Evolution of cerebral perfusion techniques in type a aortic dissection surgery: a single center experience

Abstract

Background:

The purpose of this study was to investigate the effect of using antegrade selective cerebral perfusion (ASCP) with moderate hypothermia on hospital mortality after surgery for acute type A aortic dissection (AAAD).

Methods:

Between January 1998 and December 2008, 142 consecutive patients were operated on for AAAD. Patients were divided into two subgroups: the cohort of patients operated on from January 1998 until December 2003 (without ASCP) (P1998-2003, n=64) and the cohort operated on from January 2004 until December 2008 (with ASCP)(P2004-2008, n=78).

Results:

The difference in hospital mortality was statistically significant (P1998-2003: 42.2%; P2004-2008: 14.1%, p<0.0005). Survival rates were 51.6±6.2% vs. 75.1±5.5% and 45.9±6.2% vs. 69.7±7.3% for one and four years, respectively (p=0.001). Multivariate logistic regression analysis revealed that ASCP was the only independent protective factor of hospital mortality (p=0.047).

Conclusion:

In patients operated on for AAAD, antegrade selective cerebral perfusion with moderate hypothermia is a significant factor in decreasing hospital mortality.

Keywords

aortic dissection hypothermia cerebral protection

Introduction

Untreated aortic dissection has a mortality rate of 50% within the first 48 hours.¹ Acute type A aortic dissection (AAAD) occurs nearly three times as frequently as rupture of an abdominal aortic aneurysm, with an estimated worldwide prevalence of 0.5 to 2.95 per 100,000 patients per year.^2,3

The most important concern during ascending aorta and arch repair remains cerebral protection. Deep hypothermic circulatory arrest (DHCA) is a well-established technique; it provides both good cerebral protection, even though time-limited, and a dry operative field.^4-6 However, it requires prolonged cardiopulmonary bypass (CPB) time and is often associated with coagulopathy and pulmonary complications.⁴ Retrograde cerebral perfusion (RCP) has been introduced to improve cerebral protection and to allow a longer time of circulatory arrest.^4,7,8 However, the complications resulting from deep hypothermia remain largely unchanged.⁴

Antegrade selective cerebral perfusion (ASCP) has proved to be a reliable method of brain protection during surgery of the thoracic aorta and it has been progressively introduced as a standard technique of brain protection.^4,9-11 In our clinic, until the year 2004, we used DHCA, RCP or ASCP for cerebral protection, depending on the surgeon’s preference. In 2004, we introduced the ASCP protocol and started using ASCP with moderate hypothermia during AAAD surgery. The purpose of this study was to review our experience in 142 consecutive patients undergoing surgery for AAAD in an 11-year period and to investigate the protective role of ASCP with moderate hypothermia in hospital mortality.

Patients and methods

Data of all consecutive patients who underwent surgery for AAAD between January 1998 and December 2008 were retrospectively evaluated. The diagnosis of acute type A aortic dissection, according to the Stanford classification,^2,12 was confirmed by transesophageal echocardiography (TEE), computed tomography (CT) or, in some cases, transthoracic echocardiography (TTE). Patients were divided into two subgroups: the cohort of patients who were operated on from January 1998 until December 2003 without ASCP (P1998-2003) and the cohort operated on from January 2004 until December 2008 with ASCP (P2004-2008). The Institutional Research Review Board approved this study and waived the need for patient consent.

Surgical technique

Our current surgical technique has previously been described by Tan et al.^13,14 Throughout the 11 years of the study, there was a substantial variability in the surgical techniques used; nine different surgeons operated on the patients included in this series. The operation was performed using a median sternotomy approach, femoral artery cannulation (Bio-Medicus^® percutaneous cannula, 19-21 Fr, Medtronic Inc., Arnhem, The Netherlands) and a venous single-two stage cannula in the right atrium (DLP 34-46 Fr, Medtronic Inc.). Total CPB was performed and cardiac arrest was achieved using cold oxygenated St. Thomas’ crystalloid cardioplegic solution directly injected into the coronary ostia. The left side of the heart was vented through the right superior pulmonary vein. Until the year 2004, cerebral protection was achieved by DHCA, a circulatory arrest, combined with either RCP or ASCP. From 2004 onwards, we have uniformly used ASCP during the circulatory arrest combined with an INVOS^® transcranial oximeter to monitor the cerebral blood flow. Details of our cannulation technique and method of ASCP have already been described.^9,15,16 The aorta was opened and the proximal anastomosis was performed. The patients were cooled to a rectal temperature of 25°C when ASCP was used and to 15°C when DHCA was used, with or without RCP. When reaching optimal temperature, the systemic circulation was arrested. For ASCP, we used a retrograde coronary sinus perfusion cannula inserted into the innominate and left common carotid arteries, through the aortic lumen. Cerebral perfusion was started at a rate of 10 ml/min/kg and adjusted to maintain a maximal pressure of 70 mmHg at the tip of the cannula and a pressure of 40 to 70 mmHg in the right radial artery. The aortic arch was explored and the intimal tear was always resected if located in the ascending aorta or in the transverse arch and replaced with a vascular prosthesis. The aortic stumps were often reinforced with strips. Whenever indicated, repair or replacement of the aortic valve was performed. The distal anastomosis was then performed. Glue (gelatin-resorcin-formalin glue (GFR^®) Colle Biologique Gelatine Resorcine, Formol; Cardial, Saint-Etienne, France or Bioglue^®, Cryolife Europa Ltd., Guildford, UK) was routinely used to ensure hemostasis.

Statistical Analysis

Continuous variables are reported as mean ± standard deviation (SD) and categorical data as frequencies and percentages. Cumulative survival was calculated using the Kaplan-Meier method supplemented with the log-rank test to compare survival between the groups. For continuous data, differences were evaluated by the Mann-Whitney U-test (independent samples t-test) and categorical variables were compared using the Pearson Chi-Square test. For univariate analyses of risk factors of hospital mortality, we used Binary Logistic Regression. Statistical analysis was performed using SPSS 15.0 statistical software for Windows (SPSS Inc., Chicago, IL). Statistical significance was considered at a 2-tailed value of p<0.05.

Results

The demographic characteristics of the two different cohorts are summarized in Table 1. Apart from neurological disorders and cardiogenic shock, data about other preoperative organ dysfunctions were lacking in the study groups. All details of operative techniques are described in Table 2. No evidence of intraoperative organ malperfusion was documented in any of the patients. However, this possibility cannot be excluded.

Table 1.

Demographic characteristics

Characteristics	P1998-2003 (n=64)	P2004-2008 (n=78)	p-value
Age, years, mean (±SD)	58 (±10.8)	59 (±12.3)	0.525
Male sex, n (%)	51 (79.7)	53 (67.9)	0.167
BMI, kg/m² mean (±SD)	26 (±4.6)	26 (±3.8)	0.670
Diabetes, n (%)	2 (3.1)	2 (2.6)	1.000
Hypertension, n (%)	25 (39.1)	40 (51.3)	0.199
COPD, n (%)	10 (15.6)	5 (6.4)	0.133
Previous cardiac surgery, n (%)	8 (12.5)	4 (5.1)	0.205
LVEF <35%, n (%)	9 (14.1)	5 (6.4)	0.215
AOI, n (%)	36 (56.3)	43 (55.1)	1.000
Previous neurologic disorder			0.213
Central, n (%)	1 (1.6)	3 (3.8)
Peripheral, n (%)	3 (4.7)	0 (0.0)
Extracardiac arteriopathy, n (%)	3 (4.7)	6 (7.7)	0.700
Preoperative serum creatinine, mmol/L, mean (±SD)	116 (±42.3)	109 (±65.3)	0.444
Unstable angina, n (%)	2 (3.1)	9 (11.5)	0.121
EuroSCORE, mean (±SD)	10 (±2.8)	10 (±2.6)	0.528
Clinical presentation			0.379
Acute pain, n (%)	51 (79.7)	55 (70.5)
Cardiogenic shock, n (%)	11 (17.2)	15 (19.2)
Cardiac tamponade, n (%)	1 (1.6)	5 (6.4)
Neurologic dysfunction at presentation			0.830
Central, n (%)	6 (9.4)	9 (11.5)
Peripheral, n (%)	6 (9.4)	1 (1.3)
Diagnosis confirmed by			<0.0005
CT, n (%)	30 (46.9)	62 (79.5)
TTE, n (%)	5 (7.8)	7 (9.0)
TEE, n (%)	29 (45.3)	9 (11.5)
Cause of dissection			0.228
Idiopathic, n (%)	57 (89.1)	70 (89.7)
Traumatic, n (%)	3 (4.7)	0 (0.0)
Iatrogenic, n (%)	1 (1.6)	2 (2.6)
Marfan’s syndrome, n (%)	3 (4.7)	6 (7.7)
Location aortic entry tear			0.550
Ascending aorta, n (%)	41 (64.1)	44 (56.4)
Aortic arch, n (%)	9 (14.1)	16 (20.5)
Unknown, n (%)	14 (21.8)	18 (23.1)

AOI = aortic valve insufficiency, BMI = body mass index (kg/m²), COPD = chronic obstructive lung disease, CT = computed tomography, EuroSCORE = European system for cardiac operative risk evaluation, LVEF = left ventricular ejection fraction, TEE = transesophageal echocardiography, TTE = transthoracic echocardiography,.

Table 2.

Operative data

Variables	P1998-2003 (n=64)	P2004-2008 (n=78)	p-value
Cannulation			<0.0005
Femoral artery and right atrium, n (%)	26 (40.6)	71 (91.0)
Ascending aorta and right atrium, n (%)	16 (25.0)	2 (2.6)
Femoral artery and bicaval, n (%)	7 (10.9)	1 (1.3)
Ascending aorta and bicaval, n (%)	1 (1.6)	0 (0.0)
Cerebral perfusion technique			<0.0005
DHCA, n (%)	33 (51.6)	4 (5.1)
RCP, n (%)	17 (26.6)	1 (1.3)
ASCP, n (%)	14 (21.9)	73 (93.6)
Operative procedure			<0.0005
Bentall, n (%)	22 (34.4)	6 (7.7)
Ascending aorta replacement (AAR), n (%)	16 (25.0)	20 (25.6)
AAR + AVRP, n (%)	10 (15.6)	29 (37.2)
Hemi-arch replacement (HAR), n (%)	0 (0.0)	4 (5.1)
HAR + AVRP, n (%)	3 (4.7)	10 (12.8)
Total arch replacement (TAR), n (%)	6 (9.4)	0 (0.0)
TAR + AVRP, n (%)	0 (0.0)	7 (9.0)
Stitching & gluing of the dissection	7 (10.9)	2 (2.6)
Use of surgical glue			<0.0005
GRF^®, n (%)	26 (40.6)	7 (9.0)
Bioglue^®, n (%)	38 (59.4)	71 (91.0)
Extracorporeal circulation time min., mean (±SD)	227 (100.3)	208 (57.9)	0.200
Aorta occlusion time min., mean (±SD)	103 (54.6)	102 (36.5)	0.961
Circulatory arrest time min., mean (±SD)	26 (17.6)	32 (26.3)	0.094
Lowest rectal temperature, °C, mean (±SD)	18 (5.3)	26 (3.7)	<0.0005
Number of transfused units
TC, mean (±SD)	1 (1.7)	2 (1.6)	0.160
PC, mean (±SD)	7 (7.8)	5 (5.9)	0.065
FFP, mean (±SD)	6 (6.2)	5 (5.6)	0.810

ASCP = antegrade selective cerebral perfusion, AVRP = aortic valve replacement or re-suspension, DHCA = deep hypothermic circulatory arrest, FFP = units of fresh frozen plasma, PC = packed cell (packed red blood cells) units, RCP = retrograde cerebral perfusion, TC = platelet (thrombocyte) concentrate.

Mortality (Table 3)

The difference in hospital mortality between the two cohorts was statistically significant (P1998-2003: 42.2%; P2004-2008: 14.1%, p<0.0005). The main cause of hospital mortality in cohort P1998-2003 was excessive blood loss during the operation or postoperatively (15 (23.4%) patients). The second cause of death was low cardiac output (9 (14.1%) patients) and 3 (4.7%) patients died because of septic shock in the intensive care unit (ICU). The two major causes of hospital death in cohort P2004-2008 were low cardiac output (6 (6.4%) patients) and excessive blood loss (5 (7.7%) patients). The difference in the cause of death was statistically significant (p=0.001). Postoperatively, there were no statistically significant differences in neurological events, infection or re-exploration (p=0.910, p=0.113 and p=0.859, respectively).

Table 3.

Postoperative data

Variables	P1998-2003 (n=64)	P2004-2008 (n=78)	P-value
Neurological events			0.910
CVA/ PND, n (%)	5 (7.8)	7 (9.0)
TIA/ TND, n (%)	4 (6.3)	6 (7.7)
Infection			0.113
Mediastinitis, n (%)	5 (7.8)	9 (11.5)
Pneumonia, n (%)	3 (4.7)	5 (6.4)
Sepsis, n (%)	3 (4.7)	1 (1.3)
Urinary infection, n (%)	0 (0.0)	6 (7.7)
Re-exploration, n (%)	18 (28.1)	23 (29.5)	0.859
Hospital mortality, n (%)	27 (42.2)	11 (14.1)	<0.0005
Cause hospital mortality, n (%)			0.001
Excessive blood loss, n (%)	15 (23.4)	5 (6.4)
Low cardiac output, n (%)	9 (14.1)	6 (7.7)
Septic shock, n (%)	3 (4.7)	0 (0.0)
Postoperative use of anti-hypertension medication
ACE inhibitors, n (%)	4 (6.3)	3 (3.8)	0.510
Beta blockers, n (%)	3 (4.7)	4 (5.1)	0.904
ACE inhibitors & Beta blockers, n (%)	27 (42.2)	57 (73.1)	<0.0005

ACE inhibitors = angiotensin-converting enzyme inhibitors, beta-blockers = beta adrenergic blocking agents, CVA = cerebrovascular accident; PND = permanent neurological dysfunction, TIA = transient ischemic attack, TND = temporary neurological dysfunction.

The results of univariate and multivariate analyses of predictors of hospital mortality are presented in Table 4. Univariate preoperative predictors of hospital mortality were age ≥60 years, left ventricle ejection fraction (LVEF) <35% and EuroSCORE >12. Other significant factors were postoperative infection and perfusion technique: DHCA (p=0.030; OR 2.43; 95% CI 1.09-5.43). Antegrade selective cerebral perfusion proved to be a protective factor in the univariate analysis (p=0.005; OR 0.34; 95%CI 0.16-0.73). Significant preoperative and perioperative factors were entered into the multivariate logistic regression analysis. The multivariate logistic regression revealed that ASCP (p=0.047; OR 0.29; 95%CI 0.09-0.98) was the only independent significant factor in lowering hospital mortality.

Table 4.

Logistic regression analysis for predictors of early mortality

	Univariate			Multivariate
Risk factor	P- value	Odds ratio	95% CI	p- value	Odds ratio	95% CI
Age, ≥60 years	.019	2.52	1.16-5.47	0.286	1.63	0.66-4.02
Sex, male	.722	1.16	0.51-2.66
BMI, >25	.464	1.32	0.63-2.80
Diabetes	.936	1.10	0.11-10.90
Hypertension	.363	1.42	0.67-3.02
COPD	.545	1.42	0.45-4.47
Previous cardiac surgery	.231	2.10	0.62-7.07
LVEF <35%	.002	6.15	1.91-19.78	0.051	3.83	0.10-14.71
AOI	.479	1.31	0.62-2.80
Extracardiac arteriopathy	.227	2.33	0.59-9.18
Preoperative serum creatinine >200 µmol/l	.502	1.87	0.30-11.65
Unstable angina	.968	1.03	0.26-4.10
EuroSCORE, >12	.003	3.36	1.52-7.41	0.058	2.61	0.97-7.06
Cerebral perfusion technique
DHCA	.030	2.43	1.09-5.43	0.933	1.01	0.29-3.56
RCP	.219	1.91	0.68-5.35
ASCP	.005	0.34	0.16-0.73	0.047	0.29	0.09-0.98
Postoperative CVA	.935	1.03	0.37-2.87
Postoperative infection	.046	3.13	1.02-9.63
Re-exploration	.411	1.43	0.61-3.37

AOI = aortic valve insufficiency, ASCP = antegrade selective cerebral perfusion, BMI = body mass index (kg/m²), COPD = chronic obstructive lpulmonary disease, CVA = cerebrovascular accident, DHCA = deep hypothermic circulatory arrest, EuroSCORE = European system for cardiac operative risk evaluation, LVEF = left ventricle ejection fraction, RCP = retrograde cerebral perfusion.

Figure 1 shows the Kaplan-Meier survival curves of the two cohorts over a period of ten years (Log Rank (Mantel Cox) p=0.002). One- and four-year survival rates (including hospital mortality) for the two cohorts were 51.6±6.2% vs. 75.1±5.5% and 45.9±6.2% vs. 69.7±7.3%, respectively (Wilcoxon (Gehan) p=0.001).

Discussion

Several therapeutic and diagnostic advances have been introduced to improve the surgical outcome of AAAD patients, namely DHCA, open distal anastomosis, aortic root reconstruction, and ASCP.^2,19-24 Despite these advances, perioperative mortality and morbidity remain considerably high; operative mortality can be as high as 32%.¹ Many predictors of hospital mortality have been identified by previous studies, including shock, malperfusion, cardiac tamponade, neurologic disorder, ischemia, older age and previous cardiac surgery.^1,13,25,26 In our study, we revealed ASCP to be the only independent protective factor of hospital mortality.

In our study, ASCP with moderate hypothermia (rectal temperature ≥25°C) represented a significant factor in improving hospital outcome. Previous studies reported that moderate systemic hypothermia at a nasopharyngeal temperature of at least 26°C appears to be a safe and sufficient tool for cerebral protection and the well-known side effects of DHCA may be avoided.²⁷ Examples of these side effects are coagulopathy, postoperative bleeding and postoperative pulmonary insufficiency.²⁷

Improvement of hospital mortality in our patient population is directly related to our ASCP protocol which was introduced in 2004. This improvement cannot be explained by a lower incidence of postoperative complications, since we did not see any significant difference between the two cohorts regarding the incidence of CVA, infection or re-exploration. However, by analysis of the cause of death in both cohort groups, we found a significant difference regarding postoperative bleeding and systemic infections. The incidence of fatal complications is reduced in the group where the ASCP protocol was used.

One of the major criteria included in our protocol was cooling to a rectal temperature of 25°C before arresting the systemic circulation. The mean rectal temperature in the cohort P2004-2008 was 26±3.7°C and most of the patients did not even reach the lowest temperature of 25°C. This technique reduces the problems caused by deep hypothermia and prevents ischemic injury to the abdominal viscera and to the spinal cord.⁴ However, our study did not show a significant reduction of postoperative hypothermia-related complications, such as bleeding and neurological complications, in the mild-hypothermia group of patients. This is probably because this group of patients underwent more complex and time-consuming operations, which are associated with a higher incidence of postoperative complications.

Selective or “bihemispheric” cerebral perfusion was considered by many authors more effective because it overcomes the anomalies of Willis’s circle.²⁸ Byrne et al. proposed “non-selective” cerebral perfusion by using the right axillary artery as a route for ACP during HCA. According to these authors, this method is safe, less time-consuming, and it avoids complications as a result of maneuvers for the selective cannulation of aortic arch branches.²⁹

In a non-randomized study concerning the early outcomes of hemispheric and bihemispheric ACP, Dossche et al.³⁰ showed that: (a) there were no differences regarding the neurological complications, but a significant favorable impact of the bihemispheric ACP on hospital mortality did appear; (b) in 8% of their patients, Willis’s circle was incomplete or absent and, in those patients, left-hemispheric perfusion was put at risk. These investigators suggested an application of a deeper systemic hypothermia in cases of hemispheric ACP.³⁰

Compared to DHCA, the ASCP technique offers a virtually unlimited safety period. However, the risk of embolization is still high, especially in older patients with atherosclerotic vessels. It has been advised that one should minimize manipulation of the cannulae and arch vessels during this technique.³¹ The same authors have suggested axillary artery cannulation instead of using the femoral artery in order to facilitate ASCP. In this case, it is possible to perform both systemic cooling on CPB and ASCP through the same cannula. Using this method, continuous brain perfusion is always guaranteed.³¹

Careful monitoring of cerebral blood flow is mandatory to identify and correct cerebral malperfusion and possibly improve neurological outcome.³² Different methods of cerebral monitoring during complex aortic repairs have been described, including 2-channel transcranial Doppler (TCD), near-infrared spectroscopy (NIRS), electroencephalography (EEG), and jugular venous oxygenation monitoring.³³

In the present study, there was a difference in circulatory arrest time between the two cohorts (26±17.6 vs. 32±26.3), although not statistically significant (p=0.094). Nevertheless, previous studies have demonstrated that the duration of ASCP did not affect hospital mortality.^4,9,15,16,23 This means that the period of circulatory arrest can be safely prolonged with the aid of ASCP as compared to deep hypothermic circulatory arrest with or without retrograde cerebral perfusion. This allows more demanding and more complex repairs to be performed and permits unhurried and accurate reconstruction of aortic tissue or more extended aortic replacement.⁹

Manipulation of the supra-aortic arteries, which could be calcified or even dissected, may cause more cerebral complications. To minimize this drawback, care should be taken during insertion of the cannula used for antegrade perfusion. However, Eusanio et al. stated that the technical complexity and cumbersome operative field, as well as manipulation and cannulation of the arch vessels which might be involved in the dissection, do not have to be possible drawbacks for the use of ASCP.⁹

Our hospital mortality of 14.1% from 2004 onwards is comparable with previous studies which report hospital mortality between 10-25%.^13,34,35 However, comparison remains difficult because of different patient populations, preoperative patient condition, different surgical and perfusion techniques and the experience of the different centers with surgery of the AAAD.

Limitations

We have to consider the retrospective, single-center, non-randomized nature of this study and the results of different surgeons using a variety of available techniques. The improvement in surgical techniques and postoperative care (especially the aggressive management of postoperative hypertension) over the past decade has definitely contributed to the improvement of hospital mortality. Some surgeons had used ASCP before introducing this protocol. This could have been a selection bias in our analysis and could have blurred our results. Information regarding preoperative organ malperfusion, which represents the main factor of hospital mortality in these patients, was not completely available.

Footnotes

Funding

This research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors.

Conflict of Interest Statement

None declared.

References

Mehta

Suzuki

Hagan

. Predicting death in patients with acute type A aortic dissection. Circulation 2002; 105: 200–206.

Cohn

. Cardiac surgery in the adult. 3rd Edition. New York: McGraw-Hill Professional; 2007.

Coady

Rizzo

Goldstein

Elefteriades

. Natural history, pathogenesis, and etiology of thoracic aortic aneurysms and dissections. Cardiol Clin 1999; 17: 615–635; vii. Review.

Di Bartolomeo

Pacini

Di Eusanio

Pierangeli

. Antegrade selective cerebral perfusion during operations on the thoracic aorta: our experience. Ann Thorac Surg 2000; 70: 10-15; discussion 15–16.

Ergin

Galla

Lansman

Quintana

Bodian

Griepp

. Hypothermic circulatory arrest in operations on the thoracic aorta. Determinants of operative mortality and neurologic outcome. J Thorac Cardiovasc Surg 1994; 107: 788-797; discussion 797–789.

Svensson

Crawford

Hess

. Deep hypothermia with circulatory arrest. Determinants of stroke and early mortality in 656 patients. J Thorac Cardiovasc Surg 1993; 106: 19-28; discussion 28–31.

Pagano

Boivin

Faroqui

Bonser

. Retrograde perfusion through the superior vena cava perfuses the brain in human beings. J Thorac Cardiovasc Surg 1996; 111: 270–272.

Safi

Brien

Winter

. Brain protection via cerebral retrograde perfusion during aortic arch aneurysm repair. Ann Thorac Surg 1993; 56: 270–276.

Di Eusanio

Tan

Schepens

. Surgery for acute type A dissection using antegrade selective cerebral perfusion: experience with 122 patients. Ann Thorac Surg 2003; 75: 514–519.

10.

Dossche

Schepens

Morshuis

Muysoms

Langemeijer

Vermeulen

. Antegrade selective cerebral perfusion in operations on the proximal thoracic aorta. Ann Thorac Surg 1999; 67: 1904-1910; discussion 1919–1921.

11.

Kazui

Washiyama

Muhammad

. Total arch replacement using aortic arch branched grafts with the aid of antegrade selective cerebral perfusion. Ann Thorac Surg 2000; 70: 3-8; discussion 8–9.

12.

DeBakey

McCollum

Crawford

. Dissection and dissecting aneurysms of the aorta: twenty-year follow-up of five hundred twenty-seven patients treated surgically. Surgery 1982; 92: 1118–1134.

13.

Tan

Dossche

Morshuis

. Operative risk factors of type A aortic dissection: analysis of 252 consecutive patients. Cardiovasc Surg 2003; 11: 277–285.

14.

Tan

Morshuis

Dossche

Kelder

Waanders

Schepens

. Long-term results after 27 years of surgical treatment of acute type A aortic dissection. Ann Thorac Surg 2005; 80: 523–529.

15.

Di Bartolomeo

Di Eusanio

Pacini

. Antegrade selective cerebral perfusion during surgery of the thoracic aorta: risk analysis. Eur J Cardiothorac Surg 2001; 19: 765–770.

16.

Dossche

Morshuis

Schepens

Waanders

. Bilateral antegrade selective cerebral perfusion during surgery on the proximal thoracic aorta. Eur J Cardiothorac Surg 2000; 17: 462–467.

17.

Bentall

De Bono

. A technique for complete replacement of the ascending aorta. Thorax 1968; 23: 338–339.

18.

Roques

Nashef

Michel

. Risk factors and outcome in European cardiac surgery: analysis of the EuroSCORE multinational database of 19030 patients. Eur J Cardiothorac Surg 1999; 15: 816-822; discussion 822–813.

19.

Bachet

Goudot

Dreyfus

. Surgery for acute type A aortic dissection: the Hopital Foch experience (1977-1998). Ann Thorac Surg 1999; 67: 2006-2009; discussion 2014–2009.

20.

Casselman

Tan

Vermeulen

Kelder

Morshuis

Schepens

. Durability of aortic valve preservation and root reconstruction in acute type A aortic dissection. Ann Thorac Surg 2000; 70: 1227–1233.

21.

Crawford

Kirklin

Naftel

Svensson

Coselli

Safi

. Surgery for acute dissection of ascending aorta. Should the arch be included? J Thorac Cardiovasc Surg 1992; 104: 46–59.

22.

Di Eusanio

Schepens

Morshuis

. Operations on the thoracic aorta and antegrade selective cerebral perfusion: our experience with 462 patients. Ital Heart J 2004; 5: 217–222.

23.

Di Eusanio

Wesselink

Morshuis

Dossche

Schepens

. Deep hypothermic circulatory arrest and antegrade selective cerebral perfusion during ascending aorta-hemiarch replacement: a retrospective comparative study. J Thorac Cardiovasc Surg 2003; 125: 849–854.

24.

Heinemann

Laas

Jurmann

Karck

Borst

. Surgery extended into the aortic arch in acute type A dissection. Indications, techniques, and results. Circulation 1991; 84: III25–30.

25.

Apaydin

Buket

Posacioglu

. Perioperative risk factors for mortality in patients with acute type A aortic dissection. Ann Thorac Surg 2002; 74: 2034-2039; discussion 2039.

26.

Chiappini

Schepens

Tan

. Early and late outcomes of acute type A aortic dissection: analysis of risk factors in 487 consecutive patients. Eur Heart J 2005; 26: 180–186.

27.

Pacini

Leone

Di Marco

. Antegrade selective cerebral perfusion in thoracic aorta surgery: safety of moderate hypothermia. Eur J Cardiothorac Surg 2007; 31: 618–622.

28.

Veeragandham

Hamilton

Jr O’Connor

Rizzo

Najafi

. Experience with antegrade bihemispheric cerebral perfusion in aortic arch operations. Ann Thorac Surg 1998; 66: 493–9.

29.

Byrne

Fitzgerald

Aranki

. Simultaneous selective cerebral perfusion and systemic circulatory arrest through the right axillary artery for aortic surgery. J Card Surg 1998; 13: 236–238.

30.

Dossche

Schepens

Morshuis

. Antegrade selective cerebral perfusion in operations on the proximal thoracic aorta. Ann Thorac Surg 1999; 67: 1904–1910.

31.

Haldenwang

Bechtel

Moustafine

. State of the art in neuroprotection during acute type a aortic dissection repair. Perfusion 2012; 27: 119–26.

32.

Estrera

Garami

Miller

3rd . Cerebral monitoring with transcranial Doppler ultrasonography improves neurologic outcome during repairs of acute type A aortic dissection. J Thorac Cardiovasc Surg 2005; 129(2): 277–285.

33.

Estrera

Garami

Miller

3rd . Determination of cerebral blood flow dynamics during retrograde cerebral perfusion using power M-mode transcranial Doppler. Ann Thorac Surg 2003; 76: 704-709; discussion 709–710.

34.

Bavaria

Brinster

Gorman

Woo

Gleason

Pochettino

. Advances in the treatment of acute type A dissection: an integrated approach. Ann Thorac Surg 2002; 74: S1848-1852; discussion S1857–1863.

35.

Trimarchi

Nienaber

Rampoldi

. Contemporary results of surgery in acute type A aortic dissection: The International Registry of Acute Aortic Dissection experience. J Thorac Cardiovasc Surg 2005; 129: 112–122.