooling time before the initiation of low flow (flow rates less than 50% of calculated blood flow) When temperatures dropped below 28°C, the pH management strategy was changed to pH stat, sustained by adding CO₂ to the oxygenator sweep gas. The hematocrit during cardiopulmonary bypass was maintained at a minimum of 27%. During bypass, 100% FiO₂ (hyperoxygenation strategy) was used, low flow or DHCA was initiated only after achieving a minimum of 20 minutes of cooling and the venous pO₂ was above 300. While some patients received a short amount of DHCA, there was no minimal time limit. Along with these changes, during ACP the patients were supported with a cerebral perfusion blood flow rate of 20 cc · kg^–1 · min^–1 with arterial line pressure maintained below 60 mm Hg.

Surgical Technique
The surgical procedure follows widely reported techniques for performance of modified stage-one palliation or for Damus-Kay-Stansel procedures when no coarctation or aortic hypoplasia was present. In most cases, the pulmonary artery was cannulated just above the pulmonary valve, bypass initiated, and the pulmonary arteries controlled with tourniquets. Cooling was instituted immediately.

In most cases, a modified Blalock-Taussig shunt of expanded polytetrafluoethylene (ePTFE) from the right innominate-subclavian artery junction to the right pulmonary artery was constructed. Shunt size was typically chosen by weight, using 3.5-mm shunts above 3.0 kg, 3.0-mm in babies less than 2.5 kg, and either 3.0 or 3.5 between 2.5 kg and 3.0 kg. In the ACP group, this shunt was constructed during cooling and used for whole body perfusion during main pulmonary artery transaction and patching. In the DHCA group, the shunt was constructed after circulatory arrest during rewarming.

Six patients had right ventricle to pulmonary artery conduits, using 5.0 or 6.0 mm ePTFE. One of these patients was converted to a central shunt. These patients had ACP from a temporary 3.5-mm ePTFE shunt anastamosed to the innominate-subclavian junction or, in some cases dictated by arch anatomy, the right carotid artery.

In the ACP group, the arterial cannula was transferred to the shunt and whole-body perfusion continued while the patent ductus arteriosus was ligated and the pulmonary artery was transected. The distal main pulmonary artery was reconstructed with homograft. In the DHCA group, this step was done after infusion of cardioplegia and circulatory arrest.

After aortic crossclamping and instillation of cardioplegia, an atrial septectomy was variably performed through the atrial cannulation site or small right atriotomy, usually using a period of brief DHCA in the ACP group and the arrest period in the DHCA group.

The aorta was then opened past the coarctation (if present), the aorta and pulmonary artery were amalgamated, and augmented with pulmonary homograft onto the descending aorta, past ductal tissue and the coarctation site. During arch reconstruction in the ACP group, perfusion was maintained through the shunt. At the conclusion of arch reconstruction, the cannula was removed from the shunt, replaced in the original pulmonary artery cannulation site, whole-body perfusion resumed, and the shunt anastamosed to the right pulmonary artery. After separating from bypass and decannulating, the sternum was routinely left open in both groups, and delayed sternal closure performed several days later.

	Results

Top Abstract Introduction Material and Methods Results Comment Discussion Acknowledgments References

 
Patient demographics are shown in Table 2. There were no significant differences between groups. Perfusion data are shown in Table 3. There were significant differences in median cardiopulmonary bypass time, circulatory arrest time, and time to circulatory arrest or low flow. Shunt sizes are shown in Table 4. The 6 patients in the ACP group who had right ventricular to pulmonary artery conduits are excluded.

View larger version (11K): [in this window] [in a new window]   Fig 1. Kaplan-Meier survival curves for overall survival. (ACP = antegrade cerebral perfusion; DHCA = deep hypothermic circulatory arrest.)

View larger version (11K): [in this window] [in a new window]   Fig 2. Kaplan-Meier survival curves for usual-risk groups. (ACP = antegrade cerebral perfusion; DHCA = deep hypothermic circulatory arrest.)

View larger version (10K): [in this window] [in a new window]   Fig 3. Kaplan-Meier survival curves for high-risk groups. (ACP = antegrade cerebral perfusion; DHCA = deep hypothermic circulatory arrest.)

View larger version (11K): [in this window] [in a new window]   Fig 4. Kaplan-Meier survival curves for low birth weight groups. (ACP = antegrade cerebral perfusion; DHCA = deep hypothermic circulatory arrest.)

We also analyzed mortality data excluding patients with other cardiac diagnoses, that is, including only low birth weight patients. We did this in part because we did not identify any patients with other cardiac diagnoses in the DHCA group. Results are shown in the Kaplan-Meier survival curve in [Figure 4. Excluding patients with other cardiac diagnoses shows a trend to increased survival in low birth weight patients in the ACP group but this does not reach statistical significance. Morbidity is summarized in [Table 5. Clinical seizures, length of stay, and cardiopulmonary resuscitation showed downward trends in the ACP group, although this did not reach clinical significance. Cardiopulmonary support usage remained about the same.

The odds ratio estimates were calculated using logistic regression for overall survival, 1-year survival, and for the high-risk groups as seen in Table 6. The relative odds of overall survival for the ACP group were 2.25 times greater than the DHCA group, and approximately 2.31 times greater than the DHCA group for 1-year survival. The high-risk group also had odds of survival 2.5 times greater than the usual-risk group.

	Comment

Top Abstract Introduction Material and Methods Results Comment Discussion Acknowledgments References

 
The controversy surrounding the very complex issue of the use of DHCA versus continuous perfusion techniques in congenital heart surgery has recently been reviewed. Issues included the quality of cardiac reconstruction and impact on outcome, including mortality and, importantly, neurodevelopmental outcomes [1].

A previous retrospective report has demonstrated a survival advantage associated with the use of continuous perfusion as well as the use of phenoxybenzamine and monitoring systemic venous oxygen saturations [14]. We have not adapted the use of phenoxybenzamine but have had an increased reliance on afterload reduction, usually with milrinone, with nitroprusside added occasionally. We have also not adapted the use of indwelling SvO₂ monitoring catheters, but rather adapted a strategy of goal-directed therapy based on point-of-care serial serum lactate determinations [15].

Survival in the usual-risk group was significantly improved, and because these babies make up the majority of the study population, this resulted in a significant improvement in the overall group. There was a trend to improved survival in the high-risk group, but this trend did not reach statistical significance. The disappointing long-term results in the high-risk group mirrors previous literature reports of the dismal prognosis of babies with single ventricles and anomalous pulmonary venous drainage [16] and low birth weight children requiring stage-one palliation [5, 9, 17]. Analysis of the high-risk groups excluding patients with anomalous pulmonary venous drainage and other cardiac diagnoses shows a trend to improved survival that does not reach statistical significance. The outcome in these babies remains disappointing. The increased risk in low birth weight patients may well be associated with factors that we did not specifically study, for example, noncardiac anomalies such as tracheoesophageal fistula that appear to negatively impact long-term survival. Cox regression shows an increase in survival by 47% with a one-unit (1 kg) increase in weight. We did not specifically analyze preoperative variables such as preoperative hemodynamics, shock, or ventricular function.

Interim mortality trended downward in the usual-risk group from 30 days to 1 year. Interim mortality between 30 days and 1 year remains high in the high-risk group and accounts for a large portion of their mortality rate.

Although there was a trend toward improvement in morbidity indicators in the ACP group, including length of hospital stay, clinical seizures, and need for cardiopulmonary resuscitation in the intensive care unit, these indicators did not reach statistical significance. The stability in cardiopulmonary support usage would seem to indicate no increase in technical operative issues using ACP. In addition, the trend in clinical seizure rate would indicate some improvement in cerebral protection, using a measure that may provide indications of cerebral injury [18], although the long-term importance of this marker is uncertain [19]. The seizure rate in the DHCA group of 6.0% compares favorably to previous literature reports of seizure or coma incidence as high as 23.7% in a similar group of patients [12] operated on using DHCA. The trend to decreased seizures in the ACP may reinforce the evidence that ACP provides cerebral circulatory support [20], although recent evidence suggests that there is a significant incidence of preoperative ischemic lesions and an increase in ischemic lesions postoperatively even among patients operated on with ACP [21]. The trend to lower hospital length of stay and decrease need for cardiopulmonary resuscitation reinforces our subjective (and unproven) observation that the ACP patients exhibit great stability postoperatively. This finding may provide some clinical evidence that previously demonstrated somatic impact of ACP [22] may have a clinical impact. As noted, postoperative serum lactate levels were not routinely obtained in the era of the DHCA group, making comparison between the groups impossible.

Operative times were clearly longer in the ACP group and did not result in worsened outcomes. This finding reinforces the concept that cardiopulmonary bypass probably results in an "ongoing constant but low instantaneous risk that accumulates with the duration of CPB" with "no linear dose response curve" [1].

A clear limitation of this study is the inability to control for a large number of other complex intraoperative and postoperative variables. The care of these patients is an evolving process and identifying a proximate cause for improvement in results is difficult, especially when changes in care occur over short periods of time. Confounding variables include changes in perioperative and postoperative management. In the DHCA period, a second surgeon began performing these cases in 1998. Also, cooling times were lengthened in 1999 with changes in the perfusion protocols. Specific changes occurred in the perioperative management of these patients in the same period as the initiation of the use of ACP. A dedicated cardiac anesthesia division was created, with a reduced number of anesthesiologists participating in the care of these patients. In addition, we introduced the use of near-infrared spectroscopy in the operating room to monitor and attempt to optimize cerebral perfusion [23]. Significant changes in perfusion strategy also coincided with the change to ACP. These changes included modification of pH strategy from alpha stat to mixed alpha and pH stat strategy [24, 25]. In addition, we adopted a strategy of maintaining a higher hematocrit on bypass [26] and hyperoxygenation during the procedure.

There were also significant changes in the postoperative management of these patients, also coincidentally concomitant with the advent of ACP. These include the initiation of point-of-care testing and goal-directed therapy. Serial serum lactate levels were used to direct postoperative management. In addition, a greater reliance was placed on postoperative afterload reduction, using increased dosing of milrinone in the usual case, or the addition of sodium nitroprusside. The overall survival of all patients in our institution has improved since 2001, even among patients in whom no DHCA or ACP was used, suggesting that these other changes play an important role in the improved outcome in the ACP group [15].

It is clear that the outcome for these complex patients has improved in the ACP group. The coincidentally contemporaneous changes in perioperative and postoperative management and the improvement in outcomes in other patients (RACHS-1 categories 1 through 5) in our institution make it clear that the improvement in outcome is multifactorial, and makes isolating the relative importance of ACP compared with the multitude of other simultaneous changes is impossible.

We believe that, despite the acknowledged difficulty of determining causality for improved results given confounding variables, the use of ACP has contributed to improved outcomes in our institution when used as part of an integrated program in the care of these complex neonates.

	Discussion

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DR CARL L. BACKER (Chicago, IL): This seems to be a very timely topic. I think there are 3 or 4 papers on the current program regarding antegrade cerebral perfusion or low-flow regional perfusion. It's going to be difficult for you to prove this to us, though, with all those simultaneous changes. What are you going to say in the paper to convince us that we should use antegrade cerebral perfusion?

DR HANNAN: We wrote in the paper exactly same thing that we said here, that although I believe that it improved our results that it's impossible to prove. And certainly I'd be interested to hear from the audience if anyone who has switched to antegrade cerebral perfusion has then switched back to prolonged DHCA.

DR BACKER: Why don't we take a vote? How many people in the audience are now routinely using antegrade cerebral perfusion? Let's see a show of hands. [Show of hands.] It looks like about 80% to 90% of the audience. How many people here are still only using deep hypothermic circulatory arrest? [Show of hands.] We've got 3 outliers, only 3 or 4 outliers.

DR HANNAN: Has anyone switched back? Has anyone gone to ACP and then gone back to DHCA? [Show of hands.]

DR BACKER: One person. Carlo, do you want to make a comment?

DR CARLO F. MARCELLETTI (Palermo, Italy): I think that when we attempted to do cerebral perfusion, it became very troublesome. I think that the suture line of the Gore-Tex and the innominate artery can be troublesome in trying to take a dry field. And in the reconstruction of the arch, we didn't find basically any advantage with relation of time, I mean, the time of reconstructing the arch was the same, maybe a bit shorter with deep hypothermic circulatory arrest. And we haven't found any difference in seizures after surgery. And we haven't seen any real advantages, so we went back to deep hypothermic circulatory arrest.

DR FRANK A. PIGULA (Boston, MA): As we talked about, it's very difficult to separate the era effects and the other associated changes that happen at or around the same time. And I guess that the only way to really get to that is to actually organize and perform a true randomized, prospective study to examine these things. And I think that's my comment. I did enjoy your talk, and I would like to believe that that's true, but I don't think we can actually prove that without pursuing that strategy. Thank you.

DR JOHN E. MAYER, JR (Boston, MA): One other phase that I think we may not pay enough attention to is the reperfusion phase after your period of deep hypothermia with or without circulatory arrest. Are there any things that you do during that phase? And let me give you a little bit of background. We did a lot of work—it probably didn't get much attention—several years ago on ischemia reperfusion injury in isolated neonatal lamb hearts. And one of the things that we found pretty consistently was that when you started modifying the conditions of reperfusion, you could actually significantly affect what happened with the recovery of both mechanical function as well as coronary vascular function.

And in fact, I have been working for some time with the hypothesis that frequently the issues in effects of deep hypothermic circulatory arrest or myocardial ischemia are as much vascular events as they are parenchymal cellular events. So whether it's a neuron or a myocyte, if you can't get the blood flow there during the reperfusion period, it's not going to recover, and it may in fact go on to necrose.

So I think that that's a particularly important time in the ischemia-reperfusion process, and I think it's something that we might want to, as a group, think pretty carefully about when we're comparing not only whether you turn the pump off or not but how you manage the vasculature during the reperfusion phase.

DR BACKER: So John, what do you recommend, how do you do it?

DR MAYER: Well, again, this is all based on old laboratory work that we did, but it's pretty clear that the endothelium in the post–deep hypothermic ischemic state is dysfunctional, so that it almost certainly doesn't release normal amounts of nitric oxide in the same way that it would in a normal situation. So we did experiments that showed that if you gave a nitric oxide precursor, L-arginine, or if you gave nitroglycerin, which is a lot easier to come by, you could significantly affect the recovery of function. So every patient that I either crossclamped the aorta or arrest the circulation to the head, nitroglycerin is running when reperfusion starts. And I think what happens in the first 10 minutes or 15 minutes after reperfusion is a very important phase, and I personally think that that's an area that probably stands a little more scrutiny and investigation.

DR HANNAN: I think that underscores the subtle institutional and surgeon-specific differences can have a large difference in the outcome of these operations. And clearly some of the changes in our perfusion protocols affected that. I can tell you that we usually do not rewarm until we've completed the pulmonary artery end of the shunt. I worry about the shunt clamp distorting the aortic anastomosis and creating ischemia, so we don't rewarm until the clamp is off. Peter Kouretas, in my laboratory, showed that heparin had a dramatic protective effect on endothelial performance after periods of ischemia-reperfusion as part of his PhD thesis.

DR JAMES S. TWEDDELL (Milwaukee, WI): Dr Hannan, that was an excellent presentation. We recently published a series of 14 patients assessing late neurodevelopmental outcome and showed an interaction between DHCA use and the cardiac output in the postoperative period as assessed by mixed venous saturation. Not surprisingly, a patient who is subjected to a prolonged period of circulatory arrest combined with low cardiac output in the early postoperative period was at increased risk for unfavorable late neurodevelopmental outcome. So we would agree with your findings. I was wondering if you are planning on doing any late neurodevelopmental assessment of this group of patients. You might be able to identify some additional advantages to this approach.

DR HANNAN: I will say that the literature that I alluded to was from the Wisconsin group, from Dr Pigula from the Boston's Children's Group, they've had a significant influence on our practice.

When we started doing this, we actually obtained an IRB to look at neurologic outcomes, thinking that we would be able to compare patients as they came back for their Glenn and Fontan and be able to compare the two outcomes in both of these cohorts. Unfortunately, we were unable to obtain funding for these studies.

DR BRADLEY S. ALLEN (Houston, TX): Just a quick comment. I agree with Dr Mayer completely. Reperfusion injury is reperfusion injury, no matter what the organ, and it's very important how we reperfuse.

To answer your question, Dr Backer, about 2 years ago we reported our results on modifying the pump prime while the patient is undergoing hypothermic circulatory arrest, in an attempt to avoid reperfusion injury to the entire body. This study was done in neonatal piglets, although we've now begun applying these principles to patients, and are starting to examine the data. After 90 minutes of hypothermic circulatory arrest, we were able to almost completely avoid the reperfusion injury to every organ (including the brain) by modifying the pump prime during circulatory arrest. The prime was modified in much the same way we change our terminal (warm) cardioplegic reperfusate. It follows the same principles that have been shown to work in the heart, because reperfusion injury is reperfusion injury, independent of the organ.

DR HANNAN: Thank you.

DR MARCELLETTI: I'd like to ask Dr Hannan, and maybe somebody else from the audience, how warm do you rewarm before disconnecting cardiopulmonary bypass? Do you go to normal temperature or, as we like, do you stay a little bit lower on the rectal temperature? We disconnect at 34°, and we like to complete rewarming in the intensive care.

DR HANNAN: We go to 35.5° on these babies. Other babies we go to 36° or 36.5°, especially the babies when we're going to extubate. Our perfusionists are absolutely meticulous.

DR FRANÇOIS G. LACOUR-GAYET (Denver, CO): I would like to mention another technique that has been introduced by the Japanese. It's actually to do it in normothermia around 32° to 33°—by placing a second cannula in the descending aorta in opening the posterior pericardium. It is not difficult to place a no. 6 cannula in the descending aorta and do the entire operation without circulatory arrest and normothermia.

DR HANNAN: We saw the initial report from Japan, and used that technique in 1 patient in the series.

	Acknowledgments

Top Abstract Introduction Material and Methods Results Comment Discussion Acknowledgments References

 
The authors gratefully acknowledge Dr Nancy Stein and Gabriela Lopez-Mitnik from the University of Miami for their statistical assistance.

	References

Top Abstract Introduction Material and Methods Results Comment Discussion Acknowledgments References

 

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