Surgical management of acute dissections involving the ascending aorta

J

THORAC CARDIOVASC SURG

82:576-584, 1981

Surgical management of acute dissections involving the ascending aorta Early and late results in 38 patients Thirty-eight patients (32 men and six women, mean age 48.1 years) were operated upon for acute dissection involving the ascending aorta. The surgical procedure included multiple peripheral arterial cannulations, resection of the initial intimal tear if found (35 cases), and obliteration of the false channel by double cuffing with Teflon (~l the two layers of the dissecting process proximally and distally. When present (29 cases), aortic regurgitation was usually (21 cases) managed by conservative remodeling of the aortic anulus; 34 prosthetic replacements of the ascending aorta and four replacements of the arch were achieved. The operative mortality was 7.9% (3/38) and the overall hospital mortality was 23.7% (9/38). Nonfatal complications occurred in 11 patients (29%). There were three late deaths (10.3%). Mean follow-up was 3.4 years (2 months to 8 years, 8 months). Twenty-three (88.5%) of the 26 patients were asymptomatic. Contrast tomodensitometry was performed in 14 patients: In type fl (two patients), the aorta was normal; in type 1 (12 patients), residual abnormalities were noted: patency of the false channel (10 cases), aneurysmal dilatation (seven cases), and reduction 4 the true lumen by the false channel (four cases). These results emphasize the need for scrupulous long-term follow-up in surgically treated aortic dissections.

Jean-Paul Cachera, M.D., Pascal R. Vouhe, M.D., Daniel Y. Loisance, M.D., Paul Menu, M.D., Henri Poulain, M.D., Gerard Bloch, M.D., Norbert Vasile, M.D., Philippe Aubry, M.D., and Jean-Jacques Galey, M.D., Creteil, France

Acute aortic dissection involving the ascending aorta is a catastrophic, highly lethal event. In the past, management of this disease has been controversial. Medical therapy provides less than satisfactory results, while refinements in operative technique have improved increasingly the surgical results. Thus a trend toward aggressive early surgical management has developed. I However, operative repair must be considered as palliative, because usually the entire diseased aorta cannot be replaced. More information concerning the longterm prognosis of surgically treated patients is still mandatory. Since 1971, a uniform surgical approach has been used in our department. 2 The early and late results in 38 consecutive patients are reported here. From the Department of Cardiovascular Surgery, Hopital HenriMondor, Creteil, France. Received for publication Dec. 31, 1980. Accepted for publication March 3, 1981. Address for reprints: J. P. Cachera, M.D., Service de Chirurgie Cardiaque, Hopital Henri-Mondor, 51, bId de Lattre de Tassigny 94010, Creteil Cedex, France.

576

Patients Thirty-eight consecutive patients (32 men and six women), aged 31 to 69 years (mean age 48.1 years), were operated upon for acute dissection involving the ascending aorta. The operation was undertaken less than 2 days after the onset of the disease (acute dissection) in 27 patients (71 %) and between 2 and 14 days after the initial manifestation (subacute dissection) in 11 (29%). All patients were operated upon in emergency. Hypotensive drugs were given to patients with subacute dissection, the surgical decision being urged by the onset of progressive symptoms, i.e., pericardial effusion, increase in the diastolic murmur, recurrence of chest or lumbar pain, or abolition of a peripheral pulse. Twenty-seven patients (71 %) had a history of arterial hypertension, and five (13%) had Marfan's syndrome. Two of the Marfan patients previously had undergone a valvular replacement for aortic (one case) or mitral (one case) regurgitation. Typical clinical manifestations of acute aortic dis-

0022-5223/81/100576+09$00.90/0 © 1981 The C. V. Mosby Co.

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October, 1981

section were noted in most cases: unbearable thoracic pain shifting to the interscapular or lumbar areas (36 cases), discovery of a new diastolic murmur (26 cases), and loss of one or more peripheral pulses (13 cases). In 17 patients (45%), major complicating factors were present: intrapericardial hemorrhage (15 cases), shock (five cases), myocardial ischemia (three cases), acute cerebrovascular accident (six cases), and acute renal failure (three cases). The diagnosis of dissection involving the ascending aorta was confirmed by an aortogram performed in the emergency room while the operating room was being prepared. The anatomic features (extension of the dissection, location of the intimal tear), usually suspected on the arteriogram, were confirmed during the operation. The dissection was limited to the ascending aorta (DeBakey type II) in seven patients (18%). In the remaining 31, the dissecting process extended from the ascending aorta into the transverse arch and beyond (DeBakey type I); the initial intimal tear was located in the ascending aorta in 24 patients and in the arch in four; in three patients, the tear was not found at operation either in the ascending aorta or in the arch and was presumed to be located in the descending aorta. Aortic regurgitation was present in 29 patients (76%); in 21 there was a marked dilatation of the aortic anulus with loss of support of the aortic valve but without lesions of the leaflets, and in eight the aortic leaflets were diseased-perforation (six cases) and degeneration of valve tissue (two cases). Operative technique Surgical repair was performed with cardiopulmonary bypass and systemic hypothermia (250 C). During aortic cross-clamping, myocardial protection was obtained by intermittent profound topical cooling. A femoral artery was used for arterial inflow; when aortic repair required clamping of the brachiocephalic vessels, the right axillary artery, the left carotid artery, or both arteries were cannulated as well. When intrapericardial rupture was suspected, the femoral artery and vein were cannulated prior to sternotomy and circulatory assistance was started if needed (Fig. 1). Mean time of cardiopulmonary bypass was 140 minutes (85 to 235 minutes), and mean time of aortic cross-clamping was 100 minutes (57 to 160 minutes). The segment of aorta, containing the intimal tear if exposed, was resected and replaced with a preclotted woven Dacron prosthesis. When the intimal tear was located in the aortic. arch (four cases), the aortic replacement involved the ascending aorta and the arch. When the initial tear was not found despite careful

pump

!fA

fl(

\~

•

'!l

\ \i.

Fig. 1. Technique of cardiopulmonary bypass. A femoral artery was usually used for arterial inflow. Multiple arterial lines were prepared for cannulation of the brachiocephalic vessels if needed. examination of the proximal aorta (three cases), the ascending aorta alone was resected. After completion of the resection, the proximal and distal aortic stumps were oversewn by the following technique: The two aortic layers were approximated with interrupted mattress suture buttressed on one outer and one inner band of Teflon felt. At the proximal site, the suture was placed as close as possible to the aortic anulus and the

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Fig. 2. Mechanism of aortic regurgitation. In most cases (21129), aortic insufficiency was due to dilatation of the

anulus with loss of commissural support of the leaflets. coronary ostia so as to remodel the aortic anulus and compensate for the lost commissural support of the aortic valve. Thus aortic regurgitation usually was corrected. Only in the case of lesions of the aortic leaflets was valve replacement performed (eight cases, 21%), (Figs. 2 and 3). A tubular Dacron prosthesis then was secured to the two reconstructed stumps with a continuous suture (Figs. 4 and 5).

Results Early results (30 days). The overall hospital mortality was 23.7% (9/38). Three deaths (7.9%) occurred in the operating room. Two patients could not be weaned from cardiopulmonary bypass because of extension of the dissecting process into the left main coronary artery (one patient) and acute myocardial infarction resulting from unrecognized stenosis of the left anterior descending artery (one patient). One patient died of massive bleeding during reoperation for early distal redissection. Six patients (15.8%) died during the postoperative period. The causes of death are listed in Table I. Four early deaths were attributed to cardiac causes, three to neurologic complications, one to hemorrhage, and one to sepsis. Two factors were associated with a higher mortality: acute evolution versus subacute evolution (33% or 9/27

Fig. 3. Conservative management of aortic regurgitanon. Adequate calibration of the two proximal strips of Teflon felt allowed remodeling of the anulus and repair of the loss of commissural support. versus 0% or 0/ II, P - 0.08) and replacement of the aortic arch versus replacement of the ascending aorta (100% or 4/4 versus 15% or 5/34, P < 0.01). On the other hand, the presence of one or more preoperative complications (cardiac tamponade, shock, cerebrovascular accident, renal failure, or myocardial ischemia) did not correlate with operative risk (23.5% or 4/17 versus 24% or 5/21, p = NS). Nonlethal complications were frequent (11/29 patients, 38%) and usually multiple. A list of these complications is given in Table II. All patients recovered completely. Late results. During a 1 month closing interval, all surviving patients or their physicians were contacted. Follow-up periods extended from 2 months to 8 years, 8 months (mean 3.4 years). Survival rate was studied by actuarial analysis. 3 Late survival. Three late deaths occurred (10.3% of survivors). Two patients with Marfan's syndrome died of congestive heart failure 6 months and 7 months postoperatively. The third patient died of acute rupture of an aneurysm of the abdominal aorta 8 years, 6 months

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Fig. 4. The two aortic stumps were reconstructed by double internal and external cuffing. The resected segment of aorta was replaced with a Dacron prosthesis.

after the initial procedure. Actuarial survival (±SD) for the entire population of 38 patients was 70.7% ± 7.4% at 5 years. Late reoperation. Two patients (6.9% of the survivors) subsequently required reoperation, one for aortic valve replacement (aortic regurgitation) 6 months postoperatively and the other for rupture of an aneurysm of the abdominal aorta 6 years, 4 months postoperatively. Both patients survived the reoperation. Late functional status. Twenty-three of the 26 survivors (88.5%) have been free of symptoms. Three patients complained of recurrent thoracic and lumbar pain, judged to be due to redissection, 6 months, 8 months, and 24 months postoperatively. Reoperation was not mandatory. At last follow-up examination, all patients were in New York Heart Assocation Class I; 73% (19/26) required therapy for hypotension, but none of the survivors had congestive heart failure or significant aortic regurgitation. Late anatomic results. Contrast tomodensitometry (angioscan) was performed in 14 patients (54% of survivors). Mean follow-up was 4 years (6 months to 8 years, 8 months). In two asymptomatic patients with type II dissection, the thoracoabdominal aorta seemed to be normal 39 months and 60 months postoperatively. In contrast, in all 12 patients with type I dissection, residual abnormalities of the aorta were noted whether the patients were symptomatic (two patients) or not (10 patients) (Table III). The false channel of the dissecting process was obvious in all cases, either thrombosed or patent. In two patients, the whole false lumen was ob-

Fig. 5. a, Replacement of the ascending aorta (N = 30). b, Replacement of the ascending aorta extending to the concavity of the arch (N = 4). c, Subtotal replacement of the aortic arch (N = 3). d, Subtotal replacement of the thoracoabdominal aorta (N = 1).

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Table I. Causes of early deaths Patients

~

No. Intraoperati ve deaths Acute heart failure Hemorrhage Postoperative deaths Cardiac complication Myocardial infarction Arrhythmia Neurologic complication (+renal failure, 2) Sepsis

3

7.9

6

15.8

9

23.7

2 I 2

3 I

Overall hospital mortality

Table II. Postoperative morbidity in 11 patients (38% of survivors) No. of patients Cardiac complication Myocardial infarction Low cardiac output Acute renal failure Neurologic complication Pulmonary insufficiency Reoperation for hemorrhage

5 2 3

5 6 2 3

literated, and in five, only one segment of the false channel was thrombosed. A patent false lumen was present in 10 patients; this residual dissection extended from the aortic arch to the whole aorta in five patients and involved only a segment of the thoracoabdominal aorta in another five. Aneurysmal enlargement of the thoracic aorta was noted in seven patients. In four, the true lumen of the thoracic aorta was markedly reduced by the clotted false channel. Thus angioscan anomalies of the aorta in type I dissection were multiple and often associated in the same patient (Figs. 6 to 9). Discussion The early mortality is very high in patients treated medically for an acute dissection involving the ascending aorta.v " Thus it is generally agreed that early emergency surgical management is advisable in such patients. 1, 5, 9-12 The surgical treatment fulfills three main goals: (1) replacement of the ascending aorta in order to prevent intrapericardial rupture and cardiac tamponade; (2) correction of aortic regurgitation, if present; and (3) resection of the intimal tear, if possible. A tear found during exploration of the proximal aorta should be resected to lessen the likelihood of subsequent redissection.!

Otherwise, if not found, the intimal tear must be neglected. No statistically significant correlation could be documented between resection or nonresection of the tear and operative mortality, late functional status, and late mortality. I Thus we believe that the main goal in the surgical management of acute aortic dissection remains the prevention of the fatal intrapericardial rupture by resecting the ascending aorta. Initial attempts at surgical repair were very disappointing; operative mortality and morbidity rates were dissuasive (50% or more). Retrospective analysis of the deaths and poor results proved the causes of surgical failure to be numerous. Among them, three main causes were encountered: (1) arterial inflow via the false lumen with subsequent neurologic and visceral complications, (2) intractable bleeding at the anastomotic sites, and (3) early redissection distal to the graft. After the unsatisfactory early surgical results were studied, several technical modifications were developed in the early 1970s, which afforded consistent improvement in the surgical results. 2 These modifications included several improvements in the operative procedure: I. A system of cannulating multiple peripheral arteries was designed to provide adequate perfusion in all circumstances. In most cases, only femoral perfusion is needed. Sometimes the dissecting process obviates the use of the femoral approach, in which case an axillary artery, usually the left one, is perfused. Moreover, every time the brachiocephalic vessels are occluded during aortic repair, the right axillary artery and sometimes the left carotid artery must be cannulated. In order to allow multiple cannulas, the operative field is widely prepared so that there is access to both femoral and axillary arteries, and multiple arterial lines are readied. 2. Double internal and external cuffing with large strips of Teflon felt of the two layers of the aortic wall offers safe obliteration of the false channel and decreases the risk of massive bleeding at the anastomotic sites. 3. Aortic regurgitation is managed conservatively by remodeling the aortic anulus with a circumferential strip of Teflon calibrated to adequate size. This avoids valvular replacement and subsequent anticoagulant therapy. 13. 14 These technical improvements, in our experience, have reduced the early mortality to around 20%. These results allow aggressive and early surgical management in acute dissections involving the ascending aorta, a view now usually accepted. I, 5, 9. II, 15, 16 Only complications that predictably preclude operative success con-

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Fig. 6. Angioscan of aortic arch, 65 months postoperatively, shows thrombosis of the false channel (white arrow).

Table III. Fate of the false lumen in 12 patients with acute dissection type I (according to data provided by late postoperative contrast tomodensitometry) Patient I

2 3

4 5 6 7 8 9

10 II

12

Followup (rna)

60

65 56 57 104 14 71 6 52 55 60 71

Fate offalse lumen Aortic arch Thrombotic Thrombotic Patent Patent Patent Patent, aneurysmal Patent, aneurysmal Patent, aneurysmal Thrombotic, aneurysmal Thrombotic, aneurysmal Thrombotic, aneurysmal Thrombotic, aneurysmal

I

Descending aorta

I

Thrombotic Thrombotic Patent Patent Patent Patent Patent, aneurysmal Thrombotic, aneurysmal Patent, aneurysmal Thrombotic, aneurysmal Patent, aneurysmal Thrombotic, aneurysmal

Abdominal aorta Thrombotic Thrombotic Patent Patent Patent Patent Patent Thrombotic Patent Patent Patent Patent

Legend: Thrombotic, Thrombosis of the false lumen. Patent, Patent false lumen. Aneurysmal, Aneurysmal dilatation of the aorta.

stitute contraindications to operation (massive stroke, bowel infarction, and cardiogenic shock), Despite multiple refinements in the operative management of aortic dissections, postoperative morbidity and mortality remain substantial. Two main problems impair the postoperative course of the patients: neurologic complications and acute renal failure. Both are frequent even before the operation. In most cases renal and cerebral complications are related to the diffuse dissecting process involving renal and cerebral arteries, provoking ischemic areas in the kidneys or in the brain; injuries to the lumbar branches of the descending aorta are likely to provoke paraplegia. Such conditions should encourage surgeons to operate upon aortic dissections at a very early stage, since ischemia in vital

areas can be reversed by adequate surgical management occurring during the first hours of the process. Neurologic symptoms were reversible in six of nine patients, and renal failure, palliated with peritoneal dialysis, regressed in five of seven patients. Published data concerning long-term results of surgically treated aortic dissections are now available.': 5. 12, 17. 18 Long-term mortality is low, I, 5, II and the functional status of the survivors usually is satisfactory. 1, 11 However, the long-term anatomic evolution is possibly more precarious. Adequate recovery implies thrombosis of the false lumen. Angiographic and autopsy data have shown the likelihood of thrombosis. 17, 19 At least three conditions are needed to provide clotting of the false channel:

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Fig. 7. Angioscan taken 56 months postoperatively shows persistence of a patent dissection of the aortic arch.

Fig. 8. Angioscan taken 6 months postoperatively shows patent dissection of the aortic arch and thrombosis of the false channel (f'.c.) of the upper descending aorta, with aneurysmal dilatation.

Fig. 9. Angioscan taken 52 months postoperatively shows thrombosis of the false channel (f.c.) of the aortic arch with reduction of the true lumen and aneurysmal dilatation of the arch.

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resection or spontaneous closure of the initial intimal tear, correct obliteration of the false lumen at the site of distal anastomosis, and absence of additional fenestrations distal to the graft. In fact, according to our findings and those of others, complete thrombosis of the false channel following operation is unusual.F: 18 In most cases, there is persistence of a patent doublechanneled aorta whether the patients are symptomatic or not.': 17. 18 The patent chronic dissection is frequently associated with an aneurysmal dilatation of the aorta.": 18 The persistence of a patent false channel appears to be dependent on the presence of additional intimal tears distal to the surgical repair." The longterm prognosis of such anatomic disorders is incompletely understood. In some cases, blood flow to major organs is supplied through the false channel.P: 18 On the other hand, there is some evidence that persistence of a patent dissection is associated with a higher late mortality'? and a more frequent need for reoperation': 17; this may be particularly true when an aneurysmal dilatation of the aorta is present. We consider that late development of abdominal aneurysms necessitates reoperation without any delay. Among our two patients having such aneurysms, one died of rupture because reoperation had been delayed. Development of symptoms (recurrent pain, new neurologic deficit) or documented progressive enlargement of the aorta mandate re-exploration and reoperation.' Long-term prognosis for patients with typical Marfan's syndrome must be considered poor, since other intracardiac abnormalities as well as the aortic dissection are usually present. Rupture of chordae tendineae of the mitral valve and rupture of the aortic cusp may occur after repair of the dissection. Among our five patients with Marfan's syndrome, two died of intractable heart failure, owing to rupture of chordae tendineae in one case and to an unknown cause in the second. The high rate of residual anatomic abnormalities of the aorta emphasizes the necessity of scrupulous longterm follow-up in such patients, whether they are symptomatic or not. Precise managment of hypertension is imperative, and continuing clinical and radiologic evaluation should be obtained. Contrast tornodensitometry is a noninvasive and easily reproducible technique; the fate of the false lumen and the size of the thoracic and abdominal aorta is well documented, and frequently the fate of major aortic branches is studied as well. Repeat angioscan is likely to be a very useful tool for the long-term surveillance of surgically treated aortic dissections. In summary, definitive progress in the surgical management of acute aortic dissection has been recorded

during the past 10 years. Nevertheless, despite numerous advances involving the operative techniques, the early recognition of the disease, postoperative care, and the active treatment of late complications, dissection of the whole aorta remains an exceptionally severe condition. Surgical treatment must yet be considered palliative, since the entire aorta and the main visceral vessels are involved by the dissecting process and cannot be replaced. However, satisfactory recovery has been recorded in 88% of the patients undergoing operation. Thus the main risk, i.e., death by intrapericardial rupture, was avoided by resecting the ascending aorta. The ideal goal-excision of the initial intimal tear followed by complete healing of the false channel-was reached in only a very low percentage of patients but remains the best challenge to be pursued. Early recognition of the condition; adequate topographic evaluation of the lesions by the means of angiography and tomodensitornetry; undelayed operations performed to prevent irreversible damage; and refined operative techniques should provide progressive improvement of the overall surgical results in the future.

2

3

4 5 6

7 8

9

REFERENCES Miller DC, Stinson EB, Oyer PE, Rossiter SJ, Reitz BA, Griepp RB, Shumway NE: Operative treatment of aortic dissections. Experience with 125 patients over a sixteenyear period. J THoRAc CARDIOVASC SURG 78:365-382, 1979 Cachera JP, Loisance D, Carlier M, Maillet FX, Slama R, Bouvrain Y: Progres techniques dans Ie traitement chirurgical des dissections aortiques aigues totales du type I. Arch Mal Coeur 67:125-131, 1974 Grunkemeier GL, Starr A: Actuarial analysis of surgical results. Rationale and method. Ann Thorac Surg 24: 404-408, 1977 Hirst AE Jr, Johns VS Jr, Kime SW Jr: Dissecting aneurysm of the aorta. A review of 505 cases. Medicine 37:217-279, 1958 Applebaum A, Karp RB, Kirklin JW: Ascending vs descending aortic dissections. Ann Surg 183:296-300, 1976 Harris PD, Maim JR, Bigger JT Jr: Follow-up studies of acute dissecting aortic aneurysms managed with antihypertensive agents. Circulation 35:Suppl I: 183-187, 1967 Lindsay J Jr, Hurst JW: Clinical features and prognosis in dissecting aneurysm of the aorta. A re-appraisal. Circulation 35:880-888, 1967 McFarland J, Wirleston JT, Dinsmore RE, Austen WG, Buckley MJ, Sanders CA, DeSanctis EW: The medical treatment of dissecting aortic aneurysms. N Engl J Med 286: 115-119, 1972 Dalen JE, Alpert JS, Cohn LH, Black H, Collins 11: Dis-

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section of thoracic aorta. Medical or surgical therapy? Am J Cardiol 34:803-808, 1974 Seybold-Epting W, Meyer J, Hallman GL, Cooley DA: Surgical treatment of acute dissecting aneurysms of the ascending aorta. J Cardiovasc Surg 18:43-48, 1977 Wheat MW Jr: Treatment of dissecting aneurysm of the aorta. Current status. Prog Cardiovasc Dis 16:87-101, 1973 Wolf WG, Moran JF: The evolution of medical and surgical management of acute aortic dissection. Circulation 56:503-505, 1977 Koster KJ Jr, Cohn LH, Mee RBB, Collins JJ Jr: Late results of operation for acute aortic dissection producing aortic insufficiency. Ann Thorac Surg 26:461-467, 1978 Najafi H, Dye WS, Javid M, Hunter JA, Goldin MD, Julian OC: Acute aortic regurgitation secondary to aortic dissection. Surgical management without valve replacement. Ann Thorac Surg 14:474-482, 1972

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15 Anagnostopoulos CE, Prabhakar MJS, Kittle CF: Aortic dissections and dissecting aneurysms, Am J Cardiol 30:263-273, 1972 16 Kidd IN, Reul GJ Jr, Cooley DA, Sandiford FM, Kyger ER, Wukasch DC: Surgical treatment of aneurysms of the ascending aorta. Circulation 54:Suppl 3:118-122, 1976 17 Guthaner DF, Miller DC, Silverman JF, Stinson EB, Wexler L: Fate of the false lumen following surgical repair of aortic dissections. An angiographic study. Radiology 133:1-8, 1979 18 Thomas CS, Alford WC, Burrus GR, Frist RA, Stoney WS: The effectiveness of surgical treatment of acute aortic dissection. Ann Thorac Surg 26:42-49, 1978 19 Dinsmore RE, Willerson JT, Buckley MJ: Dissecting aneurysm of the aorta. Aortographic features affecting prognosis. Radiology 105:567-572, 1972