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Ann Thorac Surg 1997;64:639-650
© 1997 The Society of Thoracic Surgeons

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Original Article: Cardiovascular

Impact of Previous Thoracic Aneurysm Repair on Thoracoabdominal Aortic Aneurysm Management

Department of Surgery, Baylor College of Medicine, The Methodist Hospital, Houston, Texas

	Abstract

Top Footnotes Abstract Introduction Patients and Methods Results Comment References

 
Background. The purpose of this study was to determine the impact of previous thoracic aortic aneurysm repair (PTAR) on subsequent thoracoabdominal aortic aneurysm operations.

Methods. A retrospective review of 723 thoracoabdominal aortic aneurysm repairs over a 10-year period facilitated comparison of 179 patients (24.8%) with PTAR and 544 patients (75.2%) without PTAR.

Results. Patients with PTAR had more chronic dissections and extensive thoracoabdominal aortic aneurysms, and consequently required longer clamp and ischemic times and more intraoperative transfusions. Patients without PTAR were older, had more preoperative comorbid disease, and had more symptomatic or ruptured aneurysms. Although differences did not reach statistical significance, patients without PTAR tended toward increased in-hospital mortality (8.5% versus 4.5%; p = 0.078) and postoperative paraplegia/paraparesis rates (6.5% versus 2.8%; p = 0.069). More patients without PTAR had cardiac complications (11.3% versus 5.6%; p = 0.028) and required chronic hemodialysis (5.9% versus 1.1%; p = 0.009).

Conclusions. The presence of a PTAR did not adversely affect the outcome of thoracoabdominal aortic aneurysm repair. After thoracic aortic aneurysm repair, life-long radiologic surveillance and early surgical treatment are justified.

	Introduction

Top Footnotes Abstract Introduction Patients and Methods Results Comment References

 
See also page 650.

Patients with thoracic aortic aneurysms are at substantial risk for the development of multiple aortic aneurysms. In patients who originally presented with aortic aneurysms involving the ascending, transverse arch, or descending segments, Crawford and Cohen [1] reported that multiple aneurysms developed in 59.6%; in contrast, multiple aneurysms developed in only 12% of patients who initially had abdominal aortic aneurysms. New or recurrent aortic aneurysms accounted for 36 of the 130 (27.7%) thoracic aortic reoperations in the 120 patients reported by Carrel and associates [2]. Natural history studies have demonstrated that in at least 25% of patients initially presenting with a thoracic aortic aneurysm a separate aneurysm develops involving the abdominal aorta [3]. Pressler and McNamara [4] found separate abdominal aortic aneurysms in 26 of 90 (28.9%) patients with nondissecting thoracic aortic aneurysms; 4 of these 26 patients (15.4%) died of ruptured abdominal aortic aneurysms.

Patients with multilevel or recurrent aortic aneurysmal disease represent a complex cardiovascular therapeutic challenge. Rupture of a second aneurysm is a frequent cause of death after a successful aortic aneurysm repair [5, 6]. Although surgical treatment is necessary to prevent rupture and improve survival in patients with multiple aneurysms, data regarding the risks associated with multiple aortic operations have been conflicting.

Most data available in the literature concerning surgical treatment of recurrent and multiple aneurysms present the results of more proximal aortic operations after infrarenal abdominal aortic aneurysm repair [7, 8]. Previous reports of small series have described early mortality rates ranging from 25% to 28.6% [9–11]. Recently, we reported on subsequent proximal aortic aneurysm repair in 123 patients with previous infrarenal abdominal aortic aneurysm repair and found that both emergency and elective proximal repairs can be performed in such patients with acceptably low levels of mortality (12.2%, overall) and morbidity [12].

Reports addressing thoracoabdominal aortic aneurysm (TAAA) repair in patients with previous thoracic aortic aneurysm repair (PTAR) are limited. Gloviczki and colleagues [13] reviewed The Mayo Clinic experience with 102 consecutive patients with multiple aortic aneurysms who underwent 201 aortic reconstructions. The initial operations involved the thoracic aorta in 65 patients (63.7%) and were isolated to the lower abdominal aorta in 37 (36.3%); TAAA repair was performed as a subsequent procedure in 37 patients (36.3%). The investigators found that overall operative mortality increased with the ordinal number of procedures: 4.4% for the first operation, 10.4% for the second, and 33.3% for the third. Of the 1,509 patients in Crawford's complete TAAA experience, reported by Svensson and colleagues [14], 181 (12%) had a previous proximal aortic operation; compared to the patients without PTAR, this group was characterized by a lower 30-day mortality rate (4% with PTAR versus 9% without PTAR; p = 0.025) and a lower incidence of postoperative renal failure (8% versus 19%; p = 0.0004), but an increased incidence of paraplegia (20% versus 15%; p = 0.051).

The reported outcomes after surgical repair of multilevel and recurrent aortic aneurysms vary widely. Furthermore, specific information regarding the results of TAAA repair after PTAR are limited. Therefore, the safety of TAAA repair in patients with PTAR remains uncertain. To clarify these issues, we retrospectively evaluated our 10-year experience with TAAA repair to compare results in patients with and without PTAR. The purpose of this study was to evaluate the impact of PTAR on subsequent TAAA operations.

	Patients and Methods

Top Footnotes Abstract Introduction Patients and Methods Results Comment References

 
Between January 11, 1986, and March 19, 1996, 723 consecutive patients underwent surgical reconstruction for TAAAs by the senior author (J.S.C.). Records from a data base established on each patient at the time of admission were evaluated retrospectively. There were 420 men (58.1%) and 303 women (41.9%). Patient ages ranged from 21 to 88 years (median, 68 years). There were 46 patients (6.4%) with Marfan's syndrome. Acute aortic dissection was present in 25 patients (3.4%), chronic dissection in 156 (21.6%), and nondissecting aneurysms in 542 (75%). The TAAAs were symptomatic in 490 patients (67.8%); 55 of these were ruptured. There were 233 asymptomatic patients (32.2%) in whom the aneurysm was discovered during routine check-up or during evaluation of an unrelated clinical problem. On the basis of classification by Crawford and associates [15] of TAAA extent, 254 (35.1%) aneurysms were extent I, 209 (28.9%) were extent II, 120 (16.6%) were extent III, and 140 (19.4%) were extent IV.

Of the 723 patients, 298 (41.2%) had previously undergone a total of 342 previous aortic aneurysm operations, with 44 patients (6.1%) having had multiple previous aortic aneurysm procedures. To evaluate the impact of PTAR on the results of TAAA replacement, patients were divided into two groups according to the presence or absence of a PTAR; there were 179 patients (24.8%) with PTAR and 544 patients (75.2%) without PTAR. The presenting characteristics of the patients in the two groups are detailed in Table 1. The previous thoracic aortic aneurysm repairs included 104 (58.1%) prior ascending aortic aneurysm repairs; 30 (16.8%) descending thoracic aortic repairs (Fig 1); 22 (12.3%) thoracoabdominal repairs; 12 (6.7%) ascending and descending thoracic aortic repairs (Figs 2, 3); 7 (3.9%) ascending and thoracoabdominal repairs; and 4 (2.2%) descending and thoracoabdominal repairs. Among the 179 patients undergoing TAAA repair after PTAR, there were 17 (9.5%) with elephant trunk completions [16]; 10 of these patients (58.8%) had Crawford extent I TAAAs and 7 (41.2%) had extent II aneurysms.

View larger version (77K): [in this window] [in a new window]   Fig 1. . (A) Preoperative drawing and aortogram demonstrating previous proximal descending thoracic tube graft replacement and aortic bifurcation graft replacement in a patient in whom an aneurysm of the intervening thoracoabdominal aorta later developed secondary to chronic fusiform medial degeneration. (B) Postoperative drawing and aortogram after graft replacement of the thoracoabdominal aortic aneurysm with island reattachment of the celiac axis, superior mesenteric, and right renal arteries, and separate reattachment of the left renal artery.

View larger version (75K): [in this window] [in a new window]   Fig 2. . (A) Preoperative drawing and aortogram demonstrating previous composite valve graft replacement of the ascending aorta and descending thoracic aortic tube graft replacement in a patient with Marfan's syndrome in whom an extent IV thoracoabdominal aortic aneurysm subsequently developed secondary to localized dissection. (B) Postoperative drawing and aortogram after thoracoabdominal graft replacement with reattachment of the celiac, superior mesenteric, and both renal arteries.

View larger version (87K): [in this window] [in a new window]   Fig 3. . (A) Preoperative drawing and aortogram demonstrating previous ascending, descending, and aortic bifurcation graft replacements in a patient in whom an intervening thoracoabdominal aneurysm developed. (B) Postoperative drawing and aortogram after thoracoabdominal aortic aneurysm replacement with preservation of intercostal arteries, island reattachment of the celiac axis, superior mesenteric artery, and right renal artery, and separate tube graft bypass to the left renal artery.

In the elective setting, pulmonary function testing and transthoracic echocardiography were routinely used before TAAA repair. Patients with a forced expiratory volume in 1 second of more than 1 L and an arterial carbon dioxide tension at less than 45 mm Hg were considered to have adequate pulmonary reserve to tolerate operation. In patients with borderline pulmonary reserve, preoperative optimization—including cessation of smoking, bronchodilator therapy, weight loss, and an exercise program—was attempted. Coronary angiography was performed in patients with either angina or an ejection fraction less than 0.30; those with significant coronary artery occlusive disease underwent myocardial revascularization before aneurysm repair.

Our methods for resection and graft replacement of TAAAs have been recently described in detail [18–21]. All operations were performed through a left thoracoabdominal incision with selective right lung ventilation. The surgical techniques used were similar in patients with and without PTAR; however, some additional precautions were undertaken in patients with PTAR, especially in those who had had a previous posterolateral thoracotomy or thoracoabdominal incision. A deliberate effort was made to enter the thorax through a different intercostal space than used in the previous repair. To decrease potential bleeding from raw surfaces, the division of pleural adhesions was limited to those essential for obtaining the necessary exposure to carry out the planned reconstruction. Excessive pulmonary trauma and parenchymal hemorrhage were prevented by minimizing lung retraction during anticoagulation. Dissection around the aneurysm was also limited in an attempt to reduce hemorrhage and avoid injuries to adjacent structures.

Permissive mild hypothermia was used routinely. Centrifugal pump bypass from the left atrium to the femoral artery or distal descending aorta was selectively used for distal perfusion in patients with extensive aneurysms (Crawford extents I and II) or aortic dissection. Aneurysm resection was performed with simple aortic cross-clamping in 574 patients (79.4%) and atriodistal bypass in 149 (20.6%). Direct cold perfusion of the renal arteries with Ringer's lactate solution at 4°C was used in 286 (39.6%) patients and renal endarterectomy or renal artery bypass were concomitantly performed in 107 (14.8%) patients. Celiac and superior mesenteric endarterectomies were required in 17 patients (2.4%) and 15 patients (2.1%), respectively. The mean aortic clamp time was 43.5 ± 17.6 minutes and the mean visceral ischemic time was 40.5 ± 15.5 minutes.

Statistical Analysis
Preoperative variables evaluated included sex, age, aneurysm cause and extent, symptoms, rupture, and prevalence of major risk factors. Intraoperative variables included surgical technique (single cross-clamping or bypass), splenectomy, blood product requirements (red blood cells, blood from the cell-saving device, fresh frozen plasma, platelets, cryoprecipitate), concurrent aneurysm operation, aortic clamp time, visceral ischemic time, and intraoperative mortality. Postoperative variables included incidence of paraparesis and paraplegia (lower limb weakness and paralysis, respectively), stroke, reoperation for bleeding, renal failure (need for hemodialysis or creatinine >3.0 mg/dL), pulmonary complications (ventilator support for >48 hours or pneumonia), cardiac complications (myocardial infarction, inotropic support >48 hours, or dysrhythmias), number of days in intensive care, and 30-day and in-hospital mortality rates.

The statistical analysis was performed using the SAS (release 6.10; SAS Institute, Inc, Cary, NC) and SPSS (release 6.1.3; SPSS, Inc, Chicago, IL) systems for Windows. The preoperative, intraoperative, and postoperative variables were compared between the PTAR and no PTAR groups using univariate analysis—Pearson's ² test, Fisher exact test (two-tailed), or Student's t test—and multivariate stepwise logistic regression. Associations were considered statistically significant when the p value was less than 0.05. Data for aortic clamp and visceral ischemic times are presented as the mean ± one standard deviation.

	Results

Top Footnotes Abstract Introduction Patients and Methods Results Comment References

 
The overall 30-day and in-hospital mortality rates for the 723 patients treated with TAAA replacement were 5.1% (37 patients) and 7.5% (54 patients), respectively. There were three intraoperative deaths (0.4%), two of cardiac failure (intraoperative myocardial infarction) and one of hemorrhage secondary to rupture; these 3 patients were excluded when calculating and analyzing morbidity rates. The incidence of paraplegia or paraparesis was 5.6% (40 patients). Only 13 patients (1.8%) were returned to the operating room for postoperative bleeding. Postoperative cardiac complications developed in 70 patients (9.7%), stroke in 13 patients (1.8%), pulmonary complications in 268 patients (37.2%), and renal failure in 94 patients (13%), 48 of which required temporary or chronic hemodialysis.

The preoperative variables in patients with and without PTAR are presented in Table 1. Patients without PTAR were significantly older and had an increased prevalence of preoperative renal failure, atherosclerotic coronary artery disease, renal arterial occlusive disease, and cerebrovascular disease. Chronic obstructive pulmonary disease was also more common in patients without PTAR, although this difference did not reach statistical significance. Although patients with PTAR were more likely to have extent II TAAAs and chronic dissection, patients without PTAR were more likely to present with symptomatic or ruptured aneurysms. Of the 46 patients with Marfan's syndrome, 32 (69.9%) had PTAR.

With regard to intraoperative techniques (Table 2), the use of simple cross-clamping versus atriodistal bypass did not differ significantly between the groups. The mean total aortic clamp time and mean visceral ischemic time were both longer in patients with PTAR. Patients with PTAR also exhibited greater transfusion requirements during TAAA repair, receiving larger amounts of blood from the cell-saving device, packed red blood cells, fresh frozen plasma, platelets, and cryoprecipitate.

	Comment

Top Footnotes Abstract Introduction Patients and Methods Results Comment References

In contrast to the patients with PTAR, those without PTAR were older and had significantly more comorbid disease. Rupture was also more common in the latter group. Despite having less extensive aneurysms and shorter clamp and ischemic times, the mortality and paraplegia/paraparesis rates in patients without PTAR tended to be higher, with differences that approached statistical significance. Because of the increased prevalence of atherosclerotic disease involving the coronary and renal arteries in the patients without PTAR, their higher incidences of cardiac complications and need for prolonged hemodialysis are not surprising.

An intrinsic selection bias for the PTAR group may have contributed to their lower morbidity and mortality rates. Careful medical follow-up after the initial operation may have resulted in risk factor prevention and, therefore, a better overall preoperative condition in these patients. In addition, because some patients who would have needed future TAAA repair did not survive their initial aortic operation, several patients with significant comorbid disease may have been automatically eliminated from the PTAR group. Therefore, by surviving the previous operation, the group of patients with PTAR may have been inherently more likely to tolerate the TAAA repair, compared with those who had not undergone the "stress test" of a previous thoracic aortic operation.

Patients with PTAR received significantly larger amounts of blood product transfusion intraoperatively. The low incidence of return to the operating room for postoperative bleeding after aortic reoperations, however, suggests a justification for obtaining adequate hemostasis intraoperatively, even at the expense of larger blood product transfusion requirements. Despite the volume associated with such transfusions, there was no significant difference in postoperative pulmonary failure between the groups with and without PTAR. Meticulous surgical technique, selective use of blood products, avoidance of unnecessary dissection, and use of impermeable graft materials all contribute to perioperative hemostasis and substantially affect the overall results.

The relative increase in dissection as a cause of TAAA development in patients with PTAR did not affect either mortality or the development of postoperative paraplegia or paraparesis in this series. This is consistent with our recent analysis of aortic dissection [23], which demonstrated that chronic dissection should no longer be considered a risk factor regarding the development of postoperative paraplegia/paraparesis in patients undergoing TAAA repair.

Current hypotheses regarding the cause of aortic aneurysms support the notion of an ongoing generalized disease process that can involve any combination of aortic segments over time [17, 24]. This propensity for multifocal aortic aneurysmal disease has prompted recommendations regarding meticulous lifetime radiologic surveillance after an initial aortic aneurysm repair [8, 11, 13]. We concur with these researchers and recommend at least biannual computed tomography or magnetic resonance imaging scanning of the chest and abdomen for follow-up in these patients. The fact that fewer patients in the PTAR group presented with symptomatic or ruptured aneurysms may be related to their postoperative surveillance.

In conclusion, the presence of a PTAR did not adversely affect the outcome of TAAA repair. Rather, the patients with PTAR fared well compared with those without PTAR, especially when considering the more extensive TAAA repairs undertaken in the former group. The primary explanation for this difference lies in the higher prevalence of comorbid disease in the patients without PTAR. Thus, an accurate assessment of a patient's physiologic reserve remains the primary factor when determining the risks of surgical intervention. Although PTAR has important implications for the technical aspects of subsequent TAAA operation, it should not affect the decision to proceed with an otherwise indicated operation. Because rupture of a concomitant or newly developed aneurysm is a frequent cause of death in patients with thoracic aortic aneurysms, life-long follow-up and early appropriate surgical treatment are justified.

	Footnotes

Top Footnotes Abstract Introduction Patients and Methods Results Comment References

Address reprint requests to Dr Coselli, 6560 Fannin, #1144, Houston, TX 77030.

	References

Top Footnotes Abstract Introduction Patients and Methods Results Comment References

 

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This Article Abstract Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): Joseph S. Coselli Scott A. LeMaire Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Coselli, J. S. Articles by LeMaire, S. A. Search for Related Content PubMed PubMed Citation Articles by Coselli, J. S. Articles by LeMaire, S. A. Related Collections Related Article