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Early and Midterm Outcomes Following Surgery for Acute Type A Aortic Dissection Sebastian Pagni, M.D., Brian L. Ganzel, M.D., Jaimin R. Trivedi, M.D., M.P.H., Ramesh Singh, M.D., Christopher E. Mascio, M.D., Erle H. Austin, M.D., Mark S. Slaughter, M.D., and Matthew L. Williams, M.D. Division of Thoracic and Cardiovascular Surgery, University of Louisville, Louisville, Kentucky ABSTRACT Objective: Surgical repair of acute Type A aortic dissection (AADA) is still associated with high inhospital mortality. We evaluated the impact of perioperative risk factors on early and midterm survival. Methods: Retrospective (2002–2011) database analysis at a single institution of 132 consecutive AADA patients (88 male, age 59.8 W 13.6). All but five patients underwent repair with open distal anastomoses and hypothermic circulatory arrest: aortic valve replacement/root replacement (n = 44, 33.3%) and valve re-suspension/repair (n = 88, 66.7%). Ascending aorta, hemi-arch, and total arch repairs were performed in 11, 113, and eight patients, respectively. Antegrade and retrograde cerebral perfusion were used in all but six patients. Results: Overall in-hospital mortality was 17.4% (n = 23). Actuarial survival at one, five, and eight years was 82%, 72%, and 62%, respectively. Perfusion time (cardiopulmonary bypass) (226.5 W 71.3 vs. 177.5 W 51.7, p = 0.0002), aortic cross-clamp time (min) (132.8 W 45.7 vs. 109.8 W 41.2, p = 0.01), aortic arch (T2) tear (31% vs. 14%, p = 0.03), instability (26% vs. 11%, p = 0.02), postoperative stroke (38% vs. 14%, p = 0.009), and low cardiac output (50% vs. 15%, p = 0.04) all correlated with increased perioperative mortality. A Cox proportional hazard model showed perfusion time (hazard ratio [HR] = 1.01), postoperative stroke (HR = 2.73), age (HR = 1.03), and unstability (HR = 1.8) as significant risk factors (p < 0.05) affecting the overall survival. Conclusion: There is a modern trend towards improving overall perioperative outcomes after surgical repair of AADA; however, early mortality and morbidity remain high even in aortic surgery referral centers. doi: 10.1111/jocs.12170 (J Card Surg 2013;28:543–549)
BACKGROUND Acute type A aortic dissection (AADA) is a surgical emergency still associated with high mortality and morbidity. Despite reports showing improved outcomes after early repair, both the perioperative and one-year mortality remain high, with a 30-day hospital mortality varying from 9% to 30%1–4 and with survival rates at five years varying from 50% to 80%.1–4 Hemodynamic status at presentation, various comorbidities, the use of different surgical strategies, and postoperative complications all have an undefined impact on early and late surgical mortality. In this study, we retrospectively reviewed 132 consecutive surgically treated patients with AADA in
Conflict of interest: The authors acknowledge no conflict of interest in the submission. Address for correspondence: Sebastian Pagni, M.D., Baptist Health, 3900 Kresge Way, Suite 46, Louisville, KY 40207. Fax: 502-899-3878; e-mail: [email protected]
the recent decade, with the aim to better define the risk factors impact early outcomes and overall survival. PATIENTS AND METHODS Patients Between January 2002 and December 2011, 132 consecutive patients (88 men, mean age 59.8 13.6 years) underwent emergent surgical repair for AADA at Jewish Hospital (University of Louisville), Louisville, Kentucky. Patient information in our database was retrospectively reviewed. Postoperative follow-up information was obtained by review of the hospital and office medical records and physician referral letters. The study was approved by the institutional review board at the University of Louisville. All patients were operated within 48 hours of an established diagnosis. The onset of symptoms varied from hours to several days (but within two weeks) before surgery. Patients with aortic intramural hematomas, chronic AADAs, and Type B dissections with
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known retrograde extension were excluded. Data from patients with AADA who were not surgical candidates, died before arrival to the surgical suite, or declined surgery were not included in the analysis. Patient characteristics are described in Table 1. Surgical technique All procedures consisted of a median sternotomy with the use of cardiopulmonary bypass (CPB). The femoral and right axillary arteries were more frequently used for arterial perfusion, and the right atrium and/or common femoral vein were used to establish venous drainage. Myocardial protection was obtained by selective coronary and retrograde cold blood cardioplegia. A left ventricular drain was placed through the right superior pulmonary vein to decompress the left ventricle and CPB was established with progressive systemic cooling to 15–20 8C. Once myocardial fibrillation occurred, we cross clamped the mid-ascending aorta, transected the aorta proximally to the clamp, and instilled cardioplegia into the coronary ostia. While cooling, we evaluated the aortic valve and started the root repair or replacement. At a core temperature below 20 8C, with an isoelectric electro encephalo gram (EEG) tracing and/or a cooling time greater than 45 minutes, we then placed the patient in Trendelenburg position and removed the aortic clamp. The distal ascending aorta and arch were examined to localize the location of the tear/s to decide the extent of arch replacement. We
TABLE 1 Patient Characteristics Variable Age Age > 65 years Gender—female Hypertension Diabetes mellitus Chronic lung disease Peripheral vascular disease Cerebrovascular disease EF (%) Stimulant drugs use Creatinine 1.4 Hemodynamic instability Shock/tamponade Malperfusion Coronary artery disease AI 2þ Connective tissue disorder Bicuspid valve Previous cardiac surgery Tear location T1 (ascending aorta) T2 (aortic arch) T2–3 (aortic arch extending to descending aorta) Acute coronary ischemia
Mean W SD or N (%) 59.8 13.6 51 (38.6%) 44 (33.3%) 106 (80%) 13 (9.9%) 23 (17.5%) 24 (18%) 13 (9.9%) 50.3 13.6 10 (7.4%) 33 (26.2%) 52 (39.4%) 20 (15%) 37 (28%) 18 (13.6%) 52 (39.4%) 10 (7.6%) 6 (4.5%) 10 (7.6%) 94 (71.3%) 32 (24.2%) 6 (4.5%) 8 (6%)
Cocaine and amphetamine. Limb ischemia, stroke, transient ischemic attack, visceral ischemia, and coronary ischemia.
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tried to avoid total arch replacements by using extended hemi-arch procedures or by plicating a distal tear when possible. The ascending aorta and/or arch with the tear was resected. Complete ascending aortic replacement with a beveled anastomosis or proximal hemi-arch replacements were typically used. We repaired or re-suspended the aortic valve when feasible, but we performed root replacements with valve conduits when it was deemed necessary. Surgical procedures are described in Table 2. The replacement technique always included replacement of the affected aorta with a Dacron (Vascutek, Terumo, Inc., Scotland, UK) tube graft. An outside Teflon strip was used for reinforcement in most cases and BioGlue (Cryolife, Inc., Kennesaw, GA, USA) was used to adhere the aortic layers and prepare the aortic cuffs for anastomosis, though two surgeons used the felt-Bioglue ‘‘neomedia’’ technique described by Bavaria et al.2 Five patients (3.8%) had closed distal anastomoses: three patients had localized (DeBakey type II) proximal
TABLE 2 Surgical Procedures and Operative Data Surgical Procedures
N (%)
Ascending aortic replacement Root repair Mechanical Biologic Proximal/hemi arch replacement Root repair Mechanical Biologic Total arch/elephant trunk replacement Root repair Mechanical Concomitant procedures CABG MVR VAD/ECMO Intra-aortic balloon pump C-section Atrial septal defect Aorto-right atrial fistula Subclavian artery bypass Operative data Cannulation site Femoral artery Axillary artery Aortic arch CPB time (min) X-C time (min) HCA time (min) Cerebral perfusion Antegrade axillary Retrograde jugular Both None
11 (8.3%) 5 3 3 113 (85.6%) 77 26 10 8 (6.1%) 6 2 25 (19%) 14 2 2 2 1 2 1 1 N (%) or Mean W SD 82 (62.1%) 42 (34.8%) 3 (2.3%) 186.4 58.6 113.9 42.9 34.1 16.7 50 75 4 3
(39.7%) (59.5%) (3%) (2.3%)
VAD, ventricular assist device; ECMO, extracorporeal membrane oxygenator; CPB, cardiopulmonary bypass; X-C, crossclamp; CABG, coronary artery bypass graft; HCA, hypothermic circulatory arrest. Re-suspension.
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dissection, and two were a prohibitive risk for hypothermic circulatory arrest (HCA). Cerebral protection was established by the use of antegrade cerebral perfusion (ACP) (n ¼ 50, 37.9%), retrograde (n ¼ 75, 56.8%), or both (n ¼ 4). We routinely used a multimodality neuro-monitoring protocol with a 12-channel EEG, cerebral Doppler flow, and transcutaneous O2 cerebral saturations and the technique is described elsewhere.5 In addition, we routinely gave methylprednisolone (1 g) IV and phosphofenitoin (500–800 mg) on anesthetic induction. Operative data are described in Table 2. Follow-up Outcome data were obtained retrospectively by review of hospital and office records, letters from referring physicians, and notification of readmission to hospitals. Typically, we followed local patients yearly with an office visit and a chest CT. For non-local patients, we relied upon referring physicians notes and radiologic and echocardiograpic reports. Follow-up for death was obtained by chart death certificates, notification of death by referring doctors and relatives, and by the Social Security Death Index. Statistical analysis Demographics, preoperative risk factors, and perioperative clinical variables were collected through cardiac surgery database and retrospective chart review. In-hospital/30-day mortality was the primary end-point of the study. Secondary end-points were major complications during the index hospitalization. Various risk factors and operative factors were analyzed as predictors of primary and secondary end-points using univariate statistical methods. Kaplan–Meier curve and Cox proportional hazard model were computed to analyze mid-term (five to eight years) survival. SAS statistical software (SAS, Inc., Cary, NC, USA) was used for all the analyses. RESULTS Demographics can be found in Table 1. Patients were predominantly male and hypertensive. Surgical procedures performed and operative data are summarized in Table 2. In-hospital and 30-day mortality was 17.4% (n ¼ 23). Mortality rate at three and 12 months was 18.3% (n ¼ 24) and 19% (n ¼ 25), respectively. Intraoperative death occurred in four (3%) patients (right ventricular failure in three and rupture with exsanguinations in one). Cause of death was predominantly cardiac (n ¼ 8) and neurologic (n ¼ 8) (Table 3). Major complications occurred in 58.3% (n ¼ 77) of patients. Mortality and morbidity data are summarized in Table 3. Hospital length of stay was 16.3 12.3 days and intensive care unit (ICU) stay was 8.6 7.1 days. Pulmonary complications (including ventilator time 48 hours) occurred in 90 (68%) patients, with a need for tracheostomy in only four. Neurologic complications occurred in 32 patients (24.2%): stroke (n ¼ 18)
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TABLE 3 Postoperative Outcomes Outcomes In-hospital mortality Mortality: cardiac causes Mortality: neurologic causes Mortality: multisystem organ failure Mortality: other Total ICU (hours) Length of stay (days) Vent time (hours) Discharge—home Major complications Low cardiac output Stroke Transient neurologic deficit (TND) Prolong vent (>48 hours) Renal failure—hemodialysis Reoperation for bleeding/effusion Atrial arrhythmias Other surgical intervention
N (%) or Mean W SD 23 (17.4%) 8 8 5 2 207 173.25 (158) 16.3 12.3 (13) 149.2 159.9 (89) 66 (60.5%) 77 (58.3%) 8 (6%) 18 (13.6%) 14 (10.6%) 89 (67.4%) 17 (12.9%) 21 (15.9%) 38 (28.8%) 19 (14.4%)
Median duration.
was primarily fatal in eight and present in another patient with fatal multisystem organ failure (MOF). Transient neurologic disorder (TND) was present in 14 patients (10.6%). Discharge to rehabilitation center, nursing home, or nursing skilled facility was required in 39.5% (n ¼ 43) of patients due to clinical or socioeconomic need. Twentyone (16%) patients required reoperation for bleeding or tamponade, and three patients required a pacemaker. Other procedures for complications included: exploratory laparotomy (n ¼ 3), lower extremity (LE) amputation (n ¼ 1), removal of ventricular assist device (VAD) (n ¼ 2), LE fasciotomy (n ¼ 3), LE revascularization (n ¼ 2), intra aortic balloon pump (IABP) (n ¼ 2), and right ventricular assist device (RVAD) (n ¼ 2). Ventilation greater than 72 hours correlated with increased risk of major complications (71% vs. 40%, p < 0.05) and the presence of malperfusion resulted in a significant risk of renal insufficiency requiring hemodialysis (29% vs. 9%, p ¼ 0.008). Univariate analysis (Table 4) showed a significantly higher in-hospital mortality in patients with prolonged CPB (226.5 minutes vs. 177.5 minutes, p ¼ 0.0002), prolonged cross-clamp (132.8 minutes vs. 109.8 minutes, p ¼ 0.01) and HCA times (39.6 minutes vs. 33.1 minutes, p ¼ 0.09). The site of arterial perfusion was not significantly associated with perioperative mortality (femoral vs. axillary, 13% vs. 23%, p ¼ 0.2). Individually, high-risk perioperative variables such as shock/tamponade, malperfusion, myocardial ischemia, renal insufficiency, and age did not correlate with early mortality but did increase the risk of major morbidity. Patients unstable at presentation (shock, tamponade, malperfusion, coronary ischemia, and/or neurologic deficit) fare worst with an early mortality of 32% vs. 12.5% in the more stable group, p < 0.05). Permanent postoperative stroke (38% vs. 14%, p ¼ 0.009) and low
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TABLE 4 Univariate Factors Associated With In-Hospital Mortality Variable Age Perfusion time Cross-clamp time Creatinine Shock Circ arrest time Arch tear Low cardiac output Postoperative stroke
Dead
Alive
P-Value
60.5 15.8 226.0 71.3 132.8 45.7 1.3 0.5 6 (30%) 39.6 25.1 10 (31.2%) 4 (50%) 7 (38%)
59.6 13.1 177.5 51.7 109.8 41.2 1.2 0.6 17 (15.2%) 33.1 14.1 13 (14.1%) 4 (15%) 16 (15%)
0.7 0.0002 0.01 0.4 0.1 0.09 0.03 0.04 0.009
TABLE 5 Cox Proportional Hazard Model for Overall Survival Risk Factor Malperfusion Perfusion time Cardiogenic shock Stroke permanent Age
N (%) or Mean W SD
P-Value
Hazard Ratio
24 (18.1%) 186.4 58.6 20 (15.1%) 18 (13.6%) 59.8 13.6
0.1681 0.0004 0.0269 0.0098 0.0357
1.671 1.009 2.332 2.738 1.031
cardiac output (50% vs. 15%, p ¼ 0.04) and location of the tear in the arch (T2) versus a proximal location (31% vs. 14%, p ¼ 0.003) (10/32) all correlated significantly with higher early mortality. At a mean follow-up of 4.0 0.2 years, the multivariate analysis using Cox proportional hazards model showed age, permanent stroke, perfusion time,
and shock/tamponade to correlate significantly with decreased survival (Table 5). Overall actuarial survival (Fig. 1) at one, five, and eight years was 82%, 72%, and 62%, respectively. Survival stratified by hemodynamic stability versus instability at one, five, and eight years was 85% versus 75%, 78% versus 50%, and 75% versus 45% (p ¼ 0.01), respectively (Fig. 2).
Figure 1. Actuarial survival.
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Figure 2. Actuarial survival stratified by hemodynamic instability at presentation. Hemodynamic instability (HDMI) defined as presence of cardiac arrest, cardiogenic shock, or hypotension (tamponade, malperfusion, myocardial infarction, aortic insufficiency, acute ventricular dysfunction) requiring volume and pressers to keep the systolic pressure above 90 mmHg. HDMI 0 (solid line), no instability; HDMI 1 (dotted line), hemodynamic instability.
Re-intervention at the operative site beyond three months (aortic insufficiency, re-dilatation, or false aneurysm) occurred in six patients (5.7%) and surgery in the descending thoracic aorta was necessary in four (3.6%). DISCUSSION Early postoperative outcomes after treatment of AADA remain suboptimal, with a mortality rate up to 30%.4,6–8 Over the last decade, some centers have shown a decrease in the 30-day hospital mortality to 10–20% and even lower.1,3,9–11 Improved perioperative management and surgical techniques allow patients nowadays to survive major complications and to convalesce in nursing homes or skilled nursing facilities, but often with less than optimal quality of life. Early mortality (between 3 and 12 months) is likely related to the impact of the initial surgery and its complications, but is seldom described in detail even in major studies. As we began our study, we speculated that the mortality within the first 3 months and even up to 12 months of surgery might make our low initial perioperative mortality rate a hollow victory and expected a significant early (one to six months) ongoing attrition rate among our repaired aortic dissection patients. However, the period prior to hospital discharge appeared to contain the vast majority of the ‘‘early risk’’ after surgery. This is consistent with longterm data from the International Registry of Acute
Aortic Dissection (IRAD) database and it is encouraging that a durable survival can be achieved in patients who survived hospital discharge. Risk assessment in AADA is difficult. Most published studies to date are from single centers with a small number of patients that have a total event rate that precludes valid multivariable modeling for short-term outcomes. Even the few larger studies of AADA have a difficult time summarizing the perioperative risk due to the complexity of presentation in this disease (e.g., the various forms of malperfusion that are possible). Despite these difficulties, the analysis by Trimarchi et al.12 on behalf of the IRAD reported an overall inhospital mortality of 25.1% in a cohort of 526 patients at 18 participating centers and made it clear the risk in unstable patients is markedly increased. The IRAD investigators reported mortality in unstable patients (shock, stroke, myocardial ischemia, renal-mesenteric ischemia, and other malperfusion) of 31.4% versus 16.7% in the stable group. Recently, Conzelmann et al.13 reported the experience of the German Registry of AADA, with a mortality of 16.9% and a neurologic morbidity of 20.3% in a cohort of 2137 patients, but the proportion of unstable patients was not reported. A survey from Goda et al.14 from the Japanese Association for Thoracic Surgery in 2007 reported an overall mortality of 10.9% after proximal aortic replacement for AADA, and 14.5% after total arch replacement. The difference of these results when compared to the ones in Western centers is remarkable and not clearly
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understood, especially when a higher proportion of full arch replacements were present in Japanese patients. But perhaps these differences are related to selection criteria, different patient population or even the surgical approach to AADA. Our approach to AADA repair has been prompt surgical repair whenever feasible. We routinely transfer patients directly to the operative suite from outside hospitals. We seldom perform coronary angiography, but five patients (3.8%) underwent this study due to a misdiagnosis of acute coronary syndrome or iatrogenic dissection during a diagnostic cath. Preoperative malperfusion and stroke are not contraindications for early surgery, unless the patient is moribund or coma is present. Although likely small, we do not know the number of patients who did not undergo surgery because they either declined surgery or surgery was not offered or expired in transit to the hospital or the operating room. Coma, visceral malperfusion with multiorgan failure, both concomitant to advanced age or to a reoperative status, were reasons not to offer surgery in a few patients. We concur with others that AADA repair is a life-saving complex operation and the main goal should be hospital survival and avoidance of major cardiac and neurologic morbidity.1,15 We believe in the ‘‘tear resection’’ concept limiting the extent of aortic resection to accomplish that goal. In addition, restoration of aortic valve competence and the use of an open distal anastomosis to assure quality and avoid bleeding as well as aortic arch inspection to avoid missing secondary tears are the key to complete a more successful repair. We routinely use biologic glue to construct a neo-media and liberally use Teflon material to reinforce the suture lines. We try whenever possible to avoid more complex operations such as root replacement or total arch replacement, as the overarching goal is patient survival rather than a perfect technical result. Despite this outlook, we are at times forced to perform these more complex operations. We have reserved the use of total arch replacement chiefly
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for large arch tears that could not be reconstructed primarily. Root replacement with a valved conduit was indicated when the intimal tear involved the coronary ostia, or when the patient had severe aortic valvular disease or severe aortic root enlargement. We decreased the CPB times by clamping the mid-ascending aorta while systemically cooling and often repairing the root before HCA is initiated. We used femoral cannulation almost exclusively until 2006 but now favor axillary cannulation with ACP unless faced with a salvage situation. Due to its complexity, we have not used aortic valve sparing procedures for AADA in this series, but some groups are now utilizing them with encouraging results.16 We approached patients with malperfusion using axillary cannulation. Prior to 2006, detected malperfusion was treated by changing cannulas from the femoral to the axillary artery and ascending aorta in a few patients. We have not performed concomitant aortic endografting or distal fenestrations in this series. Our mortality of 17% compares well to centers in North America and Europe with high surgical volume and an interest in aortic surgery (Table 6).13,17 Our mortality rate in unstable patients was 27%, similar to others, pointing to the importance of preoperative treatment with stabilization and early intervention. Our operative mortality on stable patients of 12% supports that approach. However, the rate of major complications seen was still high. Contrary to our initial suspicion, our mortality rates at three and six months were low (18.3% and 19%), even in patients discharged to nursing homes and skilled nursing facilities. The survival curve declined slowly but steadily up to five years after surgery, likely due to the competing illness as well as dissection-related problems in the remaining aorta. Poor compliance to anti-hypertensive treatment, low socio-economic status and access to health care are likely factors that affect survival as well. Like any retrospective review on AADA surgical patients, this study has many limitations. It is a relatively small cohort of unselected patients and the
TABLE 6 Outcomes After AADA Repair: Contemporary Series
Refs.
Year
No. of Patients
30-Day Mortality (%)
David et al.15 Tan et al.8 Westaby et al.1 Bavaria et al.2 Trimarchi et al.12 (IRAD) Kazui et al.10 Nakajima et al.16 Goda et al.14 Estrera et al.9 Chavanon et al.11 Santini et al.4 Conzelmann et al.13 (GERAADA) Pagni et al. (this study)
1999 2001 2002 2002 2005 2002 2007 2010 2010 2007 2007 2012 2012
109 252 95 163 526 130 100 301 281 217 311 2137 132
15 25 6.3 9.8 25.1 19.2 9 13.6 16 19.8 23 16.9 17.4
1-Year Survival (%) 85
80 89
82
Unstable (%) 13.8 21 2.1 15 53.5 40 NS 27 25 38.9 51 NS 39.4
NS—not specified for shock, tamponade, malperfusion, and coronary ischemia altogether as unstable group.
Mortality Unstable Patients (%) NS 39.5 NS NS 31.4 NS NS 39 NS 31 NS 26.9
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denominator of patients that declined or were not offered surgery is unknown. Our technique has evolved over the study period (i.e., cannulation site, root replacement type, surgical skill, cerebral perfusion, etc.) and it is also affected by the different surgeons involved. In addition, the number of deaths was small, therefore, decreasing the power for risk factor analysis. Lastly, because AADA is relatively uncommon in small and medium volume cardiac centers, this may reflect the practice pattern of more active aortic referral centers only. In summary, these results and the ones from multicenter studies show the encouraging trend toward improving early mortality in the surgical treatment of AADA over the last decade. Additionally, it appears that if patients can ‘‘make it’’ to hospital discharge, their ongoing risk of death over the next few years is relatively low. Despite the trend of improving outcomes, seen in centers with experience and an interest in aortic surgery, early mortality and morbidity still remain high after surgery. ‘‘Real world’’ crude data from surgical databases in the United States are needed to further elucidate results after surgical treatment of AADA and to better define the impact of perioperative factors on outcome.
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7.
8.
9.
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11.
12.
13.
REFERENCES 1. Westaby S, Saito S, Katsumata T: Acute type A dissection: Conservative methods provide consistently low mortality. Ann Thorac Surg 2002;73(3):707–713. 2. Bavaria JE, Brinster DR, Gorman RC, et al: Advances in the treatment of acute type A dissection: An integrated approach. Ann Thorac Surg 2002;74(5):S1848–S1852, discussion S1857–S1863. 3. Kawahito K, Adachi H, Yamaguchi A, et al: Preoperative risk factors for hospital mortality in acute type A aortic dissection. Ann Thorac Surg 2001;71(4):1239–1243. 4. Santini F, Montalbano G, Casali G, et al: Clinical presentation is the main predictor of in-hospital death for patients with acute type A aortic dissection admitted for surgical treatment: A 25 years experience. Int J Cardiol 2007;115(3):305–311. 5. Ganzel BL, Edmonds HL, Jr, Pank JR, et al: Neurophysiologic monitoring to assure delivery of retrograde cerebral
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perfusion. J Thorac Cardiovasc Surg 1997;113(4):748– 755, discussion 755–757. Apaydin AZ, Buket S, Posacioglu H, et al: Perioperative risk factors for mortality in patients with acute type A aortic dissection. Ann Thorac Surg 2002;74(6):2034– 2039, discussion 2039. Khaladj N, Shrestha M, Peterss S, et al: Ascending aortic cannulation in acute aortic dissection type A: The Hannover experience. Eur J Cardiothorac Surg 2008;34(4):792– 796, disussion 796. Tan ME, Kelder JC, Morshuis WJ, et al: Risk stratification in acute type A dissection: Proposition for a new scoring system. Ann Thorac Surg 2001;72(6):2065–2069. Estrera AL, Miller CC, Kaneko T, et al: Outcomes of acute type A aortic dissection after previous cardiac surgery. Ann Thorac Surg 2010;89(5):1467–1474. Kazui T, Washiyama N, Bashar AH, et al: Surgical outcome of acute type A aortic dissection: Analysis of risk factors. Ann Thorac Surg 2002;74(1):75–81, discussion 81–82. Chavanon O, Costache V, Bach V, et al: Preoperative predictive factors for mortality in acute type A aortic dissection: An institutional report on 217 consecutives cases. Interact Cardiovasc Thorac Surg 2007;6(1):43–46. Trimarchi S, Nienaber CA, Rampoldi V, et al: Contemporary results of surgery in acute type A aortic dissection: The International Registry of Acute Aortic Dissection experience. J Thorac Cardiovasc Surg 2005;129(1):112– 122. Conzelmann LO, Hoffmann I, Blettner M, et al: Analysis of risk factors for neurological dysfunction in patients with acute aortic dissection type A: Data from the German Registry for Acute Aortic Dissection Type A (GERAADA). Eur J Cardiothorac Surg 2012;42(3):557–565. Goda M, Imoto K, Suzuki S, et al: Risk analysis for hospital mortality in patients with acute type A aortic dissection. Ann Thorac Surg 2010;90(4):1246–1250. David TE, Armstrong S, Ivanov J, et al: Surgery for acute type A aortic dissection. Ann Thorac Surg 1999;67 (6):1999–2001, discussion 2014–2019. Nakajima T, Kawazoe K, Kataoka T, et al: Midterm results of aortic repair using a fabric neomedia and fibrin glue for type A acute aortic dissection. Ann Thorac Surg 2007;83 (5):1615–1620. Tsagakis K, Pacini D, Di Bartolomeo R, et al: Multicenter early experience with extended aortic repair in acute aortic dissection: Is simultaneous descending stent grafting justified? J Thorac Cardiovasc Surg 2010;140(6 Suppl.): S116–S120, discussion S142–S146.
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Early and Midterm Outcomes Following Surgery for Acute Type A Aortic Dissection Sebastian Pagni, M.D., Brian L. Ganzel, M.D., Jaimin R. Trivedi, M.D., M.P.H., Ramesh Singh, M.D., Christopher E. Mascio, M.D., Erle H. Austin, M.D., Mark S. Slaughter, M.D., and Matthew L. Williams, M.D. Division of Thoracic and Cardiovascular Surgery, University of Louisville, Louisville, Kentucky ABSTRACT Objective: Surgical repair of acute Type A aortic dissection (AADA) is still associated with high inhospital mortality. We evaluated the impact of perioperative risk factors on early and midterm survival. Methods: Retrospective (2002–2011) database analysis at a single institution of 132 consecutive AADA patients (88 male, age 59.8 W 13.6). All but five patients underwent repair with open distal anastomoses and hypothermic circulatory arrest: aortic valve replacement/root replacement (n = 44, 33.3%) and valve re-suspension/repair (n = 88, 66.7%). Ascending aorta, hemi-arch, and total arch repairs were performed in 11, 113, and eight patients, respectively. Antegrade and retrograde cerebral perfusion were used in all but six patients. Results: Overall in-hospital mortality was 17.4% (n = 23). Actuarial survival at one, five, and eight years was 82%, 72%, and 62%, respectively. Perfusion time (cardiopulmonary bypass) (226.5 W 71.3 vs. 177.5 W 51.7, p = 0.0002), aortic cross-clamp time (min) (132.8 W 45.7 vs. 109.8 W 41.2, p = 0.01), aortic arch (T2) tear (31% vs. 14%, p = 0.03), instability (26% vs. 11%, p = 0.02), postoperative stroke (38% vs. 14%, p = 0.009), and low cardiac output (50% vs. 15%, p = 0.04) all correlated with increased perioperative mortality. A Cox proportional hazard model showed perfusion time (hazard ratio [HR] = 1.01), postoperative stroke (HR = 2.73), age (HR = 1.03), and unstability (HR = 1.8) as significant risk factors (p < 0.05) affecting the overall survival. Conclusion: There is a modern trend towards improving overall perioperative outcomes after surgical repair of AADA; however, early mortality and morbidity remain high even in aortic surgery referral centers. doi: 10.1111/jocs.12170 (J Card Surg 2013;28:543–549)
BACKGROUND Acute type A aortic dissection (AADA) is a surgical emergency still associated with high mortality and morbidity. Despite reports showing improved outcomes after early repair, both the perioperative and one-year mortality remain high, with a 30-day hospital mortality varying from 9% to 30%1–4 and with survival rates at five years varying from 50% to 80%.1–4 Hemodynamic status at presentation, various comorbidities, the use of different surgical strategies, and postoperative complications all have an undefined impact on early and late surgical mortality. In this study, we retrospectively reviewed 132 consecutive surgically treated patients with AADA in
Conflict of interest: The authors acknowledge no conflict of interest in the submission. Address for correspondence: Sebastian Pagni, M.D., Baptist Health, 3900 Kresge Way, Suite 46, Louisville, KY 40207. Fax: 502-899-3878; e-mail: [email protected]
the recent decade, with the aim to better define the risk factors impact early outcomes and overall survival. PATIENTS AND METHODS Patients Between January 2002 and December 2011, 132 consecutive patients (88 men, mean age 59.8 13.6 years) underwent emergent surgical repair for AADA at Jewish Hospital (University of Louisville), Louisville, Kentucky. Patient information in our database was retrospectively reviewed. Postoperative follow-up information was obtained by review of the hospital and office medical records and physician referral letters. The study was approved by the institutional review board at the University of Louisville. All patients were operated within 48 hours of an established diagnosis. The onset of symptoms varied from hours to several days (but within two weeks) before surgery. Patients with aortic intramural hematomas, chronic AADAs, and Type B dissections with
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known retrograde extension were excluded. Data from patients with AADA who were not surgical candidates, died before arrival to the surgical suite, or declined surgery were not included in the analysis. Patient characteristics are described in Table 1. Surgical technique All procedures consisted of a median sternotomy with the use of cardiopulmonary bypass (CPB). The femoral and right axillary arteries were more frequently used for arterial perfusion, and the right atrium and/or common femoral vein were used to establish venous drainage. Myocardial protection was obtained by selective coronary and retrograde cold blood cardioplegia. A left ventricular drain was placed through the right superior pulmonary vein to decompress the left ventricle and CPB was established with progressive systemic cooling to 15–20 8C. Once myocardial fibrillation occurred, we cross clamped the mid-ascending aorta, transected the aorta proximally to the clamp, and instilled cardioplegia into the coronary ostia. While cooling, we evaluated the aortic valve and started the root repair or replacement. At a core temperature below 20 8C, with an isoelectric electro encephalo gram (EEG) tracing and/or a cooling time greater than 45 minutes, we then placed the patient in Trendelenburg position and removed the aortic clamp. The distal ascending aorta and arch were examined to localize the location of the tear/s to decide the extent of arch replacement. We
TABLE 1 Patient Characteristics Variable Age Age > 65 years Gender—female Hypertension Diabetes mellitus Chronic lung disease Peripheral vascular disease Cerebrovascular disease EF (%) Stimulant drugs use Creatinine 1.4 Hemodynamic instability Shock/tamponade Malperfusion Coronary artery disease AI 2þ Connective tissue disorder Bicuspid valve Previous cardiac surgery Tear location T1 (ascending aorta) T2 (aortic arch) T2–3 (aortic arch extending to descending aorta) Acute coronary ischemia
Mean W SD or N (%) 59.8 13.6 51 (38.6%) 44 (33.3%) 106 (80%) 13 (9.9%) 23 (17.5%) 24 (18%) 13 (9.9%) 50.3 13.6 10 (7.4%) 33 (26.2%) 52 (39.4%) 20 (15%) 37 (28%) 18 (13.6%) 52 (39.4%) 10 (7.6%) 6 (4.5%) 10 (7.6%) 94 (71.3%) 32 (24.2%) 6 (4.5%) 8 (6%)
Cocaine and amphetamine. Limb ischemia, stroke, transient ischemic attack, visceral ischemia, and coronary ischemia.
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tried to avoid total arch replacements by using extended hemi-arch procedures or by plicating a distal tear when possible. The ascending aorta and/or arch with the tear was resected. Complete ascending aortic replacement with a beveled anastomosis or proximal hemi-arch replacements were typically used. We repaired or re-suspended the aortic valve when feasible, but we performed root replacements with valve conduits when it was deemed necessary. Surgical procedures are described in Table 2. The replacement technique always included replacement of the affected aorta with a Dacron (Vascutek, Terumo, Inc., Scotland, UK) tube graft. An outside Teflon strip was used for reinforcement in most cases and BioGlue (Cryolife, Inc., Kennesaw, GA, USA) was used to adhere the aortic layers and prepare the aortic cuffs for anastomosis, though two surgeons used the felt-Bioglue ‘‘neomedia’’ technique described by Bavaria et al.2 Five patients (3.8%) had closed distal anastomoses: three patients had localized (DeBakey type II) proximal
TABLE 2 Surgical Procedures and Operative Data Surgical Procedures
N (%)
Ascending aortic replacement Root repair Mechanical Biologic Proximal/hemi arch replacement Root repair Mechanical Biologic Total arch/elephant trunk replacement Root repair Mechanical Concomitant procedures CABG MVR VAD/ECMO Intra-aortic balloon pump C-section Atrial septal defect Aorto-right atrial fistula Subclavian artery bypass Operative data Cannulation site Femoral artery Axillary artery Aortic arch CPB time (min) X-C time (min) HCA time (min) Cerebral perfusion Antegrade axillary Retrograde jugular Both None
11 (8.3%) 5 3 3 113 (85.6%) 77 26 10 8 (6.1%) 6 2 25 (19%) 14 2 2 2 1 2 1 1 N (%) or Mean W SD 82 (62.1%) 42 (34.8%) 3 (2.3%) 186.4 58.6 113.9 42.9 34.1 16.7 50 75 4 3
(39.7%) (59.5%) (3%) (2.3%)
VAD, ventricular assist device; ECMO, extracorporeal membrane oxygenator; CPB, cardiopulmonary bypass; X-C, crossclamp; CABG, coronary artery bypass graft; HCA, hypothermic circulatory arrest. Re-suspension.
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dissection, and two were a prohibitive risk for hypothermic circulatory arrest (HCA). Cerebral protection was established by the use of antegrade cerebral perfusion (ACP) (n ¼ 50, 37.9%), retrograde (n ¼ 75, 56.8%), or both (n ¼ 4). We routinely used a multimodality neuro-monitoring protocol with a 12-channel EEG, cerebral Doppler flow, and transcutaneous O2 cerebral saturations and the technique is described elsewhere.5 In addition, we routinely gave methylprednisolone (1 g) IV and phosphofenitoin (500–800 mg) on anesthetic induction. Operative data are described in Table 2. Follow-up Outcome data were obtained retrospectively by review of hospital and office records, letters from referring physicians, and notification of readmission to hospitals. Typically, we followed local patients yearly with an office visit and a chest CT. For non-local patients, we relied upon referring physicians notes and radiologic and echocardiograpic reports. Follow-up for death was obtained by chart death certificates, notification of death by referring doctors and relatives, and by the Social Security Death Index. Statistical analysis Demographics, preoperative risk factors, and perioperative clinical variables were collected through cardiac surgery database and retrospective chart review. In-hospital/30-day mortality was the primary end-point of the study. Secondary end-points were major complications during the index hospitalization. Various risk factors and operative factors were analyzed as predictors of primary and secondary end-points using univariate statistical methods. Kaplan–Meier curve and Cox proportional hazard model were computed to analyze mid-term (five to eight years) survival. SAS statistical software (SAS, Inc., Cary, NC, USA) was used for all the analyses. RESULTS Demographics can be found in Table 1. Patients were predominantly male and hypertensive. Surgical procedures performed and operative data are summarized in Table 2. In-hospital and 30-day mortality was 17.4% (n ¼ 23). Mortality rate at three and 12 months was 18.3% (n ¼ 24) and 19% (n ¼ 25), respectively. Intraoperative death occurred in four (3%) patients (right ventricular failure in three and rupture with exsanguinations in one). Cause of death was predominantly cardiac (n ¼ 8) and neurologic (n ¼ 8) (Table 3). Major complications occurred in 58.3% (n ¼ 77) of patients. Mortality and morbidity data are summarized in Table 3. Hospital length of stay was 16.3 12.3 days and intensive care unit (ICU) stay was 8.6 7.1 days. Pulmonary complications (including ventilator time 48 hours) occurred in 90 (68%) patients, with a need for tracheostomy in only four. Neurologic complications occurred in 32 patients (24.2%): stroke (n ¼ 18)
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TABLE 3 Postoperative Outcomes Outcomes In-hospital mortality Mortality: cardiac causes Mortality: neurologic causes Mortality: multisystem organ failure Mortality: other Total ICU (hours) Length of stay (days) Vent time (hours) Discharge—home Major complications Low cardiac output Stroke Transient neurologic deficit (TND) Prolong vent (>48 hours) Renal failure—hemodialysis Reoperation for bleeding/effusion Atrial arrhythmias Other surgical intervention
N (%) or Mean W SD 23 (17.4%) 8 8 5 2 207 173.25 (158) 16.3 12.3 (13) 149.2 159.9 (89) 66 (60.5%) 77 (58.3%) 8 (6%) 18 (13.6%) 14 (10.6%) 89 (67.4%) 17 (12.9%) 21 (15.9%) 38 (28.8%) 19 (14.4%)
Median duration.
was primarily fatal in eight and present in another patient with fatal multisystem organ failure (MOF). Transient neurologic disorder (TND) was present in 14 patients (10.6%). Discharge to rehabilitation center, nursing home, or nursing skilled facility was required in 39.5% (n ¼ 43) of patients due to clinical or socioeconomic need. Twentyone (16%) patients required reoperation for bleeding or tamponade, and three patients required a pacemaker. Other procedures for complications included: exploratory laparotomy (n ¼ 3), lower extremity (LE) amputation (n ¼ 1), removal of ventricular assist device (VAD) (n ¼ 2), LE fasciotomy (n ¼ 3), LE revascularization (n ¼ 2), intra aortic balloon pump (IABP) (n ¼ 2), and right ventricular assist device (RVAD) (n ¼ 2). Ventilation greater than 72 hours correlated with increased risk of major complications (71% vs. 40%, p < 0.05) and the presence of malperfusion resulted in a significant risk of renal insufficiency requiring hemodialysis (29% vs. 9%, p ¼ 0.008). Univariate analysis (Table 4) showed a significantly higher in-hospital mortality in patients with prolonged CPB (226.5 minutes vs. 177.5 minutes, p ¼ 0.0002), prolonged cross-clamp (132.8 minutes vs. 109.8 minutes, p ¼ 0.01) and HCA times (39.6 minutes vs. 33.1 minutes, p ¼ 0.09). The site of arterial perfusion was not significantly associated with perioperative mortality (femoral vs. axillary, 13% vs. 23%, p ¼ 0.2). Individually, high-risk perioperative variables such as shock/tamponade, malperfusion, myocardial ischemia, renal insufficiency, and age did not correlate with early mortality but did increase the risk of major morbidity. Patients unstable at presentation (shock, tamponade, malperfusion, coronary ischemia, and/or neurologic deficit) fare worst with an early mortality of 32% vs. 12.5% in the more stable group, p < 0.05). Permanent postoperative stroke (38% vs. 14%, p ¼ 0.009) and low
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TABLE 4 Univariate Factors Associated With In-Hospital Mortality Variable Age Perfusion time Cross-clamp time Creatinine Shock Circ arrest time Arch tear Low cardiac output Postoperative stroke
Dead
Alive
P-Value
60.5 15.8 226.0 71.3 132.8 45.7 1.3 0.5 6 (30%) 39.6 25.1 10 (31.2%) 4 (50%) 7 (38%)
59.6 13.1 177.5 51.7 109.8 41.2 1.2 0.6 17 (15.2%) 33.1 14.1 13 (14.1%) 4 (15%) 16 (15%)
0.7 0.0002 0.01 0.4 0.1 0.09 0.03 0.04 0.009
TABLE 5 Cox Proportional Hazard Model for Overall Survival Risk Factor Malperfusion Perfusion time Cardiogenic shock Stroke permanent Age
N (%) or Mean W SD
P-Value
Hazard Ratio
24 (18.1%) 186.4 58.6 20 (15.1%) 18 (13.6%) 59.8 13.6
0.1681 0.0004 0.0269 0.0098 0.0357
1.671 1.009 2.332 2.738 1.031
cardiac output (50% vs. 15%, p ¼ 0.04) and location of the tear in the arch (T2) versus a proximal location (31% vs. 14%, p ¼ 0.003) (10/32) all correlated significantly with higher early mortality. At a mean follow-up of 4.0 0.2 years, the multivariate analysis using Cox proportional hazards model showed age, permanent stroke, perfusion time,
and shock/tamponade to correlate significantly with decreased survival (Table 5). Overall actuarial survival (Fig. 1) at one, five, and eight years was 82%, 72%, and 62%, respectively. Survival stratified by hemodynamic stability versus instability at one, five, and eight years was 85% versus 75%, 78% versus 50%, and 75% versus 45% (p ¼ 0.01), respectively (Fig. 2).
Figure 1. Actuarial survival.
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Figure 2. Actuarial survival stratified by hemodynamic instability at presentation. Hemodynamic instability (HDMI) defined as presence of cardiac arrest, cardiogenic shock, or hypotension (tamponade, malperfusion, myocardial infarction, aortic insufficiency, acute ventricular dysfunction) requiring volume and pressers to keep the systolic pressure above 90 mmHg. HDMI 0 (solid line), no instability; HDMI 1 (dotted line), hemodynamic instability.
Re-intervention at the operative site beyond three months (aortic insufficiency, re-dilatation, or false aneurysm) occurred in six patients (5.7%) and surgery in the descending thoracic aorta was necessary in four (3.6%). DISCUSSION Early postoperative outcomes after treatment of AADA remain suboptimal, with a mortality rate up to 30%.4,6–8 Over the last decade, some centers have shown a decrease in the 30-day hospital mortality to 10–20% and even lower.1,3,9–11 Improved perioperative management and surgical techniques allow patients nowadays to survive major complications and to convalesce in nursing homes or skilled nursing facilities, but often with less than optimal quality of life. Early mortality (between 3 and 12 months) is likely related to the impact of the initial surgery and its complications, but is seldom described in detail even in major studies. As we began our study, we speculated that the mortality within the first 3 months and even up to 12 months of surgery might make our low initial perioperative mortality rate a hollow victory and expected a significant early (one to six months) ongoing attrition rate among our repaired aortic dissection patients. However, the period prior to hospital discharge appeared to contain the vast majority of the ‘‘early risk’’ after surgery. This is consistent with longterm data from the International Registry of Acute
Aortic Dissection (IRAD) database and it is encouraging that a durable survival can be achieved in patients who survived hospital discharge. Risk assessment in AADA is difficult. Most published studies to date are from single centers with a small number of patients that have a total event rate that precludes valid multivariable modeling for short-term outcomes. Even the few larger studies of AADA have a difficult time summarizing the perioperative risk due to the complexity of presentation in this disease (e.g., the various forms of malperfusion that are possible). Despite these difficulties, the analysis by Trimarchi et al.12 on behalf of the IRAD reported an overall inhospital mortality of 25.1% in a cohort of 526 patients at 18 participating centers and made it clear the risk in unstable patients is markedly increased. The IRAD investigators reported mortality in unstable patients (shock, stroke, myocardial ischemia, renal-mesenteric ischemia, and other malperfusion) of 31.4% versus 16.7% in the stable group. Recently, Conzelmann et al.13 reported the experience of the German Registry of AADA, with a mortality of 16.9% and a neurologic morbidity of 20.3% in a cohort of 2137 patients, but the proportion of unstable patients was not reported. A survey from Goda et al.14 from the Japanese Association for Thoracic Surgery in 2007 reported an overall mortality of 10.9% after proximal aortic replacement for AADA, and 14.5% after total arch replacement. The difference of these results when compared to the ones in Western centers is remarkable and not clearly
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understood, especially when a higher proportion of full arch replacements were present in Japanese patients. But perhaps these differences are related to selection criteria, different patient population or even the surgical approach to AADA. Our approach to AADA repair has been prompt surgical repair whenever feasible. We routinely transfer patients directly to the operative suite from outside hospitals. We seldom perform coronary angiography, but five patients (3.8%) underwent this study due to a misdiagnosis of acute coronary syndrome or iatrogenic dissection during a diagnostic cath. Preoperative malperfusion and stroke are not contraindications for early surgery, unless the patient is moribund or coma is present. Although likely small, we do not know the number of patients who did not undergo surgery because they either declined surgery or surgery was not offered or expired in transit to the hospital or the operating room. Coma, visceral malperfusion with multiorgan failure, both concomitant to advanced age or to a reoperative status, were reasons not to offer surgery in a few patients. We concur with others that AADA repair is a life-saving complex operation and the main goal should be hospital survival and avoidance of major cardiac and neurologic morbidity.1,15 We believe in the ‘‘tear resection’’ concept limiting the extent of aortic resection to accomplish that goal. In addition, restoration of aortic valve competence and the use of an open distal anastomosis to assure quality and avoid bleeding as well as aortic arch inspection to avoid missing secondary tears are the key to complete a more successful repair. We routinely use biologic glue to construct a neo-media and liberally use Teflon material to reinforce the suture lines. We try whenever possible to avoid more complex operations such as root replacement or total arch replacement, as the overarching goal is patient survival rather than a perfect technical result. Despite this outlook, we are at times forced to perform these more complex operations. We have reserved the use of total arch replacement chiefly
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for large arch tears that could not be reconstructed primarily. Root replacement with a valved conduit was indicated when the intimal tear involved the coronary ostia, or when the patient had severe aortic valvular disease or severe aortic root enlargement. We decreased the CPB times by clamping the mid-ascending aorta while systemically cooling and often repairing the root before HCA is initiated. We used femoral cannulation almost exclusively until 2006 but now favor axillary cannulation with ACP unless faced with a salvage situation. Due to its complexity, we have not used aortic valve sparing procedures for AADA in this series, but some groups are now utilizing them with encouraging results.16 We approached patients with malperfusion using axillary cannulation. Prior to 2006, detected malperfusion was treated by changing cannulas from the femoral to the axillary artery and ascending aorta in a few patients. We have not performed concomitant aortic endografting or distal fenestrations in this series. Our mortality of 17% compares well to centers in North America and Europe with high surgical volume and an interest in aortic surgery (Table 6).13,17 Our mortality rate in unstable patients was 27%, similar to others, pointing to the importance of preoperative treatment with stabilization and early intervention. Our operative mortality on stable patients of 12% supports that approach. However, the rate of major complications seen was still high. Contrary to our initial suspicion, our mortality rates at three and six months were low (18.3% and 19%), even in patients discharged to nursing homes and skilled nursing facilities. The survival curve declined slowly but steadily up to five years after surgery, likely due to the competing illness as well as dissection-related problems in the remaining aorta. Poor compliance to anti-hypertensive treatment, low socio-economic status and access to health care are likely factors that affect survival as well. Like any retrospective review on AADA surgical patients, this study has many limitations. It is a relatively small cohort of unselected patients and the
TABLE 6 Outcomes After AADA Repair: Contemporary Series
Refs.
Year
No. of Patients
30-Day Mortality (%)
David et al.15 Tan et al.8 Westaby et al.1 Bavaria et al.2 Trimarchi et al.12 (IRAD) Kazui et al.10 Nakajima et al.16 Goda et al.14 Estrera et al.9 Chavanon et al.11 Santini et al.4 Conzelmann et al.13 (GERAADA) Pagni et al. (this study)
1999 2001 2002 2002 2005 2002 2007 2010 2010 2007 2007 2012 2012
109 252 95 163 526 130 100 301 281 217 311 2137 132
15 25 6.3 9.8 25.1 19.2 9 13.6 16 19.8 23 16.9 17.4
1-Year Survival (%) 85
80 89
82
Unstable (%) 13.8 21 2.1 15 53.5 40 NS 27 25 38.9 51 NS 39.4
NS—not specified for shock, tamponade, malperfusion, and coronary ischemia altogether as unstable group.
Mortality Unstable Patients (%) NS 39.5 NS NS 31.4 NS NS 39 NS 31 NS 26.9
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denominator of patients that declined or were not offered surgery is unknown. Our technique has evolved over the study period (i.e., cannulation site, root replacement type, surgical skill, cerebral perfusion, etc.) and it is also affected by the different surgeons involved. In addition, the number of deaths was small, therefore, decreasing the power for risk factor analysis. Lastly, because AADA is relatively uncommon in small and medium volume cardiac centers, this may reflect the practice pattern of more active aortic referral centers only. In summary, these results and the ones from multicenter studies show the encouraging trend toward improving early mortality in the surgical treatment of AADA over the last decade. Additionally, it appears that if patients can ‘‘make it’’ to hospital discharge, their ongoing risk of death over the next few years is relatively low. Despite the trend of improving outcomes, seen in centers with experience and an interest in aortic surgery, early mortality and morbidity still remain high after surgery. ‘‘Real world’’ crude data from surgical databases in the United States are needed to further elucidate results after surgical treatment of AADA and to better define the impact of perioperative factors on outcome.
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