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Operation for acute and chronic aortic dissection: recent outcome with regard to neurologic deficit and early death
Operation for Acute and Chronic Aortic Dissection: Recent Outcome With Regard to Neurologic Deficit and Early Death Hazim J. Safi, MD, Charles C. Miller III, PhD, Michael J. Reardon, MD, Dimitrios C. Iliopoulos, MD, George V. Letsou, MD, Rafael Espada, MD, and John C. Baldwin, MD Department of Surgery, The Methodist Hospital and Baylor College of Medicine, Houston, Texas
Background. We reviewed our experience in the repair of acute and chronic aortic dissection with regard to early neurologic deficit and death. Methods. Between February 1991 and June 1996, we performed 206 operations on 195 patients for aortic dissection. Ascending or arch repair, or a combination (type A dissection) was performed on 92 of 206 patients (45%); 44 of 92 (48%) were acute dissection and 48 of 92 (52%) were chronic. Descending or thoracoabdominal repair (type B dissection) was performed on 114 of 206 patients (55%); 22 of 114 (19%) were acute and 92 of 114 (81%) were chronic. Results. Among type A cases, strokes occurred in 6 of 92 patients (7%) overall; 4 of 44 (9%) were acute cases and 2 of 48 (4%) were chronic (p < 0.34). Early deaths for type A were 11 of 92 (12%) overall; 9 of 44 (20%) acute and 2 of 48 (4%) chronic (p < 0.02). In type B cases, neurologic complications were 15 of 114 (13%) overall; 7 of 22 (32%)
were acute cases and 8 of 92 (9%) were chronic (p < 0.004). Early deaths for type B were 12 of 114 (11%) overall; 3 of 22 (14%) acute and 9 of 92 (10%) chronic (p < 0.6). Preoperative hypotension was significant in acute type A patients, with strokes in 2 of 7 (29%) hypotensives compared with 2 of 37 (5%) normotensives (p < 0.05) and early death in 4 of 7 (57%) hypotensives versus 5 of 37 (14%) normotensives (p < 0.009). Conclusions. Morbidity and mortality for repair of chronic dissection types A and B were acceptable. Preoperative hypotension in acute type A dissection was a major predisposing factor toward stroke (29% versus 5%, p < 0.05). Acute type B dissection had acceptable mortality (14%) but a high rate of neurologic complications (32%).
I
Material and Methods
n the frequent catastrophic cascade of events immediately after an aortic dissection, patient survival relies on rapid diagnosis and early therapeutic intervention [1-3]. The patient is at the greatest risk in the acute phase, within 14 days of the initial dissection, when complications brought on by hemorrhage or rupture are most likely. The decision to manage surgically or medically depends on the time elapsed since onset, the dissection location, and urgency of presentation. Most often the treatment of type A, which originates in the ascending aorta, is surgical. Type B, in the descending thoracic aorta, is more often treated medically in the acute stage and surgically in the chronic stage. In this study we examined the results of our operative treatment of aortic dissection during the past 5 years, with particular attention to the differences in morbidity and mortality between acute and chronic aortic dissection patients.
Presented at the Forty-fourth Annual Meeting of the Southern Thoracic Surgical Association, Naples, FL, Nov 6 – 8, 1997. Address reprint requests to Dr Safi, 6550 Fannin, Suite 1603, Houston, TX 77030.
© 1998 by The Society of Thoracic Surgeons Published by Elsevier Science Inc
(Ann Thorac Surg 1998;66:402–11) © 1998 by The Society of Thoracic Surgeons
Patient Population Between February 1991 and June 1996, 206 operations were performed on 195 patients by one surgeon (H.J.S.). Patient characteristics are as follows for the 92 type A patients: acute dissection, 44 (48%); stroke, 6 (7%); 30-day mortality, 11 (12%); hypotensive crisis (systolic blood pressure ,60 mm Hg or moribund presentation, ie, cardiopulmonary arrest, pulseless, or in shock), 7 (8%); cerebrovascular disease (stroke, transient ischemic attack, or atheroocclusive disease of the carotid arteries), 12 (13%); heart disease (aortic valve disease, atheroocclusive disease of the coronary arteries, or cardiomyopathy), 20 (22%); previous aortic operation, 32 (35%); hypertension, 56 (61%); current smoker, 22 (24%); and for the 114 type B patients: acute dissection, 22 (19%); neurologic deficit (paraplegia or paraparesis), 15 (13%); 30-day mortality, 12 (11%); renal insufficiency, 13 (11%); heart disease, 28 (25%); previous proximal aortic operation, 28 (25%); hypertension, 91 (80%); and current smoker, 41 (28%). The selected risk factors for stroke in type A dissection and for spinal cord neurologic deficit in type B are shown in Table 1. Men comprised more than two-thirds of all 0003-4975/98/$19.00 PII S0003-4975(98)00533-5
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patients. Patients were divided roughly in half between operation for repair of the ascending aorta (type A dissection) and repair of the descending thoracic or thoracoabdominal aorta (type B dissection). A greater number of type A repairs, however, took place in the acute phase (44 of 92 or 48%) compared with type B repairs (22 of 114 or 19%) (p , 0.001). Age did not differ significantly between these two groups. Six of 92 (7%) of the type A repairs were in patients with Marfan’s syndrome, as were 7 of 114 (6%) of type B repairs. Twentyfive of 92 type A patients (27%) underwent the first stage of aortic repair with the elephant trunk technique; 1 had an acute dissection, the remainder had chronic dissections. Twelve of 24 patients had completed the second half of this two-stage repair at the time of this study. The specific operations performed for the 92 type A patients were as follows: aortic valve and ascending aorta, 9 (10%); aortic valve, ascending aorta and arch, 16 (17%); ascending aorta, 20 (22%); ascending aorta and proximal arch, 9 (10%); ascending aorta and transverse arch, 11 (12%); transverse arch, 2 (2%); elephant trunk, stage 1, 25 (27%); and for the 114 type B patients: elephant trunk, stage 2, 12 (11%); descending thoracic aorta, type A, 1 (0.8%); descending thoracic aorta, types A, B, 9 (8%); descending thoracic aorta, types A, B, C, 16 (14%); thoracoabdominal aortic aneurysm, type I, 29 (25%); thoracoabdominal aortic aneurysm, type II, 42 (37%); thoracoabdominal aortic aneurysm, type III, 4 (4%); and abdominal aorta, 1 (0.8%). Among acute type A patients, 7 were hypotensive, with preoperative cardiopulmonary arrest in 4 patients and blood pressure below 60 mm Hg in 3. In September 1992, we abandoned the simple cross-clamp technique in favor of the adjuncts of distal aortic perfusion and cerebrospinal fluid drainage, which was consequently used in 73 of 114 type B patients (64%). Similarly, retrograde cerebral perfusion, in addition to hypothermic circulatory arrest, was added to the surgical protocol for ascending and arch patients in February 1994 for 77 of 92 type A patients (84%).
Statistical Methods Univariate categoric data were analyzed by contingency table methods. Continuous variables were divided into quartiles for contingency table analysis, and were also analyzed as continuous by univariate logistic regression. The p values were computed using x2 statistics for contingency tables, and odds ratios were computed for dichotomous variables. Confidence intervals for contingency table odds ratios are test based. Multivariate analysis was conducted by multiple logistic regression. The p values for logistic regression analyses were computed by maximum-likelihood methods. All calculations were performed using SAS software version 6.12 (SAS Institute, Inc, Cary, NC).
Patient Selection and Operative Methods Our protocol for treating acute aortic dissection depends on the patient presentation. If a patient had a moribund presentation to the emergency department he or she was sent directly to the operating room for anesthesia induc-
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tion and transesophageal echocardiography to identify the site and extent of the intimal disruption. A patient who presented with acute symptoms, but was not moribund, was admitted to the surgical intensive care unit where he or she was evaluated with transesophageal echocardiography and prepared for operation as soon as possible. After transfer to the operating room, median sternotomy was performed and the patient was placed on cardiopulmonary bypass and the systemic temperature cooled for profound hypothermia. Cannulation was femoral–femoral for cardiopulmonary bypass, and to the superior vena cava for retrograde cerebral perfusion. Myocardial protection was provided throughout the procedure by cardioplegic perfusion through the coronary sinus, keeping the myocardial temperature less than 15°C. Venting through the left superior pulmonary vein or artery prevented ventricular distention and allowed optimal decompression of the left ventricle. When the electroencephalogram was isoelectric and the nasopharyngeal temperature reached approximately 12°C, the pump was stopped, and retrograde cerebral perfusion was begun through the superior vena cava. The rate of pump flow did not exceed 500 mL/min and the pressure did not exceed 25 mm Hg. The ascending aorta was inspected for the site and extent of the tear, the involvement of the transverse arch, and assessment of intimal disruption requiring repair. The ascending aorta was opened longitudinally and then transected just proximal to the innominate artery. Provided the transverse arch was free of reentry, we sutured the intima and adventitia together with fine 4-0 and 5-0 polypropylene suture (Fig 1A). A gelatin woven Dacron graft was sutured to the reinforced proximal aortic arch in end-toend fashion, and reinforced from both inside and outside with 4-0 pledgeted sutures (Figs 1B, 1C). When the distal anastomosis was completed, retrograde cerebral perfusion was stopped and cardiopulmonary bypass restarted through the femoral artery to evacuate all air and debris from the brachiocephalic vessels. The graft was clamped proximal to the origin of the innominate artery. Flow to the cerebral and systemic circulation was restored and the head of the table was elevated. On rare occasions when the brachiocephalic arterial flow was not adequate, as manifested by low radial artery pressure and due to a dissecting flap, we cannulated the ascending aortic graft and delivered flow to the head in antegrade fashion. The patient was rewarmed with restoration of antegrade flow. If the aortic valve was morphologically normal and the root without dilatation, we resuspended the aortic valve with 4-0 polypropylene pledgeted sutures. The intima and adventitia of the supracoronary aorta were sutured together using 4-0 polypropylene sutures, and reinforced with 4-0 pledgeted suture, usually from inside the graft (Figs 1D, 1E). A composite valve graft was selected if the valve and root were dilated. The coronary arteries were reattached by button technique or modified Cabrol in
ACUTE TYPE A DISSECTION.
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Table 1. Selected Risk Factors No. of Patients (%)
No. With Event (%)
10 (22.7) 11 (25.0) 12 (27.3) 11 (25.0)
1 (10.0) 2 (18.2) 0 (0.0) 1 (9.1)
Female Male
12 (27.3) 32 (72.7)
1 (8.3) 3 (9.4)
0.88 1
0.08 –9.38
0.92
Current smokers Nonsmokers
9 (20.5) 35 (79.5)
0 (0.0) 4 (11.4)
0.37
0.02–7.49
0.29
Hypertensive Normotensive
24 (54.6) 20 (45.4)
0 (0.0) 4 (20.0)
0.08 1
0.01–1.49
0.03
Hypotensive crisis Otherwise
7 (15.9) 37 (84.1)
2 (28.6) 2 (5.4)
7.00 1
0.80 – 61.46
0.051
12 (27.3) 11 (25.0) 10 (22.7) 11 (25.0)
1 (8.3) 0 (0.0) 1 (10.0) 2 (18.2)
0.53
12 (25.0) 11 (22.9) 12 (25.0) 13 (27.1)
0 (0.0) 0 (0.0) 1 (8.3) 1 (7.7)
0.59
Female Male
10 (20.8) 38 (79.2)
1 (10.0) 3 (2.6)
4.11 1
0.23–72.21
0.29
Current smokers Nonsmokers
13 (27.1) 35 (72.9)
1 (7.7) 4 (2.9)
2.83
0.16 – 48.93
0.46
Hypertensive Normotensive
32 (66.7) 16 (33.3)
2 (6.3) 4 (0.0)
2.71 1
0.12–59.74
0.31
12 (25.0) 12 (25.0) 12 (25.0) 12 (25.0)
0 (0.0) 1 (8.3) 0 (0.0) 1 (8.3)
0.56
4 (18.2) 7 (31.8) 5 (22.7) 6 (27.3)
2 (50.0) 2 (28.6) 3 (60.0) 0 (0.0)
0.15
TAAAI Otherwise
5 (22.7) 17 (77.3)
1 (20.0) 6 (35.3)
0.458 1
0.04 –5.08
0.52
TAAAII Otherwise
6 (27.3) 16 (72.7)
4 (66.7) 3 (18.8)
8.67 1
1.05–71.59
0.04
TAAAIII Otherwise
1 (4.6) 21 (95.4)
1 (100.0) 6 (28.6)
7.15 1
0.26 –199.7
0.14
Descending Otherwise
10 (45.5) 12 (54.5)
1 (10.0) 6 (50.0)
0.11
0.01–1.17
0.07
Variable Acute type A dissection: stroke Age 8 –58 59 – 67 68 –72 73– 88
Pump time (min) 74 –96 97–127 128 –195 196 – 461 Chronic type A dissection: stroke Age 8 –58 59 – 67 68 –72 73– 88
Pump time (min) 21–116 117–150 151–191 192– 408 Acute type B dissection: spinal cord neurologic deficit Age 8 –58 59 – 67 68 –72 73– 88
Odds Ratioa
95% CIb
p Valuec
0.51
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Table 1. Continued No. of Patients (%)
No. With Event (%)
Odds Ratioa
Female Male
9 (40.9) 13 (59.1)
1 (11.1) 6 (46.2)
0.15 1
0.01–1.52
0.09
Current smokers Nonsmokers
12 (54.6) 10 (45.4)
3 (25.0) 4 (40.0)
0.50
0.08 –3.08
0.46
Hypertensive Otherwise
16 (72.7) 6 (27.3)
6 (37.5) 1 (16.7)
3.00 1
0.28 –32.21
0.36
7 (31.8) 5 (22.7) 5 (22.7) 5 (22.7)
3 (42.8) 1 (20.0) 2 (40.0) 1 (20.0)
0.19
32 (34.8) 19 (20.7) 19 (20.7) 22 (23.9)
4 (12.5) 0 (0.0) 1 (5.3) 3 (13.6)
0.34
TAAA, type I Otherwise
27 (29.4) 65 (70.7)
1 (3.7) 7 (10.8)
0.32 1
0.04 –2.72
0.27
TAAA, type II Otherwise
43 (46.7) 49 (53.3)
7 (16.3) 1 (2.0)
9.33 1
1.10 –79.28
0.02
TAAA, type III Otherwise
4 (4.4) 88 (95.7)
0 (0.0) 8 (9.1)
1.05 1
0.05–21.26
0.53
TAAA, type IV Otherwise
1 (1.1) 91 (98.9)
0 (0.0) 8 (8.8)
3.28 1
0.12– 86.8
0.76
Descending Otherwise
18 (19.6) 74 (80.4)
0 (0.0) 8 (10.8)
0.21
0.01–3.84
0.14
Female Male
17 (18.5) 75 (81.5)
2 (11.8) 6 (8.0)
1.53 1
0.28 – 8.35
0.62
Current smokers Nonsmokers
29 (31.5) 63 (68.5)
4 (13.8) 4 (6.4)
2.36
0.55–10.19
0.24
Hypertensive Otherwise
75 (81.5) 17 (18.5)
6 (8.0) 2 (11.8)
0.65 1
0.12–3.55
0.62
Pump time (min) 15– 42 43–57 58 –76 77–196
23 (25.0) 21 (22.8) 23 (25.0) 25 (27.2)
2 (8.7) 1 (4.8) 2 (8.7) 3 (12.0)
Variable
Pump time (min) 27– 45 46 – 63 64 – 87 88 –169 Chronic type B dissection: spinal cord neurologic deficit Age 28 – 47 48 –59 60 – 66 67– 81
a
Common odds ratio computed by the contingency table method. probability of a type 1 statistical error for the comparison.
b
95% CIb
Ninety-five percent confidence interval for the odds ratio.
p Valuec
0.86
c
Nominal x2
TAAA 5 thoracoabdominal aortic aneurysm.
which a 12-mm Dacron tube graft from the composite valve/graft prosthesis was attached to the left main coronary artery. The right coronary artery orifice was either attached directly to the graft or connected by a length of Dacron tube or saphenous vein (Fig 2). In 2 patients, the coronary orifices were involved in the dissection and the coronary arteries were ligated and reversed saphenous vein grafts were used for bypass from the composite graft to the left anterior descending, the
circumflex, and the right coronary arteries. Finally, the sump was terminated, the heart filled to aspirate the heart chamber from air and debris, and the patient weaned from cardiopulmonary bypass. For patients in whom dissection involved the transverse aortic arch, either the proximal arch or the total arch was replaced. In total arch replacements the brachiocephalic arteries were preserved as an island and reattached to the graft as previously described [4]. The
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Fig 1. (A) The intima and adventitia are sutured together. (B, C) Reinforcement of graft and aortic arch with pledgeted sutures. (D, E) Pledgeted reinforcement of supracoronary intima and adventitia.
elephant trunk technique [5] was used in 1 of 44 (2%) acute dissection patients in which the dissection extended into the descending thoracic aorta. CHRONIC TYPE A DISSECTION. Chronic type A dissection was treated in the same manner as ascending/arch aortic aneurysm [4]. Graft replacement is the treatment of choice, and the main indications for operation for chronic type A dissection were aortic size or presence of symptoms. The operation was performed with or without aortic valve and root replacement as required (Figs 3A, 3B). The elephant trunk technique was used in 24 of 48 (50%) chronic dissection patients in which the dissection extended into the descending thoracic aorta.
ACUTE TYPE B DISSECTION. Operations for acute type B dissection were performed selectively, and only when complications of the dissection arose. The indications were persistent pain, aneurysmal dilatation ($5 cm), endorgan (kidney, bowel) or limb ischemia, or evidence of retrograde dissection to the ascending aorta. Patients who did not meet these criteria were treated with aggressive medical therapy, which included immediate admission to the intensive care unit, urgent pharmacologic blood pressure control, complete intensive care unit monitoring, and immediate imaging studies. If pain was controlled and aortic expansion beyond 5 cm was not present, patients were weaned from intravenous antihypertensives and converted to oral antihypertensive ther-
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Fig 2. Composite valve graft with modified Cabrol reattachment of left coronary artery.
apy. Chest radiographs were obtained daily and computed tomographic scans weekly during hospitalization. Stable patients were discharged after 14 days. Patients
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were urged at follow-up to undergo quarterly computed tomographic scans in the first year, semiannual scans in the next 2 years, and thereafter to undergo annual scans. Any change in symptoms or aortic diameter were considered indications for surgical reevaluation. Operative technique for acute dissection of the descending thoracic or thoracoabdominal aorta was not unlike the techniques previously described for aneurysms occurring in this portion of the aorta [6]. The proximal descending thoracic aorta distal to the left subclavian was transected completely and lifted off the esophagus. Both proximal and distal intima and adventitia of the transected aorta were reinforced in the same manner as that for the ascending aorta with a 4-0 polypropylene suture. A gelatin woven Dacron graft was sewn directly to the reinforced acutely dissected proximal thoracic aorta with the posterior row reinforced using interrupted polypropylene sutures. The descending thoracic graft was cut to length and sutured to the reinforced distal aorta, rechanneling blood into the true lumen of the distal aorta. The adjuncts of cerebrospinal fluid drainage and distal aortic perfusion were used in all patients after 1992 [6]. When most of the descending and abdominal aorta required replacement (type II thoracoabdominal aortic aneurysm), we opened the entire thoracoabdominal
Fig 3. Chronic type A dissection; completed valve and graft replacement using the elephant trunk technique.
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Fig 4. Chronic type B dissection; completed graft replacement with intercostal artery reattachment.
aorta, excised the septum between the false and true lumen, and reattached the visceral vessels and renal arteries to the graft either directly or using a woven Dacron graft. We ligated all the intercostal and lumbar arteries because the friable tissue was likely to lead to catastrophic bleeding and a fatal outcome. Chronic type B aortic dissection was treated in the same manner as descending thoracic or thoracoabdominal aortic aneurysm [6]. In patients with chronic dissection, we preferred to reimplant intercostal arteries T-9 through T-12 [7] using either a sidearm
CHRONIC TYPE B DISSECTION.
graft or a side hole to which we reattached the arteries directly (Figs 4A, 4B).
Results Type A Dissection The overall incidence of stroke in ascending and arch or type A dissection patients was 6 of 92 (7%). None of the patient characteristics other than pump time and hypotension, such as sex, hypertension, or smoking were significant in the development of stroke. Patients with
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Table 2. Type A Aortic Dissection: Multiple Logistic Regression Model Risk Factors for Strokea
Variable Intercept Total pump time Severe hypotension a
Parameter Estimate
Adjusted Odds Ratio
25.7195 0.0129 3.6460
1.01 38.32
95% CI
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Table 4. Type B Aortic Dissection: Multiple Logistic Regression Model Risk Factors for Neurologic Deficita p Value
0.0001 1.004 –1.02 0.007 3.15– 466.77 0.004
Model developed by stepwise multiple logistic regression analysis.
Variable Intercept Acute dissection TAAAII extent a
Parameter Estimate
Adjusted Odds Ratio
95% CI
p Value
23.8394 2.3600 2.1964
10.59 8.99
2.45– 45.82 2.01– 40.15
0.0001 0.002 0.004
Model developed by stepwise multiple logistic regression analysis.
CI 5 confidence interval; total pump time 5 total cardiopulmonary bypass time, which includes cooling, operation, and rewarming time; severe hypotension 5 systolic blood pressure ,50 mm Hg.
CI 5 confidence interval; total pump time 5 acute aortic dissection; TAAAII extent 5 aortic dissection of extent equal to Crawford thoracoabdominal type II aortic aneurysm extent.
acute type A dissection presenting as hypotensive were at significantly greater risk for stroke (Table 2). The incidence of stroke was 2 of 7 (29%) compared with 2 of 37 (5%) in patients with stable blood pressure more than 90 mm Hg (p , 0.05). With regard to early mortality, the overall incidence of death was 11 of 92 (12%) (Table 3). The more stable chronic dissection patients had 2 of 48 (4%) deaths and fared much better than those with acute dissection, of whom 9 of 44 (20%) died (p , 0.02). Of the acutely dissecting patients, 7 severely hypotensive patients had the highest death rate, with 4 of 7 deaths (57%). This rate was significantly elevated beyond that of the “stable” acute dissectors, among whom 5 of 37 (13%) died (odds ratio 8.5; p , 0.009).
ture, but no other variable, was found to be a significant risk factor for mortality (Table 5).
Type B Dissection Overall postoperative neurologic deficit (paraplegia or paraparesis) for descending thoracic and thoracoabdominal aortic or type B dissection was 15 of 114 (13%). For patients with acute dissection, 7 of 22 (32%) had neurologic deficit compared to chronic aortic dissection and aneurysm patients with 8 of 92 (9%) (p , 0.004) (Table 4). There were 6 acute type B dissections with type II repairs and of these 4 patients had neurologic deficit The combined adjuncts of distal aortic perfusion and cerebrospinal fluid drainage showed a trend toward reduction of neurologic deficit in patients with aortic dissection, but this trend was not statistically significant. Overall, deaths occurred in 12 of 114 (11%). Three of 22 patients with acute dissection died, an incidence of 14%, versus 9 of 92 deaths (10%) among patients with chronic dissection (p , 0.06). By multiple logistic regression analysis, aortic rup-
Table 3. Type A Aortic Dissection: Multiple Logistic Regression Model Risk Factors for Mortalitya
Variable Intercept Total pump time Severe hypotension a
Parameter Estimate 24.2027 0.0095 3.1967
Adjusted Odds Ratio 1.01 24.45
95% CI
p Value
0.0001 1.002–1.02 0.014 3.31–180.47 0.002
Model developed by stepwise multiple logistic regression analysis.
CI 5 confidence interval; total pump time 5 total cardiopulmonary bypass time, which includes cooling, surgery and rewarming time; severe hypotension 5 systolic blood pressure ,50 mm Hg.
Comment Acute type A aortic dissection of the proximal aorta should be treated as a surgical emergency to avoid rupture into the pericardium and subsequent cardiac tamponade. Historically, the rates of early deaths in the treatment of this grave condition have been high, beginning with the first treatments by DeBakey and colleagues [8] in 1965, with a mortality rate of 40%. Better imaging technology has led to earlier recognition of acute aortic dissection, bringing a greater number of complex patients to operation. Improvements in supportive medical care have increased patient survivability. Consequently and paradoxically, the surgical treatment of more critically ill patients raises the likelihood of a higher early mortality rate for acute aortic dissection, whereas techniques and adjuncts have increased overall chances of survival, most noticeably for the chronic dissection patient. The current day rate of 20% to 30% mortality in acute type A dissection was reached in the late 1970s, and although it has fluctuated since then, it has changed little overall [9 –15]. In our series, early deaths in the acute type A dissection group fell within this range (9 of 44 patients or 20%). By striking comparison, early deaths occurred in only 4% of patients with chronic type A dissection. The favorable mortality rate in our population of patients who presented without hypotension upon admission supports this conviction (4 of 7 or 57% with hypotension died versus 5 of 37 or 14% with stable blood pressure; p , 0.009). Currently, neither imaging technology nor supportive medical care appears able to affect patients who present with catastrophic hypotension. Table 5. Type B Aortic Dissection: Multiple Logistic Regression Model Risk Factors for Mortalitya
Variable
Parameter Estimate
Adjusted Odds Ratio
95% CI
p Value
Intercept Rupture
22.3979 2.3979
11.00
1.93– 62.65
0.0001 0.007
a
Model developed by stepwise multiple logistic regression analysis.
CI 5 confidence interval.
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Transesophageal echocardiography is extremely useful for localizing intimal tears in the aorta. This imaging modality also simplifies management of acute aortic dissection because we are able to establish a diagnosis of type A or B dissection in acutely ill patients and immediately choose the proper mode of treatment. We believe that the pledgeted interrupted suture line, as compared with the felt sandwich technique, provides superior stabilization of the defective aortic wall and decreases problems of stenosis after the repair. Acute type B aortic dissection of the distal aorta presents an entirely different set of problems than type A of the proximal aorta. Acute type B dissection can be stabilized medically before being treated surgically with a reasonable perioperative risk and selective treatment has met with a degree of success at some institutions [16]. Antihypertensive treatment, however, does not forego the necessity to closely monitor these patients. Hospital mortality of primary medical treatment remains relatively high and a substantial percentage of patients requires operation during initial hospitalization [17]. The main causes of death in both medical and surgical groups are rupture and abdominal malperfusion. We advocate conservative medical therapy and watchful waiting for treatment of acute type B aortic dissection as described in the methods section. Improvements in surgical techniques over the past 10 years have helped to reduce morbidity and mortality in patients undergoing graft replacement for aortic aneurysms. Such improvements include refinements in circulatory support adjuncts such as retrograde cerebral perfusion also used for type A aortic dissection [4]. Although we did not see statistically significant multivariate effects of retrograde cerebral perfusion in this population, several confounding factors made it difficult to evaluate. In acute type A dissection, half of the strokes we observed occurred in patients with severe hypotension and much of the damage was done before the operation began, therefore the stroke rate could not be expected to respond to the generally beneficial effect of retrograde cerebral perfusion. Future studies on the role of retrograde cerebral perfusion in the acute type A aortic dissection population with larger sample sizes are warranted. Distal aortic perfusion and cerebrospinal fluid drainage should also be valuable aids in the prevention of spinal cord morbidity in type B aortic dissection. In this population, as with type A dissection, the relationship between acuity of the presentation and extent of the aortic injury made the effects of adjuncts difficult to summarize statistically. Patients with acute dissection are at much higher risk for developing neurologic complications and those with acute dissection of type II extent are at highest risk, but we did not have sufficient data to evaluate the usefulness of the adjuncts. As in type A dissection, further experience is required to evaluate the role of adjuncts in acute type B aortic dissection. In conclusion, our experience indicates that acute type A aortic dissection should be treated aggressively
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with operation. Surgical treatment of chronic type A aortic dissection presenting as aneurysm has improved greatly in the past 10 years and can be treated in the same manner as typical ascending and arch aortic aneurysm with similar outcome. For acute type B aortic dissection, conservative medical therapy remains the definitive therapy. Surgical repair becomes the only option when medical therapy fails, but carries a high risk of neurologic deficit, particularly in dissections that involve the total descending aorta. Although mortality for type B dissection is commensurate to that for thoracoabdominal aortic aneurysm, neurologic morbidity is by comparison disproportionately high, possibly because of inability to reattach friable intercostal arteries. Morbidity and mortality rates for chronic aortic dissection patients continue to improve, with outcomes very similar to those for aneurysm patients and attributable to the same technical advances. We emphasize the critical need for follow-up for the dissection patient by regular computed tomographic scans or transesophageal echocardiography. Whether treatment has been medical or surgical, sudden appearance of a previously undetected aneurysm or extension of the dissection is always a threat.
References 1. Anagnostopoulos CE. Acute aortic dissections. Baltimore: University Park Press, 1975. 2. Fann JI, Miller DC. Management of ascending aortic dissections. ACC Curr Jl Rev 1995;4(3):39 – 41. 3. DeSanctis RW, Doroghazi RM, Austen WG, Buckley MJ. Aortic dissection. N Engl J Med 1987;317:1060–7. 4. Safi HJ, Letsou GV, Iliopoulos DC, et al. The impact of retrograde cerebral perfusion on ascending and arch aneurysm repair. Ann Thorac Surg 1997;63:1601–7. 5. Safi HJ, Miller CC III, Iliopoulos DC, Letsou GV, Baldwin JC. Staged repair of extensive aortic aneurysm: improved neurologic outcome. Ann Surg 1997;226:599 – 605. 6. Safi HJ, Bartoli S, Hess KR, et al. Neurologic deficit in patients at high risk with thoracoabdominal aortic aneurysms: the role of cerebral spinal fluid drainage and distal aortic perfusion. J Vasc Surg 1994;20:434– 43. 7. Safi HJ, Miller CC III, Carr C, Iliopoulos DC, Dorsay DA, Baldwin JC. The importance of intercostal artery reattachment during thoracoabdominal aortic aneurysm repair. J Vasc Surg 1998,27:58– 68. 8. DeBakey ME, Henly WS, Cooley DA, Morris GG Jr, Crawford ES, Beall AC Jr. Surgical management of dissecting aneurysms of the aorta. J Thorac Cardiovasc Surg 1965;49: 130– 49. 9. Miller DC, Mitchell RS, Oyer PE, Stinson EB, Jamieson SW, Shumway NE. Independent determinants of operative mortality for patients with aortic dissections. Circulation 1984;70: 153– 64. 10. Crawford ES, Svensson LG, Coselli JS, Safi HJ, Hess KR. Aortic dissection and dissecting aortic aneurysms. Ann Surg 1988;208:254–73. 11. Massimo CG, Presenti LF, Marranci P, et al. Extended and total aortic resection in the surgical treatment of acute type A aortic dissection: experience with 54 patients. Ann Thorac Surg 1988;46:420– 4. 12. Bachet J, Brizard C, Goudot B, et al. Repeated surgery for recurrent dissection of the aorta. Eur J Cardiothorac Surg 1990;4:238– 44. 13. Fann JI, Glower DD, Miller DC, et al. Preservation of aortic
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valve in type A aortic dissection complicated by aortic regurgitation. J Thorac Cardiovasc Surg 1991;102:62–75. 14. Heineman M, Laas J, Jurmann M, et al. Surgery extended into the aortic arch in acute type A dissection. Indications, techniques, and results. Circulation 1991;84:25–34. 15. Fann JI, Smith JA, Miller DC, et al. Surgical management of aortic dissection during a 30-year period. Circulation 1995; 92:(Suppl 9):13–21.
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16. Schor JS, Yerlioglu ME, Galla JD, Lansman SL, Ergin MA, Griepp RB. Selective management of acute type B aortic dissection: long-term follow-up. Ann Thorac Surg 1996;61: 1339– 41. 17. Gysi J, Schaffner T, Mohacsi P, Aeschbacher B, Althaus U, Carrel T. Early and late outcome of operated and nonoperated acute dissection of the descending aorta. Eur J Cardio-Thorac Surg 1997;11:1163–70.
DISCUSSION DR SAFUH ATTAR (Baltimore, MD): I congratulate Dr Safi on an excellent presentation. This is in the tradition of the studies that have come up from Houston. We have reviewed our experience in acute dissection over the past 14 years and divide them into two stages. The first stage included 40 patients, and the recent episode, the past 5 years, also included 40 patients. The incidence of neurologic complications in the acute dissection in the first phase, and the first part of this review, had 5 patients with neurologic complications out of 40, giving an incidence of about 12%. The second episode, or the second part of the review, included the last 40 cases. The first series was only the acute descending thoracic aortic aneurysms, whereas the recent series, the last 40 patients for the past 5 years, included both ascending and descending thoracic aortic dissection. We had 7 patients during the past 5 years. Four events that occurred before operation and three occurred intraoperatively. One patient had brain damage and did not survive. Three died, and 1 survived with good recovery. The paralysis in the 3 patients was either hemiplegia or paraplegia, and there were 3 survivors. Using the regression analysis, we have reviewed what the factors were that really affected survival in acute dissection in the 40 cases and the only factor that we came up with was the pump time. Doctor Safi, in how many patients with acute dissections did you need to replace the aortic valve in type A or type 1, in that specific classification? DR SAFI: Thank you very much, Dr Attar. To answer your question about how many aortic valve replacements were performed; we rarely replace the aortic valve unless the patient has aortic root dilatation or the dissection involves the aortic root, rendering any sewing hazardous. Most probably the amount of valve replacements is about 5%, and most of these patients have Marfan’s syndrome. With regard to the neurologic deficit in type B, it all depends on the extent of aortic replacement. For acute dissection, if we replace just the upper third or the upper half of the descending thoracic aorta, we have seen no paraplegia with use of cerebrospinal fluid drainage and distal aortic perfusion. But this incidence increases to about 30% in replacement of the entire descending thoracic aorta and the abdominal aorta—the socalled Crawford type II thoracoabdominal aortic aneurysm. I think one of the reasons that paraplegia develops in these patients is that we oversew the intercostal arteries. I do not know any safe method to reattach the lower intercostal arteries into the graft in the acutely dissected aorta without the risk of catastrophic bleeding. DR WILLIAM A. BAUMGARTNER (Baltimore, MD): That is a very nice presentation, Dr Safi. I have one question regarding the neurologic injuries, because this seems to be the major stumbling block in this type of operation. Of the group of patients in whom you used retrograde cerebral perfusion for
protection, which included the majority of patients, is there a decrease in neurologic injury? DR SAFI: This is a very good question. But I think that we need a larger series to answer the question correctly. Because of the number of patients, retrograde cerebral perfusion did appear to be a protective agent. In our previous publication regarding the chronic or medial degenerative aortic aneurysm, we found there is a decreased incidence of stroke in patients older than 70 years, but not less than 70 years. DR KIT V. AROM (Minneapolis, MN): I have one brief question. If there is a very small transverse tear above the aortic valve, about 2 cm in length, would you still use deep hypothermia and circulatory arrest? DR SAFI: It all depends on the clinical presentation of the patient. If there is acute type A (or type I DeBakey) dissection, we do use profound hypothermia and circulatory arrest because we do not know the extent of the dissection and second, I like to see the inside of the transverse arch to determine whether it is free from a reentry point. Sometimes we replace the hemiarch thus excluding the reentry point in the transverse arch. I also found that clamping can cause injury. There are some surgeons who like to clamp. However, as an example of why I do not, 1 patient referred to me had had replacement of the ascending aorta and root using the clamp technique. By the time they released the clamp the flow went into the false lumen and he ended up with no blood pressure in the right arm and no flow to the right carotid artery and he had a stroke. We remedied things as best we could by replacing the transverse arch, although this is another thing I try to avoid. Replacing the arch increases the risk of death and neurologic deficit. In this series we replaced the arch as an elephant trunk in 1 patient, but the procedure takes too long, and again, I would rather avoid it. DR AROM: So your practice today is that you do all of the procedures under deep hypothermia and circulatory arrest and rarely cross-clamp the aorta? DR SAFI: Yes, this is correct. Once the patient is seen in the emergency room and has gone to the surgical intensive care unit, if the patient is stable, then we perform transesophageal echocardiography to establish the diagnosis (type A or B). If the patient has type A aortic dissection then after insertion of the arterial line and determining blood type we move the patient to the operating room and we repair the dissection of the ascending aorta. Following this policy the mortality and stroke rate has been very good. If we miss that window, and the patient is unstable (ie, hypotensive or cardiac tamponade), then the mortality and the stroke rate are going to be high.
Background. We reviewed our experience in the repair of acute and chronic aortic dissection with regard to early neurologic deficit and death. Methods. Between February 1991 and June 1996, we performed 206 operations on 195 patients for aortic dissection. Ascending or arch repair, or a combination (type A dissection) was performed on 92 of 206 patients (45%); 44 of 92 (48%) were acute dissection and 48 of 92 (52%) were chronic. Descending or thoracoabdominal repair (type B dissection) was performed on 114 of 206 patients (55%); 22 of 114 (19%) were acute and 92 of 114 (81%) were chronic. Results. Among type A cases, strokes occurred in 6 of 92 patients (7%) overall; 4 of 44 (9%) were acute cases and 2 of 48 (4%) were chronic (p < 0.34). Early deaths for type A were 11 of 92 (12%) overall; 9 of 44 (20%) acute and 2 of 48 (4%) chronic (p < 0.02). In type B cases, neurologic complications were 15 of 114 (13%) overall; 7 of 22 (32%)
were acute cases and 8 of 92 (9%) were chronic (p < 0.004). Early deaths for type B were 12 of 114 (11%) overall; 3 of 22 (14%) acute and 9 of 92 (10%) chronic (p < 0.6). Preoperative hypotension was significant in acute type A patients, with strokes in 2 of 7 (29%) hypotensives compared with 2 of 37 (5%) normotensives (p < 0.05) and early death in 4 of 7 (57%) hypotensives versus 5 of 37 (14%) normotensives (p < 0.009). Conclusions. Morbidity and mortality for repair of chronic dissection types A and B were acceptable. Preoperative hypotension in acute type A dissection was a major predisposing factor toward stroke (29% versus 5%, p < 0.05). Acute type B dissection had acceptable mortality (14%) but a high rate of neurologic complications (32%).
I
Material and Methods
n the frequent catastrophic cascade of events immediately after an aortic dissection, patient survival relies on rapid diagnosis and early therapeutic intervention [1-3]. The patient is at the greatest risk in the acute phase, within 14 days of the initial dissection, when complications brought on by hemorrhage or rupture are most likely. The decision to manage surgically or medically depends on the time elapsed since onset, the dissection location, and urgency of presentation. Most often the treatment of type A, which originates in the ascending aorta, is surgical. Type B, in the descending thoracic aorta, is more often treated medically in the acute stage and surgically in the chronic stage. In this study we examined the results of our operative treatment of aortic dissection during the past 5 years, with particular attention to the differences in morbidity and mortality between acute and chronic aortic dissection patients.
Presented at the Forty-fourth Annual Meeting of the Southern Thoracic Surgical Association, Naples, FL, Nov 6 – 8, 1997. Address reprint requests to Dr Safi, 6550 Fannin, Suite 1603, Houston, TX 77030.
© 1998 by The Society of Thoracic Surgeons Published by Elsevier Science Inc
(Ann Thorac Surg 1998;66:402–11) © 1998 by The Society of Thoracic Surgeons
Patient Population Between February 1991 and June 1996, 206 operations were performed on 195 patients by one surgeon (H.J.S.). Patient characteristics are as follows for the 92 type A patients: acute dissection, 44 (48%); stroke, 6 (7%); 30-day mortality, 11 (12%); hypotensive crisis (systolic blood pressure ,60 mm Hg or moribund presentation, ie, cardiopulmonary arrest, pulseless, or in shock), 7 (8%); cerebrovascular disease (stroke, transient ischemic attack, or atheroocclusive disease of the carotid arteries), 12 (13%); heart disease (aortic valve disease, atheroocclusive disease of the coronary arteries, or cardiomyopathy), 20 (22%); previous aortic operation, 32 (35%); hypertension, 56 (61%); current smoker, 22 (24%); and for the 114 type B patients: acute dissection, 22 (19%); neurologic deficit (paraplegia or paraparesis), 15 (13%); 30-day mortality, 12 (11%); renal insufficiency, 13 (11%); heart disease, 28 (25%); previous proximal aortic operation, 28 (25%); hypertension, 91 (80%); and current smoker, 41 (28%). The selected risk factors for stroke in type A dissection and for spinal cord neurologic deficit in type B are shown in Table 1. Men comprised more than two-thirds of all 0003-4975/98/$19.00 PII S0003-4975(98)00533-5
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patients. Patients were divided roughly in half between operation for repair of the ascending aorta (type A dissection) and repair of the descending thoracic or thoracoabdominal aorta (type B dissection). A greater number of type A repairs, however, took place in the acute phase (44 of 92 or 48%) compared with type B repairs (22 of 114 or 19%) (p , 0.001). Age did not differ significantly between these two groups. Six of 92 (7%) of the type A repairs were in patients with Marfan’s syndrome, as were 7 of 114 (6%) of type B repairs. Twentyfive of 92 type A patients (27%) underwent the first stage of aortic repair with the elephant trunk technique; 1 had an acute dissection, the remainder had chronic dissections. Twelve of 24 patients had completed the second half of this two-stage repair at the time of this study. The specific operations performed for the 92 type A patients were as follows: aortic valve and ascending aorta, 9 (10%); aortic valve, ascending aorta and arch, 16 (17%); ascending aorta, 20 (22%); ascending aorta and proximal arch, 9 (10%); ascending aorta and transverse arch, 11 (12%); transverse arch, 2 (2%); elephant trunk, stage 1, 25 (27%); and for the 114 type B patients: elephant trunk, stage 2, 12 (11%); descending thoracic aorta, type A, 1 (0.8%); descending thoracic aorta, types A, B, 9 (8%); descending thoracic aorta, types A, B, C, 16 (14%); thoracoabdominal aortic aneurysm, type I, 29 (25%); thoracoabdominal aortic aneurysm, type II, 42 (37%); thoracoabdominal aortic aneurysm, type III, 4 (4%); and abdominal aorta, 1 (0.8%). Among acute type A patients, 7 were hypotensive, with preoperative cardiopulmonary arrest in 4 patients and blood pressure below 60 mm Hg in 3. In September 1992, we abandoned the simple cross-clamp technique in favor of the adjuncts of distal aortic perfusion and cerebrospinal fluid drainage, which was consequently used in 73 of 114 type B patients (64%). Similarly, retrograde cerebral perfusion, in addition to hypothermic circulatory arrest, was added to the surgical protocol for ascending and arch patients in February 1994 for 77 of 92 type A patients (84%).
Statistical Methods Univariate categoric data were analyzed by contingency table methods. Continuous variables were divided into quartiles for contingency table analysis, and were also analyzed as continuous by univariate logistic regression. The p values were computed using x2 statistics for contingency tables, and odds ratios were computed for dichotomous variables. Confidence intervals for contingency table odds ratios are test based. Multivariate analysis was conducted by multiple logistic regression. The p values for logistic regression analyses were computed by maximum-likelihood methods. All calculations were performed using SAS software version 6.12 (SAS Institute, Inc, Cary, NC).
Patient Selection and Operative Methods Our protocol for treating acute aortic dissection depends on the patient presentation. If a patient had a moribund presentation to the emergency department he or she was sent directly to the operating room for anesthesia induc-
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tion and transesophageal echocardiography to identify the site and extent of the intimal disruption. A patient who presented with acute symptoms, but was not moribund, was admitted to the surgical intensive care unit where he or she was evaluated with transesophageal echocardiography and prepared for operation as soon as possible. After transfer to the operating room, median sternotomy was performed and the patient was placed on cardiopulmonary bypass and the systemic temperature cooled for profound hypothermia. Cannulation was femoral–femoral for cardiopulmonary bypass, and to the superior vena cava for retrograde cerebral perfusion. Myocardial protection was provided throughout the procedure by cardioplegic perfusion through the coronary sinus, keeping the myocardial temperature less than 15°C. Venting through the left superior pulmonary vein or artery prevented ventricular distention and allowed optimal decompression of the left ventricle. When the electroencephalogram was isoelectric and the nasopharyngeal temperature reached approximately 12°C, the pump was stopped, and retrograde cerebral perfusion was begun through the superior vena cava. The rate of pump flow did not exceed 500 mL/min and the pressure did not exceed 25 mm Hg. The ascending aorta was inspected for the site and extent of the tear, the involvement of the transverse arch, and assessment of intimal disruption requiring repair. The ascending aorta was opened longitudinally and then transected just proximal to the innominate artery. Provided the transverse arch was free of reentry, we sutured the intima and adventitia together with fine 4-0 and 5-0 polypropylene suture (Fig 1A). A gelatin woven Dacron graft was sutured to the reinforced proximal aortic arch in end-toend fashion, and reinforced from both inside and outside with 4-0 pledgeted sutures (Figs 1B, 1C). When the distal anastomosis was completed, retrograde cerebral perfusion was stopped and cardiopulmonary bypass restarted through the femoral artery to evacuate all air and debris from the brachiocephalic vessels. The graft was clamped proximal to the origin of the innominate artery. Flow to the cerebral and systemic circulation was restored and the head of the table was elevated. On rare occasions when the brachiocephalic arterial flow was not adequate, as manifested by low radial artery pressure and due to a dissecting flap, we cannulated the ascending aortic graft and delivered flow to the head in antegrade fashion. The patient was rewarmed with restoration of antegrade flow. If the aortic valve was morphologically normal and the root without dilatation, we resuspended the aortic valve with 4-0 polypropylene pledgeted sutures. The intima and adventitia of the supracoronary aorta were sutured together using 4-0 polypropylene sutures, and reinforced with 4-0 pledgeted suture, usually from inside the graft (Figs 1D, 1E). A composite valve graft was selected if the valve and root were dilated. The coronary arteries were reattached by button technique or modified Cabrol in
ACUTE TYPE A DISSECTION.
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Table 1. Selected Risk Factors No. of Patients (%)
No. With Event (%)
10 (22.7) 11 (25.0) 12 (27.3) 11 (25.0)
1 (10.0) 2 (18.2) 0 (0.0) 1 (9.1)
Female Male
12 (27.3) 32 (72.7)
1 (8.3) 3 (9.4)
0.88 1
0.08 –9.38
0.92
Current smokers Nonsmokers
9 (20.5) 35 (79.5)
0 (0.0) 4 (11.4)
0.37
0.02–7.49
0.29
Hypertensive Normotensive
24 (54.6) 20 (45.4)
0 (0.0) 4 (20.0)
0.08 1
0.01–1.49
0.03
Hypotensive crisis Otherwise
7 (15.9) 37 (84.1)
2 (28.6) 2 (5.4)
7.00 1
0.80 – 61.46
0.051
12 (27.3) 11 (25.0) 10 (22.7) 11 (25.0)
1 (8.3) 0 (0.0) 1 (10.0) 2 (18.2)
0.53
12 (25.0) 11 (22.9) 12 (25.0) 13 (27.1)
0 (0.0) 0 (0.0) 1 (8.3) 1 (7.7)
0.59
Female Male
10 (20.8) 38 (79.2)
1 (10.0) 3 (2.6)
4.11 1
0.23–72.21
0.29
Current smokers Nonsmokers
13 (27.1) 35 (72.9)
1 (7.7) 4 (2.9)
2.83
0.16 – 48.93
0.46
Hypertensive Normotensive
32 (66.7) 16 (33.3)
2 (6.3) 4 (0.0)
2.71 1
0.12–59.74
0.31
12 (25.0) 12 (25.0) 12 (25.0) 12 (25.0)
0 (0.0) 1 (8.3) 0 (0.0) 1 (8.3)
0.56
4 (18.2) 7 (31.8) 5 (22.7) 6 (27.3)
2 (50.0) 2 (28.6) 3 (60.0) 0 (0.0)
0.15
TAAAI Otherwise
5 (22.7) 17 (77.3)
1 (20.0) 6 (35.3)
0.458 1
0.04 –5.08
0.52
TAAAII Otherwise
6 (27.3) 16 (72.7)
4 (66.7) 3 (18.8)
8.67 1
1.05–71.59
0.04
TAAAIII Otherwise
1 (4.6) 21 (95.4)
1 (100.0) 6 (28.6)
7.15 1
0.26 –199.7
0.14
Descending Otherwise
10 (45.5) 12 (54.5)
1 (10.0) 6 (50.0)
0.11
0.01–1.17
0.07
Variable Acute type A dissection: stroke Age 8 –58 59 – 67 68 –72 73– 88
Pump time (min) 74 –96 97–127 128 –195 196 – 461 Chronic type A dissection: stroke Age 8 –58 59 – 67 68 –72 73– 88
Pump time (min) 21–116 117–150 151–191 192– 408 Acute type B dissection: spinal cord neurologic deficit Age 8 –58 59 – 67 68 –72 73– 88
Odds Ratioa
95% CIb
p Valuec
0.51
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Table 1. Continued No. of Patients (%)
No. With Event (%)
Odds Ratioa
Female Male
9 (40.9) 13 (59.1)
1 (11.1) 6 (46.2)
0.15 1
0.01–1.52
0.09
Current smokers Nonsmokers
12 (54.6) 10 (45.4)
3 (25.0) 4 (40.0)
0.50
0.08 –3.08
0.46
Hypertensive Otherwise
16 (72.7) 6 (27.3)
6 (37.5) 1 (16.7)
3.00 1
0.28 –32.21
0.36
7 (31.8) 5 (22.7) 5 (22.7) 5 (22.7)
3 (42.8) 1 (20.0) 2 (40.0) 1 (20.0)
0.19
32 (34.8) 19 (20.7) 19 (20.7) 22 (23.9)
4 (12.5) 0 (0.0) 1 (5.3) 3 (13.6)
0.34
TAAA, type I Otherwise
27 (29.4) 65 (70.7)
1 (3.7) 7 (10.8)
0.32 1
0.04 –2.72
0.27
TAAA, type II Otherwise
43 (46.7) 49 (53.3)
7 (16.3) 1 (2.0)
9.33 1
1.10 –79.28
0.02
TAAA, type III Otherwise
4 (4.4) 88 (95.7)
0 (0.0) 8 (9.1)
1.05 1
0.05–21.26
0.53
TAAA, type IV Otherwise
1 (1.1) 91 (98.9)
0 (0.0) 8 (8.8)
3.28 1
0.12– 86.8
0.76
Descending Otherwise
18 (19.6) 74 (80.4)
0 (0.0) 8 (10.8)
0.21
0.01–3.84
0.14
Female Male
17 (18.5) 75 (81.5)
2 (11.8) 6 (8.0)
1.53 1
0.28 – 8.35
0.62
Current smokers Nonsmokers
29 (31.5) 63 (68.5)
4 (13.8) 4 (6.4)
2.36
0.55–10.19
0.24
Hypertensive Otherwise
75 (81.5) 17 (18.5)
6 (8.0) 2 (11.8)
0.65 1
0.12–3.55
0.62
Pump time (min) 15– 42 43–57 58 –76 77–196
23 (25.0) 21 (22.8) 23 (25.0) 25 (27.2)
2 (8.7) 1 (4.8) 2 (8.7) 3 (12.0)
Variable
Pump time (min) 27– 45 46 – 63 64 – 87 88 –169 Chronic type B dissection: spinal cord neurologic deficit Age 28 – 47 48 –59 60 – 66 67– 81
a
Common odds ratio computed by the contingency table method. probability of a type 1 statistical error for the comparison.
b
95% CIb
Ninety-five percent confidence interval for the odds ratio.
p Valuec
0.86
c
Nominal x2
TAAA 5 thoracoabdominal aortic aneurysm.
which a 12-mm Dacron tube graft from the composite valve/graft prosthesis was attached to the left main coronary artery. The right coronary artery orifice was either attached directly to the graft or connected by a length of Dacron tube or saphenous vein (Fig 2). In 2 patients, the coronary orifices were involved in the dissection and the coronary arteries were ligated and reversed saphenous vein grafts were used for bypass from the composite graft to the left anterior descending, the
circumflex, and the right coronary arteries. Finally, the sump was terminated, the heart filled to aspirate the heart chamber from air and debris, and the patient weaned from cardiopulmonary bypass. For patients in whom dissection involved the transverse aortic arch, either the proximal arch or the total arch was replaced. In total arch replacements the brachiocephalic arteries were preserved as an island and reattached to the graft as previously described [4]. The
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Fig 1. (A) The intima and adventitia are sutured together. (B, C) Reinforcement of graft and aortic arch with pledgeted sutures. (D, E) Pledgeted reinforcement of supracoronary intima and adventitia.
elephant trunk technique [5] was used in 1 of 44 (2%) acute dissection patients in which the dissection extended into the descending thoracic aorta. CHRONIC TYPE A DISSECTION. Chronic type A dissection was treated in the same manner as ascending/arch aortic aneurysm [4]. Graft replacement is the treatment of choice, and the main indications for operation for chronic type A dissection were aortic size or presence of symptoms. The operation was performed with or without aortic valve and root replacement as required (Figs 3A, 3B). The elephant trunk technique was used in 24 of 48 (50%) chronic dissection patients in which the dissection extended into the descending thoracic aorta.
ACUTE TYPE B DISSECTION. Operations for acute type B dissection were performed selectively, and only when complications of the dissection arose. The indications were persistent pain, aneurysmal dilatation ($5 cm), endorgan (kidney, bowel) or limb ischemia, or evidence of retrograde dissection to the ascending aorta. Patients who did not meet these criteria were treated with aggressive medical therapy, which included immediate admission to the intensive care unit, urgent pharmacologic blood pressure control, complete intensive care unit monitoring, and immediate imaging studies. If pain was controlled and aortic expansion beyond 5 cm was not present, patients were weaned from intravenous antihypertensives and converted to oral antihypertensive ther-
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Fig 2. Composite valve graft with modified Cabrol reattachment of left coronary artery.
apy. Chest radiographs were obtained daily and computed tomographic scans weekly during hospitalization. Stable patients were discharged after 14 days. Patients
407
were urged at follow-up to undergo quarterly computed tomographic scans in the first year, semiannual scans in the next 2 years, and thereafter to undergo annual scans. Any change in symptoms or aortic diameter were considered indications for surgical reevaluation. Operative technique for acute dissection of the descending thoracic or thoracoabdominal aorta was not unlike the techniques previously described for aneurysms occurring in this portion of the aorta [6]. The proximal descending thoracic aorta distal to the left subclavian was transected completely and lifted off the esophagus. Both proximal and distal intima and adventitia of the transected aorta were reinforced in the same manner as that for the ascending aorta with a 4-0 polypropylene suture. A gelatin woven Dacron graft was sewn directly to the reinforced acutely dissected proximal thoracic aorta with the posterior row reinforced using interrupted polypropylene sutures. The descending thoracic graft was cut to length and sutured to the reinforced distal aorta, rechanneling blood into the true lumen of the distal aorta. The adjuncts of cerebrospinal fluid drainage and distal aortic perfusion were used in all patients after 1992 [6]. When most of the descending and abdominal aorta required replacement (type II thoracoabdominal aortic aneurysm), we opened the entire thoracoabdominal
Fig 3. Chronic type A dissection; completed valve and graft replacement using the elephant trunk technique.
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Fig 4. Chronic type B dissection; completed graft replacement with intercostal artery reattachment.
aorta, excised the septum between the false and true lumen, and reattached the visceral vessels and renal arteries to the graft either directly or using a woven Dacron graft. We ligated all the intercostal and lumbar arteries because the friable tissue was likely to lead to catastrophic bleeding and a fatal outcome. Chronic type B aortic dissection was treated in the same manner as descending thoracic or thoracoabdominal aortic aneurysm [6]. In patients with chronic dissection, we preferred to reimplant intercostal arteries T-9 through T-12 [7] using either a sidearm
CHRONIC TYPE B DISSECTION.
graft or a side hole to which we reattached the arteries directly (Figs 4A, 4B).
Results Type A Dissection The overall incidence of stroke in ascending and arch or type A dissection patients was 6 of 92 (7%). None of the patient characteristics other than pump time and hypotension, such as sex, hypertension, or smoking were significant in the development of stroke. Patients with
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Table 2. Type A Aortic Dissection: Multiple Logistic Regression Model Risk Factors for Strokea
Variable Intercept Total pump time Severe hypotension a
Parameter Estimate
Adjusted Odds Ratio
25.7195 0.0129 3.6460
1.01 38.32
95% CI
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Table 4. Type B Aortic Dissection: Multiple Logistic Regression Model Risk Factors for Neurologic Deficita p Value
0.0001 1.004 –1.02 0.007 3.15– 466.77 0.004
Model developed by stepwise multiple logistic regression analysis.
Variable Intercept Acute dissection TAAAII extent a
Parameter Estimate
Adjusted Odds Ratio
95% CI
p Value
23.8394 2.3600 2.1964
10.59 8.99
2.45– 45.82 2.01– 40.15
0.0001 0.002 0.004
Model developed by stepwise multiple logistic regression analysis.
CI 5 confidence interval; total pump time 5 total cardiopulmonary bypass time, which includes cooling, operation, and rewarming time; severe hypotension 5 systolic blood pressure ,50 mm Hg.
CI 5 confidence interval; total pump time 5 acute aortic dissection; TAAAII extent 5 aortic dissection of extent equal to Crawford thoracoabdominal type II aortic aneurysm extent.
acute type A dissection presenting as hypotensive were at significantly greater risk for stroke (Table 2). The incidence of stroke was 2 of 7 (29%) compared with 2 of 37 (5%) in patients with stable blood pressure more than 90 mm Hg (p , 0.05). With regard to early mortality, the overall incidence of death was 11 of 92 (12%) (Table 3). The more stable chronic dissection patients had 2 of 48 (4%) deaths and fared much better than those with acute dissection, of whom 9 of 44 (20%) died (p , 0.02). Of the acutely dissecting patients, 7 severely hypotensive patients had the highest death rate, with 4 of 7 deaths (57%). This rate was significantly elevated beyond that of the “stable” acute dissectors, among whom 5 of 37 (13%) died (odds ratio 8.5; p , 0.009).
ture, but no other variable, was found to be a significant risk factor for mortality (Table 5).
Type B Dissection Overall postoperative neurologic deficit (paraplegia or paraparesis) for descending thoracic and thoracoabdominal aortic or type B dissection was 15 of 114 (13%). For patients with acute dissection, 7 of 22 (32%) had neurologic deficit compared to chronic aortic dissection and aneurysm patients with 8 of 92 (9%) (p , 0.004) (Table 4). There were 6 acute type B dissections with type II repairs and of these 4 patients had neurologic deficit The combined adjuncts of distal aortic perfusion and cerebrospinal fluid drainage showed a trend toward reduction of neurologic deficit in patients with aortic dissection, but this trend was not statistically significant. Overall, deaths occurred in 12 of 114 (11%). Three of 22 patients with acute dissection died, an incidence of 14%, versus 9 of 92 deaths (10%) among patients with chronic dissection (p , 0.06). By multiple logistic regression analysis, aortic rup-
Table 3. Type A Aortic Dissection: Multiple Logistic Regression Model Risk Factors for Mortalitya
Variable Intercept Total pump time Severe hypotension a
Parameter Estimate 24.2027 0.0095 3.1967
Adjusted Odds Ratio 1.01 24.45
95% CI
p Value
0.0001 1.002–1.02 0.014 3.31–180.47 0.002
Model developed by stepwise multiple logistic regression analysis.
CI 5 confidence interval; total pump time 5 total cardiopulmonary bypass time, which includes cooling, surgery and rewarming time; severe hypotension 5 systolic blood pressure ,50 mm Hg.
Comment Acute type A aortic dissection of the proximal aorta should be treated as a surgical emergency to avoid rupture into the pericardium and subsequent cardiac tamponade. Historically, the rates of early deaths in the treatment of this grave condition have been high, beginning with the first treatments by DeBakey and colleagues [8] in 1965, with a mortality rate of 40%. Better imaging technology has led to earlier recognition of acute aortic dissection, bringing a greater number of complex patients to operation. Improvements in supportive medical care have increased patient survivability. Consequently and paradoxically, the surgical treatment of more critically ill patients raises the likelihood of a higher early mortality rate for acute aortic dissection, whereas techniques and adjuncts have increased overall chances of survival, most noticeably for the chronic dissection patient. The current day rate of 20% to 30% mortality in acute type A dissection was reached in the late 1970s, and although it has fluctuated since then, it has changed little overall [9 –15]. In our series, early deaths in the acute type A dissection group fell within this range (9 of 44 patients or 20%). By striking comparison, early deaths occurred in only 4% of patients with chronic type A dissection. The favorable mortality rate in our population of patients who presented without hypotension upon admission supports this conviction (4 of 7 or 57% with hypotension died versus 5 of 37 or 14% with stable blood pressure; p , 0.009). Currently, neither imaging technology nor supportive medical care appears able to affect patients who present with catastrophic hypotension. Table 5. Type B Aortic Dissection: Multiple Logistic Regression Model Risk Factors for Mortalitya
Variable
Parameter Estimate
Adjusted Odds Ratio
95% CI
p Value
Intercept Rupture
22.3979 2.3979
11.00
1.93– 62.65
0.0001 0.007
a
Model developed by stepwise multiple logistic regression analysis.
CI 5 confidence interval.
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Transesophageal echocardiography is extremely useful for localizing intimal tears in the aorta. This imaging modality also simplifies management of acute aortic dissection because we are able to establish a diagnosis of type A or B dissection in acutely ill patients and immediately choose the proper mode of treatment. We believe that the pledgeted interrupted suture line, as compared with the felt sandwich technique, provides superior stabilization of the defective aortic wall and decreases problems of stenosis after the repair. Acute type B aortic dissection of the distal aorta presents an entirely different set of problems than type A of the proximal aorta. Acute type B dissection can be stabilized medically before being treated surgically with a reasonable perioperative risk and selective treatment has met with a degree of success at some institutions [16]. Antihypertensive treatment, however, does not forego the necessity to closely monitor these patients. Hospital mortality of primary medical treatment remains relatively high and a substantial percentage of patients requires operation during initial hospitalization [17]. The main causes of death in both medical and surgical groups are rupture and abdominal malperfusion. We advocate conservative medical therapy and watchful waiting for treatment of acute type B aortic dissection as described in the methods section. Improvements in surgical techniques over the past 10 years have helped to reduce morbidity and mortality in patients undergoing graft replacement for aortic aneurysms. Such improvements include refinements in circulatory support adjuncts such as retrograde cerebral perfusion also used for type A aortic dissection [4]. Although we did not see statistically significant multivariate effects of retrograde cerebral perfusion in this population, several confounding factors made it difficult to evaluate. In acute type A dissection, half of the strokes we observed occurred in patients with severe hypotension and much of the damage was done before the operation began, therefore the stroke rate could not be expected to respond to the generally beneficial effect of retrograde cerebral perfusion. Future studies on the role of retrograde cerebral perfusion in the acute type A aortic dissection population with larger sample sizes are warranted. Distal aortic perfusion and cerebrospinal fluid drainage should also be valuable aids in the prevention of spinal cord morbidity in type B aortic dissection. In this population, as with type A dissection, the relationship between acuity of the presentation and extent of the aortic injury made the effects of adjuncts difficult to summarize statistically. Patients with acute dissection are at much higher risk for developing neurologic complications and those with acute dissection of type II extent are at highest risk, but we did not have sufficient data to evaluate the usefulness of the adjuncts. As in type A dissection, further experience is required to evaluate the role of adjuncts in acute type B aortic dissection. In conclusion, our experience indicates that acute type A aortic dissection should be treated aggressively
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with operation. Surgical treatment of chronic type A aortic dissection presenting as aneurysm has improved greatly in the past 10 years and can be treated in the same manner as typical ascending and arch aortic aneurysm with similar outcome. For acute type B aortic dissection, conservative medical therapy remains the definitive therapy. Surgical repair becomes the only option when medical therapy fails, but carries a high risk of neurologic deficit, particularly in dissections that involve the total descending aorta. Although mortality for type B dissection is commensurate to that for thoracoabdominal aortic aneurysm, neurologic morbidity is by comparison disproportionately high, possibly because of inability to reattach friable intercostal arteries. Morbidity and mortality rates for chronic aortic dissection patients continue to improve, with outcomes very similar to those for aneurysm patients and attributable to the same technical advances. We emphasize the critical need for follow-up for the dissection patient by regular computed tomographic scans or transesophageal echocardiography. Whether treatment has been medical or surgical, sudden appearance of a previously undetected aneurysm or extension of the dissection is always a threat.
References 1. Anagnostopoulos CE. Acute aortic dissections. Baltimore: University Park Press, 1975. 2. Fann JI, Miller DC. Management of ascending aortic dissections. ACC Curr Jl Rev 1995;4(3):39 – 41. 3. DeSanctis RW, Doroghazi RM, Austen WG, Buckley MJ. Aortic dissection. N Engl J Med 1987;317:1060–7. 4. Safi HJ, Letsou GV, Iliopoulos DC, et al. The impact of retrograde cerebral perfusion on ascending and arch aneurysm repair. Ann Thorac Surg 1997;63:1601–7. 5. Safi HJ, Miller CC III, Iliopoulos DC, Letsou GV, Baldwin JC. Staged repair of extensive aortic aneurysm: improved neurologic outcome. Ann Surg 1997;226:599 – 605. 6. Safi HJ, Bartoli S, Hess KR, et al. Neurologic deficit in patients at high risk with thoracoabdominal aortic aneurysms: the role of cerebral spinal fluid drainage and distal aortic perfusion. J Vasc Surg 1994;20:434– 43. 7. Safi HJ, Miller CC III, Carr C, Iliopoulos DC, Dorsay DA, Baldwin JC. The importance of intercostal artery reattachment during thoracoabdominal aortic aneurysm repair. J Vasc Surg 1998,27:58– 68. 8. DeBakey ME, Henly WS, Cooley DA, Morris GG Jr, Crawford ES, Beall AC Jr. Surgical management of dissecting aneurysms of the aorta. J Thorac Cardiovasc Surg 1965;49: 130– 49. 9. Miller DC, Mitchell RS, Oyer PE, Stinson EB, Jamieson SW, Shumway NE. Independent determinants of operative mortality for patients with aortic dissections. Circulation 1984;70: 153– 64. 10. Crawford ES, Svensson LG, Coselli JS, Safi HJ, Hess KR. Aortic dissection and dissecting aortic aneurysms. Ann Surg 1988;208:254–73. 11. Massimo CG, Presenti LF, Marranci P, et al. Extended and total aortic resection in the surgical treatment of acute type A aortic dissection: experience with 54 patients. Ann Thorac Surg 1988;46:420– 4. 12. Bachet J, Brizard C, Goudot B, et al. Repeated surgery for recurrent dissection of the aorta. Eur J Cardiothorac Surg 1990;4:238– 44. 13. Fann JI, Glower DD, Miller DC, et al. Preservation of aortic
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valve in type A aortic dissection complicated by aortic regurgitation. J Thorac Cardiovasc Surg 1991;102:62–75. 14. Heineman M, Laas J, Jurmann M, et al. Surgery extended into the aortic arch in acute type A dissection. Indications, techniques, and results. Circulation 1991;84:25–34. 15. Fann JI, Smith JA, Miller DC, et al. Surgical management of aortic dissection during a 30-year period. Circulation 1995; 92:(Suppl 9):13–21.
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16. Schor JS, Yerlioglu ME, Galla JD, Lansman SL, Ergin MA, Griepp RB. Selective management of acute type B aortic dissection: long-term follow-up. Ann Thorac Surg 1996;61: 1339– 41. 17. Gysi J, Schaffner T, Mohacsi P, Aeschbacher B, Althaus U, Carrel T. Early and late outcome of operated and nonoperated acute dissection of the descending aorta. Eur J Cardio-Thorac Surg 1997;11:1163–70.
DISCUSSION DR SAFUH ATTAR (Baltimore, MD): I congratulate Dr Safi on an excellent presentation. This is in the tradition of the studies that have come up from Houston. We have reviewed our experience in acute dissection over the past 14 years and divide them into two stages. The first stage included 40 patients, and the recent episode, the past 5 years, also included 40 patients. The incidence of neurologic complications in the acute dissection in the first phase, and the first part of this review, had 5 patients with neurologic complications out of 40, giving an incidence of about 12%. The second episode, or the second part of the review, included the last 40 cases. The first series was only the acute descending thoracic aortic aneurysms, whereas the recent series, the last 40 patients for the past 5 years, included both ascending and descending thoracic aortic dissection. We had 7 patients during the past 5 years. Four events that occurred before operation and three occurred intraoperatively. One patient had brain damage and did not survive. Three died, and 1 survived with good recovery. The paralysis in the 3 patients was either hemiplegia or paraplegia, and there were 3 survivors. Using the regression analysis, we have reviewed what the factors were that really affected survival in acute dissection in the 40 cases and the only factor that we came up with was the pump time. Doctor Safi, in how many patients with acute dissections did you need to replace the aortic valve in type A or type 1, in that specific classification? DR SAFI: Thank you very much, Dr Attar. To answer your question about how many aortic valve replacements were performed; we rarely replace the aortic valve unless the patient has aortic root dilatation or the dissection involves the aortic root, rendering any sewing hazardous. Most probably the amount of valve replacements is about 5%, and most of these patients have Marfan’s syndrome. With regard to the neurologic deficit in type B, it all depends on the extent of aortic replacement. For acute dissection, if we replace just the upper third or the upper half of the descending thoracic aorta, we have seen no paraplegia with use of cerebrospinal fluid drainage and distal aortic perfusion. But this incidence increases to about 30% in replacement of the entire descending thoracic aorta and the abdominal aorta—the socalled Crawford type II thoracoabdominal aortic aneurysm. I think one of the reasons that paraplegia develops in these patients is that we oversew the intercostal arteries. I do not know any safe method to reattach the lower intercostal arteries into the graft in the acutely dissected aorta without the risk of catastrophic bleeding. DR WILLIAM A. BAUMGARTNER (Baltimore, MD): That is a very nice presentation, Dr Safi. I have one question regarding the neurologic injuries, because this seems to be the major stumbling block in this type of operation. Of the group of patients in whom you used retrograde cerebral perfusion for
protection, which included the majority of patients, is there a decrease in neurologic injury? DR SAFI: This is a very good question. But I think that we need a larger series to answer the question correctly. Because of the number of patients, retrograde cerebral perfusion did appear to be a protective agent. In our previous publication regarding the chronic or medial degenerative aortic aneurysm, we found there is a decreased incidence of stroke in patients older than 70 years, but not less than 70 years. DR KIT V. AROM (Minneapolis, MN): I have one brief question. If there is a very small transverse tear above the aortic valve, about 2 cm in length, would you still use deep hypothermia and circulatory arrest? DR SAFI: It all depends on the clinical presentation of the patient. If there is acute type A (or type I DeBakey) dissection, we do use profound hypothermia and circulatory arrest because we do not know the extent of the dissection and second, I like to see the inside of the transverse arch to determine whether it is free from a reentry point. Sometimes we replace the hemiarch thus excluding the reentry point in the transverse arch. I also found that clamping can cause injury. There are some surgeons who like to clamp. However, as an example of why I do not, 1 patient referred to me had had replacement of the ascending aorta and root using the clamp technique. By the time they released the clamp the flow went into the false lumen and he ended up with no blood pressure in the right arm and no flow to the right carotid artery and he had a stroke. We remedied things as best we could by replacing the transverse arch, although this is another thing I try to avoid. Replacing the arch increases the risk of death and neurologic deficit. In this series we replaced the arch as an elephant trunk in 1 patient, but the procedure takes too long, and again, I would rather avoid it. DR AROM: So your practice today is that you do all of the procedures under deep hypothermia and circulatory arrest and rarely cross-clamp the aorta? DR SAFI: Yes, this is correct. Once the patient is seen in the emergency room and has gone to the surgical intensive care unit, if the patient is stable, then we perform transesophageal echocardiography to establish the diagnosis (type A or B). If the patient has type A aortic dissection then after insertion of the arterial line and determining blood type we move the patient to the operating room and we repair the dissection of the ascending aorta. Following this policy the mortality and stroke rate has been very good. If we miss that window, and the patient is unstable (ie, hypotensive or cardiac tamponade), then the mortality and the stroke rate are going to be high.