lock Open Access lock Peer-Reviewed




Early Mortality in Patients who Received Extensive Surgical Management for Acute Type A Aortic Dissection – Analysis of 452 Consecutive Cases from a Single-center Experience

Ahmed Sayed AbdelhameedI; Feng XinI; Xiang WeiI

DOI: 10.21470/1678-9741-2019-0258


Objective: To detect the potential risk factors associated with early mortality in patients who received extensive surgical management, in the form of total arch replacement plus frozen elephant trunk and arch debranching (hybrid repair technique), for acute type A aortic dissection.
Methods: The clinical and surgical data of 452 surgically treated patients with acute type A aortic dissection at our center, between March 2010 and December 2016, have been retrieved. Uni and multivariate logistic regression analyses were carried out to detect the effect of various preoperative demographics and different perioperative variables on early mortality.
Results: Overall 30-day mortality occurred in 70 out of 452 patients (15.4%). The principal causes of death were multiple organ failure (n=38), cardiac failure (n=18), and severe pulmonary infection (n=10). Risk factors for early mortality were identified with multivariate analysis. Preoperatively, overweight (P<0.025), alcohol drinking (P<0.002), coronary artery disease (P<0.014), hemodynamic shock (P<0.006), and elevated white blood cells count (P<0.002) were associated with higher mortality rate. Postoperatively, prolonged operation time (P<0.008), stroke (P<0.0001), and acute renal dysfunction (P<0.0001) were highly associated with death.
Conclusion: Considering the advantages of extensive surgical management for acute type A aortic dissection over the other less aggressive surgical approaches, it should be advised whenever indicated, provided that being carried out by experts in the field of adult aortic surgery in high-volume centers. The surgeon should be aware of the patient’s preoperative comorbidities and other risk factors for early mortality, in particular, prolonged operation time.


AAA = Abdominal aortic aneurysm

AAAD = Acute type A aortic dissection

AD = Aortic dissection

ARD = Acute renal dysfunction

AUC = Area under the curve

BMI = Body mass index

CA = Circulatory arrest

CABG = Coronary artery bypass grafting

CAD = Coronary artery disease

COPD = Chronic obstructive pulmonary disease

CPB = Cardiopulmonary bypass

DSWI = Deep sternal wound infection

DTA = Descending thoracic aorta

ESM = Extensive surgical management

FET = Frozen elephant trunk ok

GERAADA = German Registry of Acute Aortic Dissection Type A

ICU = Intensive care unit

IQR = Interquartile range

IRAD = International Registry of Acute Aortic Dissection

LVEF = Left ventricular ejection fraction

MC = Mainland of China

ROC = Receiver operating characteristics

RTAD = Retrograde type A aortic dissection

SD = Standard deviation

SPSS = Statistical Package for the Social Sciences

TAR = Total aortic arch replacement

TEVAR = Thoracic endovascular aortic repair

TIA = Transient ischemic attack

TND = Transient neurologic dysfunction

WBCs = White blood cells

WHO = World Health Organization


In acute type A aortic dissection (AAAD), the complications of either aortic rupture or malperfusion syndromes may arise if the remaining distal portion of the aorta is untreated[1]. As a result, recent surgical practice advocates a more aggressive repair approach using total aortic arch replacement (TAR) combined with the frozen elephant trunk (FET) technique[2,3]. Arch debranching is a safe alternative to FET in AAAD patients and it has the advantage of being performed without circulatory arrest in addition to being suitable in candidates who are unfit for FET[4-6].

Over the past few decades, risk factors related to mortality of AAAD have been explored widely but with a relatively small number of patients who received extensive surgical management (ESM) for AAAD. Contrarily, our study is one of the few studies in the literature which investigated a relatively large series of patients who underwent ESM for AAAD. The dominant impact factors on adverse surgical outcomes of AAAD stay a matter of controversy. This might be explained by the rarity of the disease and the lack of numerous experienced surgical centers, which resulted in lack of clear risk stratification. Also, the emergency nature and the evolving surgical techniques necessitated continuous update regarding any recognizable predictors that could aid aortic surgeons in their daily practice. The aim of the present study is to explore the effect of different peri and intraoperative variables on early mortality in a large series of patients who underwent extensive surgical repair for AAAD.


This study was approved by the institutional ethical review board and informed consent was waived as this is a retrospective study of pre-existing data. Clinical and surgical data of AAAD patients who have been treated at our aortic surgery center between March 2010 and December 2016 were collected from the institutional database. Four independent aortic surgeons performed the surgical intervention.

At our institution, the FET technique was the primary management strategy in 364 out of 452 patients (80.5%), being indicated to patients who required an extensive repair for aortopathy. Eighty-eight out of 452 patients (19.5%) underwent arch debranching (hybrid repair) for AAAD.

Diagnosis of AAAD was confirmed by multidetector computed tomographic angiography. AAAD was defined as acute if chest pain or other related symptoms were present for less than two weeks before presentation to our hospital.

Extensive repair was indicated when the site of the intimal tear was in the aortic arch, close to the descending thoracic aorta (DTA), or when the supra-arch branches were involved by the dissection process, as well as to patients with Marfan syndrome or in cases of dissection with a dilatated aortic arch.

High-risk status, obesity, surgeon’s preference, and patient’s willingness were our indications for hybrid repair, provided that the anatomy was suitable for this kind of intervention.

Excluded cases were those with chronic aortic dissection (AD) (54 cases), patients who did not undergo surgical treatment (22 cases), and those who had undergone open surgery for retrograde type I AD post thoracic endovascular aortic repair (TEVAR).

The flow chart picture (Figure 1) shows included and excluded cases.

Fig. 1 - Flow chart picture showing included and excluded cases. FET=frozen elephant trunk; RTAD=retrograde type A aortic dissection; TAR=total aortic arch replacement

Hemodynamic shock was defined as a drop in systolic blood pressure below 90 mmHg at the emergency department. Emergency surgery was the operation carried out within 24 hours after admission. Postoperative acute renal dysfunction (ARD) was defined as a serum creatinine level three-fold greater than baseline (≥ 4 mg/dl), urine output < 0.3 ml/kg/h for 24 hours, anuria for 12 hours, or a new requirement for transient hemodialysis.

Multiple organ dysfunction syndrome was defined as existence of at least two or more of the following conditions: acute liver failure, acute respiratory distress syndrome, acute heart failure, acute renal failure, diffuse or focal neurologic ischemic damage, such as permanent paraparesis or paraplegia due to deterioration of blood supply to the spinal cord or signs of central neurological damage following cerebral hypoperfusion, and septicemia.

Statistical Analysis

The Statistical Package for the Social Sciences (SPSS) software (IBM, Armonk, NY, USA), version 22.0, was used for analysis. Continuous variables were presented as mean ± standard deviation and median with interquartile range. Nominal variables were compared by c[2] tests or two-sided Fisher’s exact tests. Continuous univariate predictors for death were tested using Student’s t-tests or Wilcoxon-Mann-Whitney tests, as appropriate. A P-value < 0.05 was considered statistically significant. In order to assess the predictive risk factors for mortality and morbidity, each variable that was considered significant at univariate analysis was selected for multivariable analysis at three levels: preoperative, intraoperative, and postoperative, independently.

Receiver operating characteristics (ROC) curves were performed to estimate the capacity of prolonged operation and cardiopulmonary bypass (CPB) time in predicting mortality.

Operative Strategies and Techniques

For FET technique, general anaesthesia, supine position, and sterile draping were performed followed by exposure of the right axilla at the beginning. Then a median sternotomy was done and CPB establishment was made by placing an arterial cannula in the right axillary artery and a two-stage cannula for venous drainage. Circulatory arrest was started after completing the proximal aortic repair at 20-28 ˚C nasopharyngeal temperature. Our cerebral perfusion strategy was to use the right axillary artery alone for antegrade cerebral perfusion at a rate of 6±2 ml/kg/min. If there was a poor backward bleeding from the left-sided arch vessels, then bilateral antegrade cerebral perfusion was preferred by placing an additional balloon-tipped catheter into the lumen of the left carotid artery. We have used the Cronus prosthesis (Microport Medical, Shanghai, China), which is commercially available in China, to perform the Sun’s procedure[7], that involves implanting the stented graft into the descending aorta under direct vision, followed by total arch replacement with a four-branched vascular graft (Hemashield Platinum, Maquet, Wayne, NJ, USA). A specific anastomotic order for aortic reconstruction was conducted starting by the proximal descending aorta, followed by the left carotid artery, then the ascending aorta, the left subclavian artery, and lastly, the innominate artery (Figure 2). Rewarming and reperfusion were initiated just after the distal anastomosis to minimize cerebral and coronary ischemia (Figure 3).

Fig. 2 - Implanting the stented graft into the descending aorta under direct vision, followed by total arch replacement with a fourbranched vascular graft (Hemashield Platinum; Maquet, Wayne, NJ, USA); a specific anastomotic order for aortic reconstruction is conducted starting by the proximal descending aorta, followed by the left carotid artery, then the ascending aorta, the left subclavian artery, and lastly, the innominate artery.

Fig. 3 - Final reconstruction with frozen elephant trunk+total aortic arch replacement.

As regards to the arch debranching procedure, the same abovementioned steps were carried out plus placing an additional arterial cannula in the femoral artery to establish CPB. Use of the four-branch graft to replace the ascending aorta, starting by proximal anastomosis first, then construction of the distal anastomosis beyond the level of the innominate artery, was done. Afterward, we removed the aortic clamp and started rewarming. The arch vessels were anastomosed to the limbs of the artificial graft on pump after heavy ligatures of each branch vessel were taken off. If there was a difficult left subclavian artery, we rerouted it to the left axillary artery. After weaning off CPB, administration of a half dose of protamine was done for heparin neutralization.

Placing the endovascular stent was done before sternal closure, using the femoral artery for the stent delivery. In order to achieve about 20% oversize in diameter of the stent graft (range 28-34 mm), we were guided by the size of the pre-sutured four-branch Dacron graft. Retrograde advancement of the stiff guidewire was done from the femoral artery up to the left ventricle or by using the fourth limb of the Dacron. The implementation of the stent graft in the Dacron graft was done with an overlapping margin of about 2 cm. Occasionally, in order to cover the DTA, we needed two stent grafts instead of one, as one stent graft (15-17 cm in length) might be insufficient to cover DTA. There was no need to extend beyond the level of T8 vertebra in most cases to cover the distal territory. Assessment of endoleak or incomplete sealing was made by repeating the angiography[4].


Four hundred fifty-two surgically treated AAAD patients were included in this study. Of these, 70 patients (15.4%) died within 30 days. Regarding hybrid repair, 13 patients died out of 88 cases (14.7%), while 57 patients died out of 364 cases (15.6%) when FET+TAR technique was used. The principal causes of death were multiple organ failure (n=38), cardiac failure (n=18), and severe pulmonary infection (n=10). Two deaths were due to deep sternal infection and two deaths occurred due to surgical failure. Detailed information on demographics and peri and intraoperative data are presented in Tables 1 to 6.

Table 1 - Patients' demographics data.
Variable Value (%)
Age (years)  
    Mean ± SD 48.36±9.57
    Median (IQR) 48 (42-53)
    Male (%) 346 (76.2)
Weight (kg)  
    Mean ± SD 72.05±12.44
    Median (IQR) 71 (64-80)
    Smoking (%) 200 (44.1)
    Alcohol drinking (%) 172 (37.9)
    Previous cardiac surgery (%) 12 (2.6)
Duration of complaint  
    0-24 hours (%) 254 (55.9)
    > 24 hours (%) 188 (41.4)
Diabetes mellitus 44 (9.7)
Hypertension (%) 356 (78.4)
Hyperlipidemia (%) 30 (6.6)
COPD (%) 14 (3.1)
CAD (%) 16 (3.5)
Aortic regurgitation ≥ grade 3 84 (18.5)
Shock (%) 14 (3.1)
Malperfusion (%)  
    Stroke (%) 6 (1.3)
    TIA (%) 2 (0.4)
    Myocardial ischemia (%) 116 (25.6)
    Renal dysfunction (%) 36 (7.9)
    Mesenteric ischemia (%) 0
    Lower extremity (%) 2 (0.4)
Marfan syndrome (%) 18 (3.9)
    Mean ± SD 60.5±6.1
    Median (IQR) 60 (58-63.2)
Elevated WBCs count (%) 246 (54.2)
Anemia (%) 84 (18.5)
Low platelets count (%) 174 (38.1)

Values are presented as mean and SD and median with IQR or n (%).

CAD=coronary artery disease; COPD=chronic obstructive pulmonary disease; IQR=interquartile range; LVEF=left ventricular ejection fraction; SD=standard deviation; TIA=transient ischemic attack; WBCs=white blood cells

Table 1 - Patients' demographics data.



Table 2 - Patients' demographics data (univariate and multivariate analyses).
Variable Univariate P-value Multivariate (P-value)
Age (years) 0.855  
    Mean ± SD    
    Median (IQR)    
    Gender 0.174  
    Male (%)    
Weight (kg) 0.063 0.025
    Mean ± SD    
    Median (IQR)    
    Smoking (%) 0.869  
Alcohol drinking (%) 0.014 0.002
    Previous cardiac surgery (%) 0.999  
Duration of complaint    
    0-24 hours (%) 0.047  
    > 24 hours (%) 0.428  
Diabetes mellitus 0.733  
Hypertension (%) 0.845  
Hyperlipidemia (%) 0.345  
COPD (%) 0.282  
CAD (%) 0.124 0.014
Aortic regurgitation ≥ grade 3 0.509  
Shock (%) 0.010 0.006
Malperfusion (%)    
    Stroke (%) 0.999  
    TIA (%) >0.999  
    Myocardial ischemia (%) 0.130  
    Renal dysfunction (%) 0.054  
    Mesenteric ischemia (%)    
    Lower extremity (%) >0.999  
Marfan syndrome (%)    
    Mean ± SD    
    Median (IQR)    
Elevated WBCs count (%) 0.043 0.002
Anemia (%) 0.206  
Low platelets count (%) 0.768  

Values are presented as mean and SD and median with IQR or n (%).

CAD=coronary artery disease; COPD=chronic obstructive pulmonary disease; IQR=interquartile range; LVEF=left ventricular ejection fraction; SD=standard deviation; TIA=transient ischemic attack; WBCs=white blood cells

Table 2 - Patients' demographics data (univariate and multivariate analyses).



Table 3 - Operative variables.
Variable Value (%)
Emergency (%) 212 (46.7)
Hybrid (%) 88 (19.5)
Bentall (%) 150 (33)
CABG (%) 54 (11.9)
Arterial cannulation method  
    Right axillary artery 400 (88.1)
    Right axillary & right femoral arteries 36 (7.9)
    Distal ascending aorta 6 (1.3)
    Left femoral artery 6 (1.3)
Operation time (min)  
    Mean ± SD 513.55±101.27
    Median (IQR) 501 (440-565)
Clamp time (min)  
    Mean ± SD 120.88±31.57
    Median (IQR) 122 (96-139)
CPB time (min)  
    Mean ± SD 225.18±55.01
    Median (IQR) 217 (189.5-251.25)
    CA time (min)  
    Mean ± SD 26.77±8.73
    Median (IQR) 26 (21-30.75)
Nasopharyngeal temperature (˚C)  
    Mean ± SD 21.46±4.16
    Median (IQR)  
Cerebral perfusion  
    Unilateral antegrade 328 (72.2)
    Bilateral antegrade 92 (20.3)

CA=circulatory arrest; CABG=coronary artery bypass grafting; CPB=cardiopulmonary bypass; IQR=interquartile range; SD=standard deviation

Table 3 - Operative variables.



Table 4 - Operative variables (univariate and multivariate analyses).
Variable Univariate P-value Multivariate (P-value)
Emergency (%) 0.614  
Hybrid (%) 0.521  
Bentall (%) 0.909  
CABG (%) 0.299  
Arterial cannulation method 0.844  
    Right axillary artery    
    Right axillary & right femoral arteries    
    Distal ascending aorta    
    Left femoral artery    
Operation time (min) < 0.0001 < 0.008
    Mean ± SD    
    Median (IQR)    
Clamp time (min) 0.014  
    Mean ± SD    
    Median (IQR)    
CPB time (min) 0.0001  
    Mean ± SD    
    Median (IQR)    
CA time (min) 0.422  
    Mean ± SD    
    Median (IQR)    
Nasopharyngeal temperature (˚C) 0.278  
    Mean ± SD    
    Median (IQR)    
Cerebral perfusion 0.239  
    Unilateral antegrade    
    Bilateral antegrade    

CA=circulatory arrest; CABG=coronary artery bypass grafting; CPB=cardiopulmonary bypass; IQR=interquartile range; SD=standard deviation

Table 4 - Operative variables (univariate and multivariate analyses).



Table 5 - Early outcomes.
Variable Value (%)
30-day mortality (%) 70 (15.4)
Mortality in hybrid repair (%) 13 (14.7)
Mortality in FET+TAR (%) 57 (15.6)
Stroke (%) 30 (6.6)
TND (%) 168 (37)
Hemiplegia (%) 2 (0.4)
DSWI (%) 20 (4.4)
ARD (%) 68 (15)
Pulmonary infection (%) 144 (31.7)
Tracheotomy (%) 74 (16.3)
Ventilation time (h)  
    Mean ± SD 124.25±122.94
    Median (IQR) 89 (40-165)
ICU readmission (%) 50 (11)

ARD=acute renal dysfunction; DSWI=deep sternal wound infection; FET=frozen elephant trunk; ICU=intensive care unit; IQR=interquartile range; SD=standard deviation; TAR=total aortic arch replacement; TND=transient neurologic dysfunction

Table 5 - Early outcomes.



Table 6 - Early outcomes (univariate and multivariate analyses).
Variable Univariate P-value Multivariate (P-value)
30-day mortality (%)    
Stroke (%) < 0.0001 < 0.0001
TND (%) 0.997  
Hemiplegia (%) 0.053  
DSWI (%) 0.706  
ARD (%) < 0.0001 < 0.0001
Pulmonary infection (%) 0.009  
Tracheotomy (%) 0.002  
Ventilation time (h) 0.001  
    Mean ± SD    
    Median (IQR)    
ICU readmission (%) < 0.0001  

ARD=acute renal dysfunction; DSWI=deep sternal wound infection; ICU=intensive care unit; IQR=interquartile range; SD=standard deviation; TND=transient neurologic dysfunction

Table 6 - Early outcomes (univariate and multivariate analyses).

Preoperative Risk Factors for Death

The risk of death was significantly increased on multivariable analysis in relation to body weight (P<0.025), when the patient was positive for alcohol drinking history (P<0.002) or shocked prior to surgery (P<0.006).

Furthermore, concomitant coronary artery disease (CAD) (P<0.014) and elevated leucocytic count were also associated with an increased risk of early death (P<0.002) on multivariate logistic regression analysis (Tables 1 and 2).

Intraoperative Risk Factors for Death

Prolonged operation and CPB times were highly significant predictors of early mortality on univariable logistic regression analysis (P<0.0001) and the entire surgery time remained significantly correlated with mortality in the multivariate analysis (P<0.008) (Tables 3 and 4). ROC curves of operation time and CPB time performance in predicting mortality showed area under the curve of 74.1% (P<0.0001) and 72.8% (P<0.0001), respectively. A selected cutoff point of 511.5 minutes (8.525 hours) of operation time had sensitivity of 73.3% and specificity of 60% (Figure 4), and a cutoff value of 223 minutes (3.72 hours) of CPB time showed sensitivity of 73.5% and specificity of 60.1% in predicting mortality (Figure 5).

Fig. 4 - Cutoff point of 511.5 minutes (8.525 hours) had an accuracy of 74.1% in predicting mortality (sensitivity 73.3%, specificity 60%, P<0.0001). AUC=area under the curve; ROC=receiver operating characteristics

Fig. 5 - Cutoff point of 223 minutes (3.72 hours) had an accuracy of 72.8% in predicting mortality (sensitivity 73.5%, specificity 60.1%, P<0.0001).
Fig. 5 - AUC=area under the curve; CPB=cardiopulmonary bypass; ROC=receiver operating characteristics

Postoperative Risk Factors for Death

Both stroke and ARD were highly significant predictors of early mortality on multivariable analysis (P<0.0001) (Tables 5 and 6).


Our surgical strategies - TAR+FET and hybrid repair - are aggressive repair techniques that showed better results for the management of AAAD[8]. Validation of the FET technique has been acquired as a compatible way for repair of AAAD[9]. In the meantime, various techniques for aortic debranching were designed to achieve AAAD repair with promising outcomes[5,6].

In the year 2000, the International Registry of Acute Aortic Dissection (IRAD) group reported a 58% in-hospital death rate[10] in patients who received medical treatment for AAAD. Even when surgery is conducted in a prompt time, the adverse outcome and death rates for AAAD are still high. Other large AAAD studies, e.g. the Chinese study (mainland of China [MC]; n=270, in 2011) or IRAD (n=617, in 2004), reported mortality rates of 37.0 and 30.6%[11,12], respectively. Another important and relatively recent study is the German Registry of Acute Aortic Dissection Type A (GERAADA)[13], which investigated the early mortality of 2,137 patients after surgical intervention for AAAD (16.9%), being this the biggest number of patients till now included in an AAAD early mortality study. GERAADA’s results should define the up-to-date degree of excellence and experience in surgical management of AAAD comparable to other studies, in which 17% is the average death rate. It is noteworthy to mention that these studies had a big number of patients, but a small percentage of ESM. The great decrease in death rate is attributed to the continuous surgical advance; not only improvements in surgical techniques, but also in temperature management and perfusion strategies, as well as anaesthesia refinements.

Risk Factors for Mortality in Acute Type A Aortic Dissection Patients

The effect of obesity on perioperative and late postoperative outcomes in acute AD remains controversial. However, obese patients are significantly complex candidates to surgery in acute AD due to the demanding anatomy and difficulty of arterial access.

According to accessible data in Asia, a World Health Organization (WHO) expert consultation stated that the body fat content of Asians is generally higher than of white races of the same sex, age, and body mass index (BMI). Additionally, Asians are more vulnerable to develop type II diabetes mellitus and cardiovascular illness even if their BMI is lower than 25 kg/m2. Hence, the present WHO cutoff points for BMI are insufficient for assessment of overweight and obesity in Asian populations[14].

In this study, increased body weight was an independent factor of early mortality. Being overweight was associated with early mortality as stated in a Chinese study by Ma et al.[5]. Interestingly, another Western study demonstrated that obesity (BMI > 30 kg/m2) is significantly related to early mortality in AAAD patients[15].

In our study, a positive history of alcohol consumption was also significantly related to early mortality in univariate analysis and remained statistically significant in the multivariate logistic regression analysis. It has been stated that alcohol consumption in moderation might have a protective effect against CAD and ischemic stroke[16], however, the relationship between alcohol consumption and aortic diseases are not so clear. Several observational studies reported either positive or inverse and even U-shaped relationship between alcohol intake and abdominal aortic aneurysm (AAA)[17]. A recent Japanese cohort study suggested the same protective effect of light to moderate alcohol consumption against mortality in aortic diseases[17]; this finding might be supported by the anti-atherogenic effect of alcohol[18,19]. Atherosclerosis is a cardinal pathological feature in AAA[22] but not in thoracic aortic aneurysm or dissection[20]. On the other hand, elevated blood pressure is one of the effects of chronic alcohol consumption[21], which is a major culpable factor in the development of AD. Our finding must be further investigated as regards to drinking status, habits, and amount, beverage type, and average amount on one occasion for regular drinkers, as little is known about the relationship between alcohol consumption and mortality in AAAD patients.

Cardiogenic shock was recognized as another predictive factor of early mortality, which is mostly due to pericardial tamponade or a high-grade aortic regurgitation. Several studies addressed the adverse relationship between preoperative shock, pericardial tamponade, and pre-admission ventilation and the survival of AAAD patients[22].

Also, CAD was associated with early death. It can be a result of either concomitant coronary atherosclerosis or a consequence of aortic sinus laceration due to extensive dissection process, which in turn resulted in a longer operating time and more difficult surgery.

Leukocytosis on admission was associated with early mortality in our patients’ population. This might be explained by the inflammatory process, which plays a significant role in AD pathogenesis. An elevated white blood cells (WBCs) count has been observed in dissection patients as soon as the onset of the syndrome, suggesting a very early initiation of a cascade of inflammation in AAAD. The tissue destruction and thrombi in the false lumen created by the dissection might induce the inflammatory reaction. The activated circulating WBCs adhered to endothelium and damaged it with toxic oxygen compounds and proteolytic enzymes, this contributed a lot to the injury of the tissues. The WBCs, such as neutrophils and macrophages, have been detected in teared aortic tissues. WBCs were also responsible for the extension of the false lumen, which clearly indicated that WBCs may reflect the severity in cases of acute AD.

On the other hand, acute AD might cause malperfusion syndrome; significant WBCs elevation has been observed in the end-organ ischemic complications that resulted from cerebral, visceral, or coronary malperfusion. Higher WBCs in patients with type A AD might reflect the higher severity of malperfusion syndromes when there is end-organ involvement. Guan et al.[23] demonstrated that high WBC count was a significant predictor of higher rate of postoperative neurological complications. During the surgery, the inflammatory cytokines and cells might add insult to ischemia-reperfusion injury and lead to poor prognosis.

Our study has also demonstrated that elevated WBC count is another independent predictor of early mortality. The high leucocytic count finding and its relationship with early mortality is consistent with results from Fan et al. [24].

Concerning intraoperative risk factors for death, various studies with similar results to ours also reported that whether the preservation or replacement of the aortic root, ascending aorta, and either the total or hemiarch replacement were not independent predictors of mortality, neither were the application of different methods of cerebral perfusion or the arterial cannulation site[14,25].

While univariate logistic regression analysis showed that longer operation times (whole surgery, CPB time, and aortic cross-clamp time) were highly associated with early mortality, the total operation time remained as an independent predictor of early death in the multivariate logistic regression (P<0.008).

Postoperatively, on univariate analysis, respiratory problems in the form of prolonged mechanical ventilation, pulmonary infection, and the need for tracheotomy were also associated with early mortality. Readmission on the intensive care unit was another indicator of consecutive death. Stroke and ARD were highly significant predictors of mortality, both on univariate and multivariate analyses.


We need to acknowledge some limitations of our study. First, the retrospective observational nature is the main limitation of this study. Second, this is a single-center experience on a relatively small sample. Third, the dichotomous nature of data as regards to alcohol drinking habits, which must be investigated in more details.


The use of ESM did not result in any rise in early death or adverse events compared with other surgical approaches in the literature.

Despite the advantages of ESM for AAAD over the other less aggressive surgical approaches, the surgical team should consider the patient’s preoperative comorbidities and other risk factors for early mortality, in particular, prolonged operation time.

A positive relationship was found between preoperative regular alcohol intake and early mortality in these surgical candidates; this is - to the best of our knowledge - the first study to report this relationship.


1. Concistrè G, Casali G, Santaniello E, Montalto A, Fiorani B, Dell&apos;Aquila A, et al. Reoperation after surgical correction of acute type A aortic dissection: risk factor analysis. Ann Thorac Surg. 2012;93(2):450-5. doi:10.1016/j.athoracsur.2011.10.059.

2. Appoo JJ, Bozinovski J, Chu MWA, El-Hamamsy I, Forbes TL, Moon M, et al. Canadian cardiovascular society/Canadian society of cardiac surgeons/Canadian society for vascular surgery joint position statement on open and endovascular surgery for thoracic aortic disease. Can J Cardiol. 2016;32(6):703-13. doi:10.1016/j.cjca.2015.12.037.

3. Erbel R, Aboyans V, Boileau C, Bossone E, Bartolomeo RD, Eggebrecht H, et al. 2014 ESC guidelines on the diagnosis and treatment of aortic diseases: document covering acute and chronic aortic diseases of the thoracic and abdominal aorta of the adult. The task force for the diagnosis and treatment of aortic diseases of the European society of cardiology (ESC). Eur Heart J. 2014;35(41):2873-926. doi:10.1093/eurheartj/ehu281.

4. Ma M, Feng X, Wang J, Dong Y, Chen T, Liu L, et al. Acute type i aortic dissection: a propensity-matched comparison of elephant trunk and arch debranching repairs. Interact Cardiovasc Thorac Surg. 2018;26(2):183-9. doi:10.1093/icvts/ivx283. [MedLine]

5. Esposito G, Cappabianca G, Bichi S, Cricco A, Albano G, Anzuini A. Hybrid repair of type A acute aortic dissections with the Lupiae technique: ten-year results. J Thorac Cardiovasc Surg. 2015;149(2 Suppl):S99-104. doi:10.1016/j.jtcvs.2014.07.099. [MedLine]

6. Chang Q, Tian C, Wei Y, Qian X, Sun X, Yu C. Hybrid total arch repair without deep hypothermic circulatory arrest for acute type A aortic dissection (R1). J Thorac Cardiovasc Surg. 2013;146(6):1393-8. doi:10.1016/j.jtcvs.2012.09.041.

7. Sun LZ, Qi RD, Chang Q, Zhu JM, Liu YM, Yu CT, et al. Surgery for acute type A dissection using total arch replacement combined with stented elephant trunk implantation: experience with 107 patients. J Thorac Cardiovasc Surg. 2009;138(6):1358-62. doi:10.1016/j.jtcvs.2009.04.017.

8. Dohle DS, Tsagakis K, Janosi RA, Benedik J, Kühl H, Penkova L, et al. Aortic remodelling in aortic dissection after frozen elephant trunk. Eur J Cardiothoracic Surg. 2016;49(1):111-7. doi:10.1093/ejcts/ezv045.

9. Ma WG, Zhang W, Wang LF, Zheng J, Ziganshin BA, Charilaou P, et al. Type A aortic dissection with arch entry tear: surgical experience in 104 patients over a 12-year period. J Thorac Cardiovasc Surg. 2016;151(6):1581-92. doi:10.1016/j.jtcvs.2015.11.056.

10. Hagan PG, Nienaber CA, Isselbacher EM, Bruckman D, Karavite DJ, Russman PL, et al. The international registry of acute aortic dissection (IRAD): new insights into an old disease. JAMA. 2000;283(7):897-903. doi:10.1001/jama.283.7.897. [MedLine]

11. Wang DJ, Fan FD, Wang Q, Li QG, Zhou Q, Wu Z, et al. Preliminary characterization of acute aortic dissection in the mainland of China. Chin Med J(Engl). 2011;124(11):1726-30.

12. Collins JS, Evangelista A, Nienaber CA, Bossone E, Fang J, Cooper JV, et al. Differences in clinical presentation, management, and outcomes of acute type A aortic dissection in patients with and without previous cardiac surgery. Circulation. 2004;110(11 Suppl 1):II-237-42. doi:10.1161/01.CIR.0000138219.67028.2a.

13. Conzelmann LO, Weigang E, Mehlhorn U, Abugameh A, Hoffmann I, Blettner M, et al. Mortality in patients with acute aortic dissection type A: analysis of pre- and intraoperative risk factors from the German registry for acute aortic dissection type A (GERAADA). Eur J Cardiothorac Surg. 2016;49(2):e44-52. doi:10.1093/ejcts/ezv356.

14. WHO Expert Consultation. Appropriate body-mass index for Asian populations and its implications for policy and intervention strategies. Lancet. 2004;363(9403):157-63. Erratum in: Lancet. 2004;363(9412):902. doi:10.1016/S0140-6736(03)15268-3.

15. Kawahito K, Kimura N, Yamaguchi A, Aizawa K, Misawa Y, Adachi H. Early and late surgical outcomes of acute type A aortic dissection in octogenarians. Ann Thorac Surg. 2018;105(1):137-43. doi:10.1016/j.athoracsur.2017.06.057. [MedLine]

16. Ronksley PE, Brien SE, Turner BJ, Mukamal KJ, Ghali WA. Association of alcohol consumption with selected cardiovascular disease outcomes: a systematic review and meta-analysis. BMJ. 2011;342:d671. doi:10.1136/bmj.d671.

17. Shirakawa T, Yamagishi K, Yatsuya H, Tanabe N, Tamakoshi A, Iso H, et al. Alcohol consumption and mortality from aortic disease among Japanese men: the Japan collaborative cohort study. Atherosclerosis. 2017;266:64-8. doi:10.1016/j.atherosclerosis.2017.08.025. [MedLine]

18. Kiechl S, Willeit J, Rungger G, Egger G, Oberhollenzer F, Bonora E. Alcohol consumption and atherosclerosis: what is the relation? Prospective results from the Bruneck study. Stroke. 1998;29(5):900-7. doi:10.1161/01.str.29.5.900.

19. Johnsen SH, Forsdahl SH, Singh K, Jacobsen BK. Atherosclerosis in abdominal aortic aneurysms: a causal event or a process running in parallel? The Tromsø study. Arterioscler Thromb Vasc Biol. 2010;30(6):1263-8. doi:10.1161/ATVBAHA.110.203588.

20. Achneck H, Modi B, Shaw C, Rizzo J, Albornoz G, Fusco D, et al. Ascending thoracic aneurysms are associated with decreased systemic atherosclerosis. Chest. 2005;128(3):1580-6. doi:10.1378/chest.128.3.1580.

21. Clark LT. Alcohol-induced hypertension: mechanisms, complications, and clinical implications. J Natl Med Assoc. 1985;77(5):385-9.

22. Long SM, Tribble CG, Raymond DP, Fiser SM, Kaza AK, Kern JA, et al. Preoperative shock determines outcome for acute type A aortic dissection. Ann Thorac Surg. 2003;75(2):520-4. doi:10.1016/s0003-4975(02)04536-8.

23. Guan X, Gong M, Wang X, Zhu J, Liu Y, Sun L, et al. Low preoperative fibrinogen level is risk factor for neurological complications in acute aortic dissection. Medicine (Baltimore). 2018;97(21):e10830. doi:10.1097/MD.0000000000010830. [MedLine]

24. Fan X, Huang B, Lu H, Zhao Z, Lu Z, Yang Y, et al. Impact of admission white blood cell count on short- and long-term mortality in patients with type A acute aortic dissection: an observational study. Medicine (Baltimore). 2015;94(42):e1761. doi:10.1097/MD.0000000000001761. [MedLine]

25. Goda M, Imoto K, Suzuki S, Uchida K, Yanagi H, Yasuda S, et al. Risk analysis for hospital mortality in patients with acute type a aortic dissection. Ann Thorac Surg. 2010;90(4):1246-50. doi:10.1016/j.athoracsur.2010.05.069.

No financial support.
No conflict of interest.

Authors' roles & responsibilities

ASA Substantial contributions to the conception or design of the work; or the acquisition, analysis, or interpretation of data for the work; drafting the work or revising it critically for important intellectual content; final approval of the version to be published

FX Substantial contributions to the conception or design of the work; final approval of the version to be published

XW Agreement to be accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved; final approval of the version to be published

Article receive on Wednesday, June 26, 2019

Article accepted on Tuesday, October 22, 2019

CCBY All scientific articles published at are licensed under a Creative Commons license


All rights reserved 2017 / © 2020 Brazilian Society of Cardiovascular Surgery DEVELOPMENT BY