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Eur J Cardiothorac Surg 2007;32:255-262. doi:10.1016/j.ejcts.2007.04.012
Copyright © 2007, European Association for Cardio-Thoracic Surgery. Published by Elsevier B.V. All rights reserved

Significance of malperfusion syndromes prior to contemporary surgical repair for acute type A dissection: outcomes and need for additional revascularizations

Arnar Geirssona, Wilson Y. Szetoa, Alberto Pochettinoa, Michael L. McGarveyb, Martin G. Keanec, Y. Joseph Wooa, John G. Augoustidesd, Joseph E. Bavariaa,*

a Division of Cardiothoracic Surgery, Hospital of the University of Pennsylvania, 3400 Spruce Street, Philadelphia, PA 19104-4283, United States
b Department of Neurology, University of Pennsylvania Medical Center, Philadelphia, Pennsylvania, United States
c Department of Cardiovascular Medicine, University of Pennsylvania Medical Center, Philadelphia, Pennsylvania, United States
d Department of Anesthesiology and Critical Care, University of Pennsylvania Medical Center, Philadelphia, Pennsylvania, United States

Received 5 February 2007; received in revised form 29 March 2007; accepted 3 April 2007.

* Corresponding author. Tel.: +1 215 662 2017; fax: +1 215 349 5798. (Email: joseph.bavaria{at}uphs.upenn.edu).


   Abstract
Top
 Abstract
1. Introduction
 2. Materials and methods
 3. Results
 4. Discussion
 Appendix A
 References
 
Objective: The aim of this study was to assess the significance of malperfusion syndromes in patients with acute type A aortic dissection following a contemporary surgical management algorithm and the effects on morbidity, hospital mortality, and long-term survival. We believe that obliteration of the primary tear site with restoration of flow in the true aortic lumen results in decreased need for revascularization of malperfused organ systems. Methods: Our operative approach aims at replacing the entire ascending aorta, resuspension of the aortic valve with repair or replacement of the sinus segment, and routine open replacement of the arch under hypothermic circulatory arrest with retrograde cerebral perfusion with obliteration of false lumen at the distal arch/proximal descending thoracic aorta, thus reestablishing normal flow in the descending thoracic true lumen. From January 1993 to December 2004, 221 consecutive patients underwent repair of acute type A aortic dissection at our institution. Data were collected retrospectively and prospectively. Various types of malperfusion syndromes were present in 26.7% of patients. The organ systems with malperfusion were as follows: cardiac, 7.2%; cerebral, 7.2%; iliofemoral, 12.7%; renal, 4.1%; mesenteric, 1.4%; innominate, 5.4%; and spine, 2.2%. Results: Coronary malperfusion required coronary revascularization in 62.5% of cases. Distal revascularization was needed in 42.9% of patients with iliofemoral malperfusion. Patients with malperfusion were more likely to suffer perioperative myocardial infarction (p < 0.001), postoperative coma (p = 0.012), delirium (p = 0.011), sepsis (p = 0.006), acute renal failure (p = 0.017), dialysis (p = 0.018), and acute limb ischemia (p < 0.001). The in-hospital mortality was 30.5% in patients presenting with any malperfusion syndrome while only 6.2% in patients without malperfusion syndrome (p < 0.001). Both cardiac (p = 0.020) and cerebral malperfusions (p < 0.001) were risk factors for in-hospital mortality. The actuarial long-term survival in patients with malperfusion syndrome was estimated by Kaplan–Meier methods to be 67.8% ± 6.1% at 1 year, 54.0% ± 7.0% at 5 years, and 43.1% ± 8.0% at 10 years and for patient without malperfusion 82.7% ± 3.0% at 1 year, 66.3% ± 3.9% at 5 years, and 46.1% ± 6.7% at 10 years (log rank 2.55, p = 0.110). Cerebral malperfusion was a significant risk factor for decreased long-term survival (p = 0.0002). Conclusions: The occurrence of malperfusion in patients with acute type A dissection is associated with significant increased risk of in-hospital mortality and complications. Additional revascularization is generally needed in patients with coronary malperfusion and iliofemoral malperfusion. Patients presenting with cardiac and cerebral malperfusions have a high hospital mortality and preoperative cerebral malperfusion is associated with dismal long-term survival.

Key Words: Aortic dissection • Cerebral complications • Outcomes • Malperfusion


   1. Introduction
Top
 Abstract
 1. Introduction
2. Materials and methods
 3. Results
 4. Discussion
 Appendix A
 References
 
Acute type A dissection remains one of the most challenging diseases that the cardiothoracic surgeon faces. In the past, mortality without surgical treatment for aortic dissection was estimated to be 1–2% per hour with less than 10% surviving 3 days [1]. In a recent study the in-hospital mortality without operative management was 58% [2]. The in-hospital mortality following surgical treatment of type A aortic dissection ranges from 9 to 32.5% in published series [3–7]. Coronary malperfusion is associated with acute type A aortic dissection in 6.1–11.3% of cases and has high hospital mortality [8,9]. Distal malperfusion occurs in 25–31% cases of acute type A dissection [10,11], with significant hospital mortality, especially in patients with mesenteric malperfusion [11]. Since 1993, our group has established a uniform approach in the treatment of type A aortic dissection [12]. The primary goal of operative repair of type A aortic dissection is to prevent the four main causes of early death: ascending aortic rupture, coronary malperfusion, acute aortic valve insufficiency with associated myocardial dysfunction, and cerebral malperfusion with associated stroke or coma. Additional aims are to restore perfusion to all compromised systems and minimize complications. Successful surgical treatment involves immediate operative intervention with resection and replacement of the aortic tear site, repair or replacement of the aortic sinus segment to treat potential coronary malperfusion, resuspension or replacement of the aortic valve, obliteration of the distal false lumen, and reestablishment of flow in the true lumen. Cerebral protection strategy by our group includes uniform use of hypothermic circulatory arrest (HCA) and retrograde cerebral perfusion (RCP). Selective antegrade cerebral perfusion is used selectively when circulatory arrest time is expected to be excessive. We believe that by correcting the complex perfusion disturbance associated with the presence of proximal dissection flap, distal aortic branch malperfusion is alleviated and the need for additional procedures to revascularize malperfused organ systems potentially avoided. This report examines the incidence of malperfusion syndromes in patients presenting with acute type A aortic dissection undergoing contemporary surgical repair, and its effect on morbidity, hospital mortality, and long-term survival.


   2. Materials and methods
Top
 Abstract
 1. Introduction
 2. Materials and methods
3. Results
 4. Discussion
 Appendix A
 References
 
2.1 Patients
Patients were included if they had undergone surgical repair for acute type A aortic dissection in the years of 1993–2004 and operated by surgeons of the Complex Thoracic Aortic Disease Center at University of Pennsylvania. Patients had to have an open arch reconstruction with the use of hypothermic circulatory arrest and retrograde cerebral perfusion with or without selective antegrade perfusion. Otherwise, they were excluded from the study. Complete medical record had to be made available. A total of 244 consecutive patients underwent repair for acute type A aortic dissection. Twenty-three cases were excluded because HCA/RCP and open arch reconstruction were not used as part of operative strategy. Two hundred and twenty-one cases were included in the analysis.

2.2 Definitions
Aortic dissection was classified according to the Stanford system where type A dissection involves the ascending aorta. Acute dissection was defined by onset of symptoms within 14 days of operative treatment. Malperfusion syndromes were defined according to symptoms from each arterial system and required clinical evidence of lack of blood flow to defined organ system. That included: cerebral malperfusion – stroke; cardiac malperfusion – EKG changes, CK or troponin elevation – myocardial dysfunction; iliofemoral malperfusion – loss of pulses, sensory, or motor function; renal malperfusion – creatinine elevation, lack of urine output; innominate malperfusion – loss of pulses, sensory, or motor function; spinal malperfusion – paraplegia; mesenteric malperfusion – abdominal tenderness, bowel ischemia, elevation of liver function tests. Radiographic or surgical evidence of interruption of blood flow was also required either due to false lumen compression into ostium of the true lumen, extension of the dissection into branch vessel, or branch vessel disruption. Evidence of dissection flap in branch vessels, either surgically or radiographically without symptoms of malperfusion, was not considered as malperfusion syndrome.

2.3 Operative methods
Our standardized type A dissection algorithm was as follows: as soon as notification of a suspected type A aortic dissection is received, rapid transfer to the operating room is arranged. We do not delay operative intervention by obtaining coronary angiography. Occasionally, patients may have had cardiac catheterization outside institutions prior to our notification. Unilateral radial artery monitoring (left preferentially) is obtained with bilateral preferred if neuromonitoring is not available. Pulmonary artery catheter is placed prior to prepping and draping if the patient is hemodynamically stable or at any time during the procedure as feasible. Intraoperative transesophageal echocardiography (TEE) is obtained in all patients to confirm the diagnosis, look for any concomitant cardiac abnormalities, plan the proximal repair, and check the effectiveness of the root repair at the completion of the operation. Electroencephalographic (EEG) monitoring is obtained whenever possible (used in 120/221 (54.1%) of cases). Bilateral carotid artery flow is interrogated by duplex ultrasound in all patients at standardized times: induction of anesthesia (baseline); establishment of CPB; placement of ascending aortic cross-clamp; and resumption of antegrade CPB after completion of arch reconstruction. As soon as carotid artery malperfusion is detected, often correlated by EEG asymmetry if available, surgical maneuvers are carried out to reverse them: ascending/arch flap fenestration or revision of the arch reconstruction. Arterial access to establish cardiopulmonary bypass (CPB) is usually via the femoral 196/221 (88.7%) or the axillary artery 12/221 (5.4%), but in cases of severe malperfusions can be obtained via the dissected aortic arch 13/221 (5.9%) over a guide-wire directed into the true lumen by TEE. Venous cannulation is usually achieved with a standard right atrial double-stage cannula and a small right-angle single-stage superior vena cava cannula, unless concomitant cardiac abnormalities dictate the use of bicaval cannulation. As soon as satisfactory CPB is established and after the left ventricle is vented via the right superior pulmonary vein, core cooling is begun. Neuromonitored patients are cooled for 3 min beyond EEG silence. When EEG monitoring is not available, patients are cooled for 50 min or when nasopharyngeal temperature reaches 12 °C, whichever occurs first. Pharmacological adjuncts include methylprednisone, magnesium, lidocaine (to delay cardiac fibrillation), and aprotinin.

As soon as the heart fibrillates, a cross-clamp is placed across the distal ascending aorta, which is then transected at the level of the right pulmonary artery. Myocardial protection is achieved with a combination of intermittent antegrade and retrograde cold blood cardioplegia via the coronary ostia and the coronary sinus, respectively. Aortic valve (AV) resuspension is performed whenever feasible with aortic root repair consisting of Teflon felt ‘neo-media’ placed within the dissected portions of the sinuses and a Dacron graft sewn to the mobilized sino-tubular junction. When repair is not feasible, root replacement with a biological or mechanical valved conduit is performed. As soon as adequate cooling is achieved proximal reconstruction is stopped and focus is directed to the aortic arch. Hypothermic circulatory arrest is established with retrograde cerebral perfusion consisting of oxygenated blood at 10–12 °C infused into the snared superior vena cava cannula at a jugular venous pressure between 20 and 25 mmHg, usually at flows between 200 and 300 ml/min. All ascending aortic and most (rarely all) of the aortic arch tissues are excised. Residual dissected arch and/or proximal descending thoracic aortic tissue is reinforced with Teflon felt ‘neo-media’. When the arch reconstruction is felt to require more than 40–50 min, selective antegrade cerebral perfusion is utilized either via the axillary cannula or via balloon-tipped cannulae placed in the innominate and left common carotid arteries. The excised aortic arch is replaced with Dacron graft which is always directly cannulated to resume antegrade CPB. Proximal aortic reconstruction is then completed during rewarming. An ascending graft, or root replacement conduit-to-arch graft anastomosis completes the repair. Since 1999, small amounts of BioGlueTM have been used as anastomotic adjunct.

2.4 Follow-up
Mortality was assessed through medical records and the Social Security Death Index completed for 11/30/2006. Survival data were available for all but one patient. Survival follow-up was 904 patient years with mean follow-up of 49.1 months. Longest follow-up was 13.1 years.

2.5 Statistical analysis
The design was a retrospective observational study. Variables were collected though retrospective review of patient hospital charts and office notes, through phone calls, and by using prospectively collected STS data at the University of Pennsylvania. Variables are listed in Appendix A. The study was approved by the Investigational Review Board of University of Pennsylvania (#804788). Continuous variables were expressed as the mean ± SD and were compared with an unpaired two-tailed t-test. Categorical variables, expressed as percentage, were analyzed with a {chi} 2-test. Survival was analyzed with Kaplan–Meier actuarial method and compared with log-rank test. One year, 5 years, and 10 years are expressed as percentage ± SD.


   3. Results
Top
 Abstract
 1. Introduction
 2. Materials and methods
 3. Results
4. Discussion
 Appendix A
 References
 
Malperfusion occurred in 59 of 221 (26.7%) patients presenting with acute type A dissection. The incidence of each subtype is presented in Table 1 . Single malperfusion syndrome was present in 38 patients (64.4%): 16 (27.1%) had two, 3 (5.1%) had three, and 2 (3.4%) had four different malperfusion syndromes. The mean number of malperfusion syndromes was 1.47 per patient. The demographics and operative approach are shown in Table 2 . Malperfusion was associated with significant number of complications shown in Table 3 . Long-term survival, estimated by Kaplan–Meier method, was not different in patients with or without any malperfusion syndrome (Fig. 1 ).


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  		Table 1 Malperfusion syndromes in acute type A aortic dissection (n = 221)
 

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  		Table 2 Any malperfusion syndrome, demographics, presentation, and operative approach (n = 221)
 

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  		Table 3 Any malperfusion syndrome – morbidity (n = 216)
 

Figure 1
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  		Fig. 1. Kaplan–Meier estimate of long-term actuarial survival of patients with or without any malperfusion syndrome. One-year, 5-year, and 10-year survival for patients without malperfusion was 82.7% ± 3.0%, 66.3% ± 3.9%, and 46.1% ± 6.7%, respectively, compared to 67.8% ± 6.1%, 54.0% ± 7.0%, and 43.1% ± 8.0%, respectively, for patients with malperfusion.

 
Cardiac malperfusion was present in 16 patients (7.2%). Difference in presentation, operative approach, and outcome for this group of patients is presented in Table 4 . Six patients with cardiac malperfusion did not require CABG. In those cases the malperfusion was managed by local repair of either the root or coronary buttons. Seven patients without malperfusion required coronary revascularization. Three patients had preoperative coronary angiogram prior to diagnosis, demonstrating critical coronary atherosclerosis, and four had right coronary button torn off where the reconstruction was not felt to be adequate. As expected, postoperative myocardial infarction occurred commonly (p < 0.0001). Myocardial infarction occurred in only three cases (1.5%) without cardiac malperfusion. Hospital mortality was significantly higher in patients with cardiac malperfusion compared to patients without cardiac malperfusion. However, long-term mortality did not differ between these two groups estimated by Kaplan–Meier method (Fig. 2 ).


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  		Table 4 Cardiac malperfusion syndrome (n = 221)
 

Figure 2
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  		Fig. 2. Kaplan–Meier estimate of long-term actuarial survival of patients with or without cardiac malperfusion syndrome. 1-year, 5-year, and 10-year survival for patients without cardiac malperfusion was 80.0% ± 2.8%, 63.0% ± 3.6%, 47.2% ± 5.3%, respectively, compared to 68.8% ± 11.6%, 60.2% ± 12.9%, 36.1% ± 15.3%, respectively, for patients with cardiac malperfusion.

 
Cerebral malperfusion occurred in 16 patients (7.2%). Difference in presentation and outcome is presented in Table 5 . Cannulation strategy was not a determinant of neurological outcome. The long-term survival of patients with cerebral malperfusion was significantly worse (Fig. 3 ).


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  		Table 5 Cerebral malperfusion syndrome (n = 221)
 

Figure 3
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  		Fig. 3. Kaplan–Meier estimate of long-term actuarial survival of patients with or without cerebral malperfusion syndrome. 1-year, 5-year, and 10-year survival for patients without cerebral malperfusion was 81.5% ± 2.7%, 64.7% ± 3.6%, 49.1% ± 5.4%, respectively, compared to 50.0% ± 12.5%, 37.5% ± 12.1%, 12.5% ± 11.0%, respectively, for patients with cerebral malperfusion.

 
Iliofemoral malperfusion was the most common malperfusion syndrome and occurred in 28 cases (12.7%). None of the patients with iliofemoral malperfusion had preexisting peripheral vascular disease (PVD), while 10.4% of patients without iliofemoral malperfusion had history of PVD. We used contralateral femoral cannulation in 78.6% of iliofemoral malperfusion cases compared to 90.2% of cases without iliofemoral malperfusion. Twelve patients in the iliofemoral malperfusion group (42.9%) required additional operation to manage acute lower-extremity ischemia. Revascularization was performed by open conventional approach. Four required revascularization only, three required revascularization and fasciotomy, two revascularization and eventually amputation, two fasciotomy only, and one patient amputation only. Total of three patients (10.7%) had to undergo lower-extremity amputation. Cannulation was not a determinant of need for amputation. Hospital and long-term mortality was not significantly different between those two groups.

Nine patients presented with renal malperfusion. Only two developed postoperative renal failure; none of them required dialysis. One patient had open renal revascularization at the same time as proximal aortic repair. Innominate malperfusion occurred in 12 patients. No revascularization was required or complication associated with it. Mesenteric malperfusion occurred in three patients. One developed multiorgan failure and died shortly after surgery. The other two did well and were discharged without major complications. Spinal malperfusion was present in five patients. One patient died during hospital stay. Other four survived and were all discharged with paraplegia. Survival analysis in all these groups demonstrated no significant difference in short-term and long-term survival.


   4. Discussion
Top
 Abstract
 1. Introduction
 2. Materials and methods
 3. Results
 4. Discussion
Appendix A
 References
 
Acute type A dissection remains one of the most challenging diseases facing cardiothoracic surgeons and is associated with high mortality and morbidity. Short-term survival has improved over the years probably due to improved operative techniques, recognition of importance of immediate operative intervention, and improved anesthesia techniques and ICU care. We believe that rapid restoration of flow into true lumen and obliteration of the false lumen is the best way to treat malperfusion syndrome. Even though replacement of the ascending aorta and hemiarch repair does not always completely obliterate the false distal lumen, by correcting the complex perfusion disturbance, distal aortic branch malperfusion is alleviated and the need for additional procedures to revascularize malperfused organ systems potentially avoided. Recent analysis by the IRAD Investigators [13] revealed that certain preoperative and intraoperative factors are important predictors of surgical death following repair of type A aortic dissection. That includes age older than 70 years, pulse deficit, aortic rupture with preoperative hypotension, shock or cardiac tamponade, signs of acute myocardial ischemia or infarct, and intraoperative myocardial dysfunction. Surgical mortality in that study was 23.9%, which is markedly higher than in our series. They did not specifically address malperfusion syndromes which significantly complicate the management and outcome of these patients. In-hospital mortality for all our cases in this report was 12.7%, while the subgroup of patients with malperfusion had significantly higher in-hospital mortality of 30.5% compared to 6.2% in patients without malperfusion. The long-term mortality was not significantly different between the two subgroups. The presence of cardiac malperfusion, which by definition had to include EKG changes, enzyme elevation, and/or myocardial dysfunction, as well as evidence of dissection into coronaries, was associated with higher hospital mortality. Presence of cerebral malperfusion was also associated with worse short-term and long-term outcome. No particular preoperative factor predicted malperfusion syndromes, including Marfan syndrome, but chronic obstructive pulmonary disease (COPD) was associated with decreased risk of malperfusion. The reason for this is unclear but has also been described in other reports [10]. Presence of malperfusion was associated with significant postoperative complications including perioperative MI, coma, delirium, sepsis, acute renal failure, need for dialysis, acute limb ischemia, and multisystem organ failure.

Cardiac malperfusion was associated with increased need for root replacement and coronary revascularization, demonstrating the more extensive root involvement of the dissection in patients suffering cardiac malperfusion. We were successful in performing local repair of the root or coronary buttons in selective case and therefore able to avoid coronary bypass grafting. Postoperative myocardial infarction occurred in 64.3% of cardiac malperfusion cases but only 3.4% of cases without cardiac malperfusion. We generally do not perform planned preoperative angiography and these results support that approach, since clinically relevant coronary pathology in patients with acute type A dissection is due to malperfusion, but not primary coronary artery disease.

Cerebral malperfusion was associated with very high rates of postoperative stroke (46.7%). Importantly, as per definition, all patients with cerebral malperfusion presented with preoperative neurological deficit, so more than half of these patients recovered their neurological function following operative repair. There were never any attempts of additional cerebral revascularization. We assess the flow in the carotid arteries by using ultrasound after the patient is anesthetized, after initiation of CPB, after aortic cross-clamping, and following reestablishment of antegrade flow. We believe it to be essential to identify cerebral malperfusion that may occur intraoperatively, which can then be addressed by either acute fenestration into the arch or change in cannulation strategy. In terms of cerebral protection strategy, hypothermic circulatory arrest with retrograde cerebral perfusion is an essential part of the protocol. We have reported very favorable results in elective arch cases using that approach [14] and believe that it allows for uniform cerebral cooling, backflushing of air and debris resulting in reduced stroke risk. Short-term mortality in patients presenting with cerebral malperfusion was very high (50%) and the major reason for death was neurological. Incidence of stroke following cardiac surgery varies according to different cardiac procedures. Stroke rates following CABG are in the range of 1.5–5.2% [15,16] but much higher (8.2–8.7%) in aortic surgery [14,17]. The incidence of postoperative stroke for all patients in this series was 7.4%.

We did not have adequate data to allow us to determine if length of time from presentation to operative repair was a factor in incidence of postoperative stroke. Our approach is to rush patients to the operating room as soon as they arrive to the hospital. Majority of our cases are transfers from outside hospitals and we generally do not defer referral for critical neurological status. Some groups have advocated delay in surgical repair in patients with malperfusion syndromes [18]. We do not agree with that and believe the best way to treat malperfusion is to rapidly restore flow in the true lumen. This is supported by a recent study by Estrera et al. [19] where 80% of patients with cerebral malperfusion who underwent repair within 10 h experienced improvement in neurological status with very acceptable mortality. Long-term survival of the subgroup of patients with cerebral malperfusion is quite dismal with only 12.5% estimated survival at 10 years and is highly significant compared to patients without cerebral malperfusion (53.9%) (p = 0.0002).

As part of our cannulation strategy we favor the femoral approach. Only in the cases of clear malperfusion and pulse deficit to the lower extremities do we change to either axillary or ascending aortic cannulation. In the group of patients with iliofemoral malperfusion, 10.7% required amputation. This is a significantly high incidence. Cannulation strategy did not play a negative role in those cases according to our analysis. We did not have adequate data to determine whether time delay was a factor in worse outcome in that patient group. Mesenteric malperfusion was associated with 33.3% in-hospital mortality, but that did not reach statistical significance countering other reports [10]. Spinal malperfusion always resulted in permanent neurological damage and none of the paraplegia was affected by operative repair. However, due to small number of cases in these two groups it is difficult to draw definite conclusion regarding the clinical importance of mesenteric malperfusion or the reversibility of paraplegia. In particular, the clinical evidence of mesenteric malperfusion can be hard to detect or is diagnosed too late, and is probably a significant factor in some cases of death following multisystem organ failure. Other malperfusion syndromes were not associated with significant morbidity and mortality.

Limitations of this report include potential difficulties in establishing the true incidence of malperfusion syndromes since this is a retrospective case series. Many of the variables were collected prospectively as part of the STS Database collection at our institution, but symptoms of type A dissection and malperfusion are not included in the data collection. Also, we did not specifically collect and analyze data on patients without clinical symptoms of malperfusion but who had evidence of dissection flaps in end-organ vessels. We did not have adequate data to determine if timing and potential time delay were significant factors in worse outcome, specifically in respect to neurological outcome and the need for peripheral interventions. Our practice is immediate operative repair regardless of patient condition and time of the day. We do not delay operative intervention with additional preoperative workup including coronary and cerebral imaging once the patient has arrived at our institution. Although this is a case series the strength of the study is that we have developed standardized surgical techniques and perfusion strategy which result in homogenous cohort in term of operative approach. That may explain in part the favorable short-term outcome.

In conclusion we report the importance of malperfusion syndromes in management of patients following contemporary surgical approach for repair of acute type A aortic dissection. Rapid restoration of flow in the true lumen can alleviate malperfusion syndrome in all distal aortic branches. Proximal malperfusion generally requires root replacement and coronary bypass grafting and is associated with significant surgical mortality. Malperfusion is associated with multiple postoperative complications where postoperative neurological events are considerable and result in high in-hospital mortality. Cerebral malperfusion is associated with high in-hospital mortality and dismal long-term survival.


   Appendix A
Top
 Abstract
 1. Introduction
 2. Materials and methods
 3. Results
 4. Discussion
 Appendix A
References
 
Variables

Independent variables used were patient demographic variables including age; sex; hypertension; coronary artery disease; diabetes mellitus; peripheral vascular disease; chronic obstructive lung disease; chronic renal failure, prior history of stroke or transient ischemic attacks; bicuspid aortic valve; connective tissue disease (Marfans disease and Ehlers-Danlos disease); and prior cardiac operations (coronary artery bypass, aortic valve replacement, mitral valve operation, and other). Symptoms at presentation variables included acute chest pain; hypotension; loss of consciousness; preoperative cardiac arrest; hemopericardium; pericardial tamponade; malperfusion (overall, cardiac, cerebral, spinal, renal, mesenteric, iliofemoral, and innominate), and extent of dissection (DeBakey I and DeBakey II). Operative repair variables included type of proximal repair (aortic valve resuspension with ascending graft, aortic valve replacement with ascending graft, valve sparing root replacement with ascending graft, and composite root replacement (mechanical or biological)); distal arch repair (hemiarch or total arch replacement); use of BioGlueTM; use of felt neomedia; type of arterial cannulation (femoral artery, axillary artery, and ascending aorta); length of cardiopulmonary bypass; length of cross-clamp time; length of hypothermic circulatory arrest; length of RCP; and use of cerebral neuromonitoring, and resternotomy. Dependent outcome variables included postoperative complications (reoperation for bleeding, perioperative myocardial infarction, sternal wound infection, sepsis, cerebral complications (stroke, TIA, coma >24 h, delirium), acute renal failure, need for dialysis, more than 24 h on ventilator, pneumonia, acute limb ischemia, need for revascularization, multisystem organ failure, atrial fibrillation, and tracheostomy); overall mortality; intraoperative mortality; 30-day mortality; and in-hospital mortality.


   Acknowledgments
 
We appreciate the database management conducted by Katherine Cornelius and statistical analysis expertise contributed by Sonnad Seena.


   Footnotes
 
\#9734; Presented at the 55th Annual Meeting of the Scandinavian Association for Thoracic Surgery, Reykjavik, Iceland, August 16–19, 2006.


   References
Top
 Abstract
 1. Introduction
 2. Materials and methods
 3. Results
 4. Discussion
 Appendix A
 References
 

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