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Ann Thorac Surg 2002;73:1843-1848
© 2002 The Society of Thoracic Surgeons


Original article: cardiovascular

Surgical treatment of acute type a dissection: is rupture a risk factor?

Marek P. Ehrlich, MD*a, Martin Grabenwöger, MDa, Juliane Kilo, MDa, Alfred A. Kocher, MDa, Georg Grubhofer, MDb, Andrea M. Lassnig, MDb, Edda M. Tschernko, MDb, Bernhard Schlechta, MDa, Doris Hutschala, MDa, Hans Domanovits, MDc, Gottfried Sodeck, MDa, Ernst Wolner, MDa

a Departments of department of Cardiothoracic Surgery, University of Vienna, Vienna, Austria
b Department of Cardiac Anesthesia, University of Vienna, Vienna, Austria
c Department of Emergency Care, University of Vienna, Vienna, Austria

Accepted for publication February 17, 2002.

* Address reprint requests to Dr Ehrlich, Department of Cardiothoracic Surgery, University of Vienna, Währinger Gürtel 18-20, A-1090 Viennam, Austria
e-mail: marekehrlich{at}hotmail.com


    Abstract
 Top
 Abstract
 Introduction
 Patients and methods
 Results
 Comment
 References
 
Background. The purpose of this study was to evaluate the significance of aortic rupture on clinical outcome in patients after aortic repair for acute type A dissection.

Methods. One hundred and twenty patients underwent aortic operations with resection of the intimal tear and open distal anastomosis. Median age was 60 years (range 16 to 87); 78 were male. Thirty-six patients had only ascending aortic replacement, 82 had hemiarch repair, and 2 had the entire arch replaced. Retrograde cerebral perfusion was utilized in 66 patients (53%). Rupture defined as free blood in the pericardial space was present in 60 patients (50%). Univariate and multivariate analyses were performed to assess the risk factors for mortality and neurologic dysfunction.

Results. Overall hospital mortality rate was 24.2% ± 4.0% (± 70% confidence level) but did not differ between patients with aortic rupture or without (p = 0.83). The incidence of permanent neurologic dysfunction was 9.4% overall, 10.5% with rupture and 8.3% without rupture (p = 0.75). Multivariate analysis revealed absence of retrograde cerebral perfusion and any postoperative complication as statistically significant indicators for in-hospital mortality (p < 0.05). Overall 1- and 5-year survival was 85.3% and 33.7%; among discharged patients, survival in the nonruptured group was 89% and 37%, versus 81% and 31% in the ruptured group (p = 0.01).

Conclusions. Aortic rupture at the time of surgery does not increase the risk of hospital mortality or permanent neurologic complications in patients with acute type A dissections. However, aortic rupture at the time of surgery does influence long-term survival.


    Introduction
 Top
 Abstract
 Introduction
 Patients and methods
 Results
 Comment
 References
 
Acute type A aortic dissections represent an emergency situation in cardiac surgery, which requires immediate surgical treatment in order to prevent mortality from intrapericardial hemorrhage. Death from acute proximal aortic dissection is frequently due either to aortic rupture or to a leak of fluid, often by transudation into the pericardial cavity. The accumulation of blood and fluid in the pericardial cavity leads to cardiac tamponade or occlusion of the coronary arteries. Roberts and colleagues [1] have documented that the most common site of rupture in the acute stage is at the site of the mural tear in the aorta. Necrosis of the outer layer of the aortic wall at the site of the tear weakens the wall, allowing rupture. Thus for dissections arising in the ascending aorta, rupture within the closed confines of the pericardial cavity can cause cardiac tamponade.

As transportation of patients as well as diagnostic tools such as computed tomography (CT) or transesophageal echocardiography (TEE) became better over the last decades, more frequently patients with acute type A aortic dissections arrive at the hospital with conditions such as cardiac tamponade and hypotension in need of immediate surgery.

Although results of repair of ascending aortic aneurysms with a focus on particular patients subsets such as those with acute type A dissections have been extensively described, few broad overviews of the procedure have included patients with ruptured type A dissections [2, 3].

This study was undertaken to compare retrospectively our experiences and results in 120 patients undergoing ascending aortic repair for acute type A dissection with and without aortic rupture at the time of operation. Moreover the association between aortic rupture and clinical outcome was evaluated. Particular emphasis was directed toward mortality rate, neurologic outcome, and long-term survival.


    Patients and methods
 Top
 Abstract
 Introduction
 Patients and methods
 Results
 Comment
 References
 
Patients
Between March 1998 and February 2001, a total of 120 patients underwent surgical repair of the ascending aorta or aortic arch for acute type A aortic dissection at the University of Vienna Medical Center. Rupture was classified as follows: hematoma in the mediastinal fat or in the aortopulmonary window or frank rupture with blood in the pericardial or pleural space with or without hemodynamic compromise. Most patients in the ruptured group with hemodynamic compromise presented with signs of cardiac tamponade. Hemodynamic compromise was defined as a permanent deterioration in systolic blood pressure below 90 mm Hg. In these cases inotropic drug support was initiated to maintain adequate circulatory perfusion until the patient was put on cardiopulmonary bypass.

The nonruptured group consisted of 36 men and 24 woman with an median age of 57.5 years ranging from 16 to 87. The ruptured group was composed of 42 men and 18 women with an median age of 64 years ranging from 18 to 83. Age distribution showed a predominance in the fifth, sixth, and seventh decades in both groups (Fig 1). For the 7 patients (5 in the nonruptured group, 2 in the ruptured group) with Marfan syndrome the median age was 37 years (range 16 to 52). The groups were not significantly different with respect to a number of preoperative as well as intraoperative variables previously shown to have an impact on outcome in patients with this aneurysmal disease as shown in Table 1. There was no statistically significant difference with respect to sex, preoperative neurologic symptoms, and previous cardiac surgery between both groups. The incidence of coronary heart disease was higher in the nonruptured group than in the ruptured. Four patients in the ruptured group had undergone previous coronary artery bypass grafting. Two of these 4 patients presented with a hematothorax in the right pleural space at the time of surgery.



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Fig 1. Age distribution of patients at the time of surgery.

 

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Table 1. Selected Preoperative Clinical Characteristics and Complications in the Rupture and Nonrupture Groups

 
Hypertension was the most common preoperative medical disorder with a prevalence of more than 80% in both groups followed by coronary artery disease and pulmonary dysfunction. Hemodynamic instability as well as cardiac tamponade were both more common in the ruptured group (p < 0.05).

Attempts were made to repair and resuspend the native aortic valve whenever possible except in cases of Marfan syndrome or severe annuloaortic ectasia. Nevertheless 31 patients (16 in the nonruptured group, 15 in the ruptured group) required aortic valve replacement. Composite valve graft replacement with reimplantation of the coronary arteries was performed in 24 patients (20%).

The preoperative diagnosis of aortic dissection was made by either CT or TEE or by a combination of both methods.

Assessment of neurologic complications
The presence of neurologic dysfunction at the time of discharge from the hospital whether focal injury (stroke) or global (coma) was considered permanent neurologic injury. Temporary neurologic dysfunction, which could only be assessed on operative survivors without permanent neurologic dysfunction, was defined as the occurrence of postoperative confusion, agitation or transient delirium. CT scans when performed on patients with temporary dysfunction were usually normal.

Operative technique
All patients had replacement of the ascending aorta with an open distal anastomosis during an interval of hypothermic circulatory arrest. In patients with cardiac tamponade the left femoral vein was used for venous access and the patient was first cooled down and circulation interrupted before sternotomy.

The extent of operation was variable; the site of the tear was resected whenever possible. The surgical technique and the application of profound hypothermic circulatory arrest (HCA) throughout the study period were standard: the implementation of HCA has previously been described in detail [4]. Briefly it consists of core cooling during cardiopulmonary bypass to an average core temperature of 12° to 15°C measured in the esophagus. The part of the procedure that requires interruption of cerebral blood flow is then done during the period of circulatory arrest. The head is packed in ice to prevent warming of the central nervous system during prolonged circulatory arrest. In patients where retrograde cerebral perfusion was implemented during the period of profound HCA a bypass bridge connecting the arterial and venous lines of the extracorporeal circuit was used to reverse the flow into the superior vena cava cannula. Retrograde cerebral perfusion (RCP) flow rates were adjusted to maintain a mean central venous pressure of 20 mm Hg.

Statistical analysis
All continuous data are expressed as mean ± SD. Mortality was defined as death that occurred in the hospital. Statistical comparison between survivors and nonsurvivors was performed using {chi}2 analysis and unpaired t test. Twelve preoperative variables (operation date, gender, age, Marfan syndrome, hypertension, coronary artery disease, previous myocardial infarction, preoperative neurologic symptoms, pulmonary disease, preoperative renal dysfunction, previous cardiac surgery, preoperative resuscitation and hemodynamic compromise) as well as seven intraoperative variables (coronary bypass grafting, use of a composite graft, aortic cross-clamp time, circulatory arrest time, use of RCP, rectal and esophageal temperature before circulatory arrest) were used for the determination of statistically significant risk factors for mortality and neurologic complications. Risk factors found to have a p value of less than 0.25 in the univariate analysis were entered into a stepwise multiple logistic regression for the determination of statistically significant independent risk factors for mortality prediction. Survival rates were generated using life-tables analysis. The log-rank test was used for statistical comparisons of the Kaplan-Meier curve. All statistical analysis was performed on Sigmastat (Jandel Scientific, San Raphael, CA) and SPSS computer programs (SPSS, Inc, Chicago, IL).


    Results
 Top
 Abstract
 Introduction
 Patients and methods
 Results
 Comment
 References
 
The overall hospital mortality for all patients was 24.2% ± 4.0% (± 70% confidence level). Fourteen patients (23%) died in the nonruptured group compared with 15 patients (25%) in the ruptured group (p = 0.83). Patients with hemodynamic instability after rupture had a much higher hospital mortality than those without (36% versus 19%; p = 0.14). Intraoperative death occurred in 3 patients (all in the ruptured group). Causes of intraor postoperative death are listed in Table 2. Myocardial failure (including low cardiac output) was the most common cause of hospital mortality. Postoperative neurologic deficits were contributing factors in 3 deaths in both groups.


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Table 2. Causes of Intraoperative and Postoperative Mortality

 
Univariate analysis for hospital mortality independent of group revealed a number of preoperative, intraoperative, and postoperative risk factors: preoperative angina (p = 0.04), older age (p = 0.09), preoperative cardiopulmonary resuscitation (p = 0.002), absence of retrograde cerebral perfusion (p = 0.009), and any postoperative complication (p = 0.0002). Duration of HCA, the performance of concomitant procedures, and the year of operation all failed to show any impact on hospital mortality.

By multiple logistic regression analysis, absence of RCP and any postoperative complications were found to be independent predictors of hospital mortality (Table 3).


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Table 3. Stepwise Multiple Logistic Regression for Mortality in Patients With and Without Aortic Rupture

 
As depicted in Table 4, no differences were found in esophageal and rectal temperature before the implementation of circulatory arrest, aortic cross-clamp, and circulatory arrest time. The mean duration of the latter was 34 minutes in the nonruptured group and 30 minutes in the ruptured group. Patients with ruptured aortic aneurysms had somewhat longer extracorporeal circulation times (p = 0.01).


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Table 4. Selected Surgical Characteristics

 
Sixteen patients in the nonruptured group and 11 patients in the ruptured group exceeded HCA times of greater than 40 minutes, respectively (p = 0.28). There was no increase in hospital mortality in both groups when circulatory arrest times exceeded 40 minutes (p = 0.12).

Coronary artery bypass grafting was the most common concomitant procedure and was performed in 10 patients (8.3%) overall.

Neurologic dysfunction
Postoperative permanent cerebral complications (stroke, global) occurred in 5 patients in the nonruptured group (8.3%) and in 6 patients (10.5%) in the ruptured group (p = 0.75). Of these 11 neurologic deficits, 7 were caused by embolic strokes and were focal in nature. They were verified by enhanced computer tomography. In 4 patients the permanent injury was global and not embolic in nature as could best determined by cerebral CT scans. Univariate analysis for permanent neurologic dysfunction of the group as a whole revealed two preoperative factors: a history of previous neurologic symptoms (p = 0.03) and hemodynamic instability before surgery (p = 0.02). In the multivariate analysis of the group as a whole, independent risk factors for permanent neurologic sequelae were hemodynamic instability before surgery (p = 0.04, odds ratio [OR] 4.7) and coronary artery bypass grafting (p = 0.05, OR 23; Table 5).


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Table 5. Stepwise Multiple Logistic Regression for Permanent Neurologic Dysfunction in Patients With and Without Aortic Rupture

 
Transient neurologic dysfunction, which was evaluated only in patients surviving operation without permanent neurologic sequelae, occurred in 23 patients (28.7%). It occurred in 27% of patients with no aortic rupture and in 31% of patients with rupture (p = 0.80). Univariate analysis for temporary neurologic dysfunction of the group as a whole revealed a history of previous neurologic symptoms (p = 0.04) and the occurrence of any postoperative complications had a high correlation with transient neurologic dysfunction (p = 0.0005). It is admittedly more difficult, however, to evaluate transient neurologic dysfunction in the presence of complications that may require additional sedation for their treatment. Significant predictors of transient neurologic dysfunction in multivariate analysis of the group as a whole were the presence of any postoperative complications (p = 0.01, OR 16.5).

Survival
Overall 1- and 5-year survivals were 85% and 33%, respectively; among discharged patients (Fig 2), survival in the nonruptured group was 89% and 37% versus 81% and 31% in the ruptured group (p = 0.01).



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Fig 2. Overall 1-year and 5-year survival among discharged patients (Pts.) with rupture and without rupture at the time of operation.

 

    Comment
 Top
 Abstract
 Introduction
 Patients and methods
 Results
 Comment
 References
 
Acute type A dissection is a catastrophic event that still represents a formidable undertaking for cardiac surgeons. Treated nonoperatively 90% of all patients with acute dissection will die within 2 weeks [57]. The cause of death in this cohort is mostly related to aortic rupture and as a consequence leakage of fluid or blood into the pericardial cavity. The accumulation of blood and fluid in the pericardial cavity leads to cardiac tamponade or occlusion of the coronary arteries. The current management philosophy therefore favors immediate surgical intervention for which results have steadily been improving owing to the development of better prosthetic materials, amelioration of cardiac as well as cerebral protection, and increased surgical experience [8].

Furthermore owing to more efficient transportation of these patients to a medical center as well as enhanced preoperative diagnosis, more patients with acute type A aortic dissections arrive in the hospital in poorer conditions, cardiac tamponade due to aortic rupture and hypotension already developing in many of them and in need of immediate surgery.

This has led us to a reexamination of different prognostic indicators, especially questioning whether aortic rupture before surgery would have an impact on morbidity, mortality, and long-term survival. In this study a series of 120 patients with acute type A dissection was analyzed to determine postoperative outcome.

The overall perioperative mortality rate of 24.2% in our study is comparable with other recent studies [9, 10]. Two variables were found to be statistically significant independent risk factors for mortality in our patient population: the first was absence of RCP and any postoperative complications. The observation that RCP reduced hospital mortality is consistent with the results obtained by Coselli and Lemaire [11] and with a recent study from our department [4]. We strongly believe that the apparent superiority of RCP over profound HCA in this study can be explained by the sustained intracranial cooling during profound HCA that is afforded by retrograde cerebral perfusion and may therefore enhance the topical cooling effect of ice-bags around the head.

Interestingly, aortic rupture at the time of operation was not found to be a statistically significant risk factor. This finding once again confirms our own earlier results [12]. Similarly, but not surprisingly, hemodynamic instability after aortic rupture was found to be a better predictor for mortality than rupture alone.

The second variable identified as an independent risk factor for hospital mortality was any type of postoperative complications. These included the need for tracheostoma, the presence of infection, or the postoperative occurrence of renal, liver, or cardiac failure. The influence of any postoperative complications on hospital mortaltiy was also reported by Griepp and coworkers [13].

Cardiac failure was the most common cause of hospital death. Although special emphasis was made in the last years for optimal myocardial protection by administrating antegrade or retrograde cold blood cardioplegia continuously during the entire operation, 12 of 29 patients (41%) died postoperatively of heart failure. The reason for this postoperative complication can be explained by the severe coronary heart disease with poor left ventricular function at the time of operation. To reduce the delay in surgical intervention none of these high-risk patients had undergone cardiac catheterization. Coronary artery bypass graft surgery was performed in addition to the aortic surgery in patients in which the dissection continued into the right or left coronary artery or when signs of cardiac ischemia were present at the time of weaning the patient from the extracorporeal ciculation pump.

We were unable to find a significant effect on mortality either from the length of circulatory arrest time or from myocardial ischemic time. The observation that circulatory arrest time is not a factor for hospital mortality is consistent with the results obtained by Ergin and coworkers [14] and with a recent study from our department [15].

The absence of Marfan syndrome as a risk factor for adverse outcome is symbolic of the success that has been achieved in a particular group of high-risk patients by early elective intervention, reducing the need for emergency operations with their associated higher mortality and morbidity.

In regard to patients’ age at time of intervention, a sharp increase in mortality in older patients was observed. Age was also of borderline significance for mortality in univariate analysis. The influence of age was also reported by others as the only constant determinant of mortality [4, 14].

The emergence of coronary artery disease as an independent risk factor for the occurrence of permanent neurologic dysfunction is interesting but we cannot find a satisfactory explanation for this finding. We can only speculate that these patients had some sort of cerebrovascular disease at the time of surgery.

We also wanted to examine the syndrome termed "transient neurologic dysfunction" because previous studies have consistently shown TND to correlate with duration of cerebral ischemia in contrast with permanent neurologic injury, which is predominantly focal and for which prolonged HCA has not invariably emerged as a risk factor [14]. In addition to being a reflection of suboptimal cerebral protection recent evidence has also suggested that TND seems to be a marker of long-lasting but subtle cognitive impairment [16]. In this series a significant predictor of TND in multivariate analysis of the group as a whole was the presence of any postoperative complications. This finding is similar to a recent retrospective analysis of a large clinical series published by Ehrlich and coworkers [13].

In conclusion the results of this study reinforce dramatically the notion that patients with acute type aortic dissections should be operated on as soon as possible. Aortic rupture at the time of surgery does not increase the risk of hospital mortality. In an effort to avoid hemodynamic instability after aortic rupture, earlier diagnosis and immediate surgical intervention as well as recognition of risk factors such as hypertension and aortic dilatation should be the goal and will lead to lower mortality and morbidity.

Limitations of the study
The major limitation of the present study was that all data were analyzed retrospectively, a process that mandates caution in the interpretation of the results. For example the two groups of patients may have been quite different in spite of our efforts to eliminate any potential bias by accounting for possible known confounding factors that may have influenced the clinical outcome. Furthermore "aortic rupture" has a broad variety of definitions ranging from minimal pericardial effusion to total rupture of the aortic wall. In this study we focused only on those patients with signs of pericardial fluid, hematoma in the mediastinal fat or in the aortopulmonary window, or frank rupture with or without hemodynamic compromise.


    References
 Top
 Abstract
 Introduction
 Patients and methods
 Results
 Comment
 References
 

  1. Roberts W.C. Aortic dissection: anatomy, consequences, and causes. Am Heart J 1981;101:195-214.[Medline]
  2. Ehrlich M.P., Ergin A., McCullough J., et al. Results of immediate surgical treatment of all acute type A dissections. Circulation 2000;102(Suppl 3):248-252.
  3. Bachet J., Goudot B., Dreyfus G.D., et al. Surgery for acute type A aortic dissection: the Hopital Foch experience (1977–1998). Ann Thorac Surg 1999;67:2006-2009.[Abstract/Free Full Text]
  4. Ehrlich M.P., Fang C., Grabenwoeger M., et al. Impact of retrograde cerebral perfusion on aortic arch aneurysm repair. J Thorac Cardiovasc Surg 1999;118:1026-1032.[Abstract/Free Full Text]
  5. Fuster V., Ip J.H. Medical aspects of acute aortic dissection. Semin Thorac Cardiovasc Surg 1991;3:219-224.[Medline]
  6. Anagnostopoulos C.E., Prabhaker M.J.S., Kittle C.F. Aortic dissections and dissecting aneurysms. Am J Cardiol 1972;30:263-273.[Medline]
  7. DeBakey M.E., McCollum C.H., Crawford E.S., et al. Dissection and dissecting aneurysms of the aorta: twenty-year follow-up of five hundred twenty-seven patients treated surgically. Surgery 1982;92:1118-1134.[Medline]
  8. Laas J., Jurmann M.J., Heinemann M., Borst H.G. Advances in aortic arch surgery. Ann Thorac Surg 1992;53:227-232.[Abstract]
  9. Fann J.I., Smith J.A., Miller D.C., et al. Surgical management of aortic dissection during a 30-year period. Circulation 1995;92(Suppl 2):113-121.[Abstract/Free Full Text]
  10. Bavaria J.E., Woo J.Y., Hall R.A., Wahl P.M., Acker M.A., Gardner T.J. Circulatory management with retrograde cerebral perfusion for acute type A aortic dissection. Circulation 1996;94(Suppl 2):173-176.
  11. Coselli J.S., Lemaire S.A. Experience with retrograde cerebral perfusion during proximal aortic surgery in 290 patients. J Card Surg 1997;12(Suppl):322-325.[Medline]
  12. Ehrlich M.P., Fang W.C., Grabenwoger M., Cartes-Zumelzu F., Wolner E., Havel M. Perioperative risk factors for mortality in patients with acute type A aortic dissection. Circulation 1998;98:294-302.[Abstract/Free Full Text]
  13. Ehrlich M.P., Ergin M.A., McCullough J.N., et al. Predictors of adverse outcome and transient neurological dysfunction after ascending aorta/hemiarch replacement. Ann Thorac Surg 2000;69:1755-1763.[Abstract/Free Full Text]
  14. Ergin M.A., Galla J.D., Lansman S.L., Quintanac C., Bodian C., Griepp R.B. Hypothermic circulatory arrest in operation on the thoracic aorta: determinants of operative mortality and neurological outcome. J Thorac Cardiovasc Surg 1994;107:788-799.[Abstract/Free Full Text]
  15. Grabenwoeger M., Ehrlich M., Cartes-Zumelzu F., et al. Surgical treatment of aortic arch aneurysms in profound hypothermia and circulatory arrest. Ann Thorac Surg 1997;64:1067-1071.[Abstract/Free Full Text]
  16. Ergin M.A., Uysal S., Reich D.L., et al. Temporary neurological dysfunction after deep hypothermic circulatory arrest: a clinical marker of long-term functional deficit. Ann Thorac Surg 1999;67:1887-1890.[Abstract/Free Full Text]




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