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J Thorac Cardiovasc Surg 2008;136:1160-1166
© 2008 The American Association for Thoracic Surgery
Surgery for Acquired Cardiovascular Disease |
a Department of Cardiovascular Surgery, Saitama Medical Center, Jichi Medical University, Saitama, Japan
b Department of Cardiac Surgery, Kashiwa Hospital, Jikei University School of Medicine, Kashiwa, Japan
Received for publication October 27, 2007; revisions received February 10, 2008; accepted for publication May 20, 2008. * Address for reprints: Naoyuki Kimura, MD, Department of Cardiovascular Surgery, Saitama Medical Center, Jichi Medical University, 1-847 Amanuma-cho, Omiya, Saitama 330-0834, Japan. (Email: masashi{at}omiya.jichi.ac.jp).
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Abstract |
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 Top Abstract IntroductionPatients and MethodsResultsDiscussionConclusionsFigure E1Table E1Table E2References |
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Methods: Two hundred eighteen patients underwent emergency surgery for DeBakey type I or IIIb retrograde acute type A aortic dissection (1997–2006). Aortic arch replacement was performed in selected patients whose entry site was in or extended into the aortic arch. In-hospital mortality was 7.3% (16/218), and 193 survivors (mean age 62 years) underwent enhanced computed tomography within 1 month after the operation. These patients were divided into two groups according to the status of the false lumen, whether patent (n = 124) or thrombosed (n = 69). In each group, segment-specific aortic growth rate, distal reoperation, and late survival were examined.
Results: Growth rate was determined in 139 (72.0%) patients who underwent serial computed tomography. Average growth rate in the patent group was greater than that in the thrombosed group (aortic arch [1.1 vs –0.41 mm per year; P = .005], proximal descending aorta [1.9 vs –0.71 mm per year; P <.001], and distal descending aorta [1.3 vs –0.70 mm per year; P = .002]). However, growth was slow (<1 mmper year) in about 50% of patients in the patent group. There was no significant difference in distal reoperation or late survival between the two groups.
Conclusions: The patent false lumen influences postoperative aortic enlargement. However, with careful follow-up, a favorable prognosis is expected even for patients with a residual patent false lumen.
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Introduction |
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TopAbstractIntroductionPatients and MethodsResultsDiscussionConclusionsFigure E1Table E1Table E2References |
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the latest report from the International Registry of Acute Aortic Dissection Investigators disclosed a still high hospital mortality rate (23.9% for 682 patients with AAAD, 1996–2003).4 Prolonged surgery for patients at risk of death might increase the already high operative risk through coagulopathy, cerebral ischemia, infection, or multiorgan failure. We consider the most important goal of initial surgery for AAAD to be immediate survival; a simple and less invasive operative procedure is effective for such patients. Therefore, our surgical strategy for AAAD is based on the following: First, prompt establishment of cardiopulmonary bypass to prevent malperfusion. Second, preservation of the aortic valve whenever possible. Third, aortic arch replacement in patients whose entry site is located in or extends into the aortic arch. By following this policy, we have achieved acceptable operative outcomes for AAAD.5,6
The initial operation does not remove the entire diseased aorta, and some patients require aortic reoperation for aneurysmal dilatation of the distal aorta. The residual patent false lumen has recently been reported as a risk factor for secondary aortic enlargement.7-9 In addition, several studies have shown that a more aggressive operative approach for AAAD, such as systematic extended or total arch replacement, irrespective of the location of the entry site, might improve long-term outcomes by decreasing the incidence of residual patent false lumen.2,10-12 However, the effect of the residual patent false lumen on long-term outcomes is not fully understood. In the present study, we assessed influence of the residual patent false lumen on late aortic growth rate, distal reoperation, and late survival to evaluate the long-term effectiveness of our surgical strategy for AAAD.
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Patients and Methods |
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TopAbstractIntroductionPatients and MethodsResultsDiscussionConclusionsFigure E1Table E1Table E2References |
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We defined a patent false lumen as a false lumen that was enhanced during delayed-phase CT (90–120 seconds after the start of contrast medium injection). However, in patients who did not undergo delayed-phase CT, patency of the false lumen was judged on the basis of early-phase data. The 193 patients were divided into two groups according to the status of the residual false lumen: those with a patent false lumen in the distal aorta (124 patients, mean age 58.7 ± 11.0 years) and those with a totally thrombosed false lumen in the distal aorta (69 patients, mean age 68.5 ± 8.7 years). If contrast medium was found anywhere in the distal aorta, the false lumen was considered patent. Thus, the patent group included patients with a partially thrombosed false lumen in the distal aorta. Patients' clinical characteristics and dissection characteristics are shown in Table E1.
Our study followed the guidelines of the Ethical Review Board of Jichi Medical University. All of the patients had previously granted permission for use of their medical records for research purposes.
Surgical Procedures
All operations were performed on an emergency basis within 24 hours after admission. The surgical procedure consisted of median sternotomy with standard cardiopulmonary bypass via a subclavian artery or femoral artery cannulation. Once cardiopulmonary bypass was established, systemic cooling was started immediately. After the onset of ventricular fibrillation, the aorta was clamped. The proximal stump was trimmed and reinforced with Teflon felt (DuPont, Parkersburg, WVa) during cooling. The aortic arch was then explored under circulatory arrest at a rectal temperature of 20°C. If the entry site was found in the ascending aorta, ascending aorta replacement (including hemiarch replacement) was performed by the open aorta technique. If the entry site was present or extended into the aortic arch, partial or total arch replacement was performed with a selective cerebral perfusion technique. The placement technique always included the interposition of woven collagen-impregnated or albumin-sealed grafts with Teflon felt reinforcement of the aortic stumps. Gelatin–resorcin–formalin adhesive was not used. When the entry site could not be identified or was identified in the descending aorta by transesophageal echocardiography, we simply replaced the ascending aorta. Aortic root replacement with a composite prosthesis and reimplantation of the coronary arteries by the modified Bentall technique was performed in patients with conspicuous dilatation of the aortic root.
Follow-up
In-hospital data were obtained by retrospective review of hospital records. Follow-up CT was usually performed at our outpatient clinic or at one of several neighboring hospitals 6 to 12 months after hospital discharge and annually thereafter. Other follow-up data including survival time, general health condition, aortic reoperation or rupture, and cause of death were obtained from our outpatient clinic, through written or telephone contact with patients or relatives, or from local cardiologists. The mean follow-up period was 4.3 ± 2.8 years (0.6–10.2 years), and follow-up information was obtained for 100% of the patients.
Aortic Growth Rates
Aortic growth rate was assessed if a patient had undergone at least 2 CT studies postoperatively with at least 6 months between them. If more than 2 CT studies were performed after hospital discharge, the most recent image was used to determine the growth rate. Once an aortic segment had been subjected to reoperative intervention, the patient was excluded from further assessment of growth rate. In each patient, analyses were performed at 4 different levels of the aorta: the aortic arch, proximal (at the level of the aortic isthmus) and distal (at the level of the supradiaphragm) descending aorta, and abdominal aorta. The growth rate was calculated as follows13,14: difference in diameter between the initial (D1) and final (D2) measurements divided by the time interval (T) between the 2 measurements: that is, growth rate = (D2 – D1)/T.
As previously described,9 a number of factors were compared between patients for whom serial CT scans were available and those for whom they were not available to determine whether the group who contributed scans was representative of the entire cohort of patients. The following factors were examined: age; sex; DeBakey classification; patency of the residual false lumen; postoperative complications (stroke, need for re-exploration, renal failure, prolonged ventilator support); presence of aortic dilatation, chronic obstructive pulmonary disease (COPD), diabetes, hypertension, chronic renal failure, Marfan syndrome, or aortic valve insufficiency; surgical procedures; proximal or distal reoperation; and late survival.
Statistical Analysis
All values are expressed as mean ± standard deviation. Between-group differences in clinical and morphologic variables were analyzed by 
2 or Fisher's exact test or by the unpaired t test or Mann–Whitney U test. Multivariate logistic regression analysis was performed to identify independent risk factors for a residual patent false lumen. Time-related events studied included death and reoperation in the distal aorta after hospital discharge. Freedom from these time-related events was estimated by the nonparametric actuarial Kaplan–Meier method. For the purposes of comparison with other published data, actuarial survival and freedom from reoperation on the distal aorta for all patients with AAAD (including 25 patients with DeBakey type II) are also given. All statistical analyses were performed with SPSS 11.0.1 for Windows software (SPSS, Inc, Chicago, Ill).
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Results |
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TopAbstractIntroductionPatients and MethodsResultsDiscussionConclusionsFigure E1Table E1Table E2References |
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Of the 56 patients with type IIIb retrograde AAAD (29.0%, 56/193), 5 patients who had visible entry located in the proximal descending aorta were treated with total arch replacement for entry resection. The remaining 51 patients included 5 whose entry was identified by transesophageal echocardiography and 46 whose entry was not identified intraoperatively. Patency of the thrombosed false lumen in patients with type IIIb retrograde AAAD was 39.3% (22/56).
Results of multivariate logistic regression analysis for independent risk factors for residual patent false lumen are shown in Table 1 . Although male sex, history of smoking, and preoperative limb ischemia were identified as significant risk factors by univariate analysis, only age less than 70 years was identified as an independent risk factor for a residual patent false lumen.
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One hundred thirty-nine (72.1%) patients had sufficient image data for determination of aortic growth rate. These 139 patients included 94 patients with a patent false lumen and 45 patients with a thrombosed false lumen. Although the proportion of patients who contributed scans was higher in the patent group (75.8%, 94/124) than in the thrombosed group (65.2%, 45/69), the difference was not significant (P = .12). The mean overall CT follow-up period was 3.2 ± 2.0 years (0.6–9.1 years). The mean follow-up period for the patent group was 3.2 ± 2.1 years, and that for the thrombosed group was 2.6 ± 1.9 years (P = .23).
The mean initial diameter and growth rate for each aortic segment are shown in Table 2 . At the proximal and distal descending aorta, the mean initial aortic diameter was slightly but significantly greater in the patent group than in the thrombosed group. In both groups, the largest segment of the distal aorta on the initial CT scan was the aortic arch; this was followed by the proximal descending aorta, distal descending aorta, and abdominal aorta. At all segments of the distal aorta, the mean growth rate was greater in the patent group than in the thrombosed group, and between-group differences at the aortic arch, proximal descending aorta, and distal descending aorta were significant. The mean growth rates in the patent group ranged from 1.1 to 1.9 mm per year. However, about 50% of patients with a residual patent false lumen showed a growth rate of less than 1 mm per year at all aortic segments. In contrast, the mean growth rates in the thoracic aorta of the thrombosed group were less than 0 mm per year, and only 15% to 32% of patients with a thrombosed false lumen showed a growth rate more than 1 mm per year at all aortic segments. The distal aorta of the thrombosed group frequently became a single-barrel chamber because the thrombosed false lumen disappeared during the follow-up period. This later disappearance of the thrombosis led to the negative aortic growth found in the thrombosed group.
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Freedom from distal aortic reoperation for all hospital survivors including the patients with DeBakey type II aortic dissection (n = 226) was 99.0% ± 0.7% at 1 year, 97.4% ± 1.3% at 5 years, and 89.5% ± 4.2% at 10 years (Figure E1, A). Freedom from distal aortic reoperation in the patent group (n = 124) was 98.3% ± 1.2%, 95.6% ± 2.2%, 88.0% ± 4.7% at 1, 5, and 10 years, respectively, and that for the thrombosed group (n = 69) was 100% ± 0%, 100% ± 0%, and 91.7% ± 8.0% at 1, 5, and 10 years, respectively. Although there was a tendency for the thrombosed group to have the better distal reoperation-free rate, the difference was not significant (P = .16) (Figure 2, A).
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Long-term Survival
Twenty-four patients died during the follow-up period. The leading cause of late death was malignancy (33.3%, 8/24) (Table E2). In 2 of the 8 patients who died of malignancy, malignancy was diagnosed during hospitalization for AAAD. The second leading cause of late death was cardiac failure (29.2%, 7/24), including myocardial infarction (n = 3), congestive heart failure (n = 3), and sudden death without distal aortic aneurysm (n = 1). Four (16.7%) patients died of ruptured aortic aneurysm in the distal aorta; all 4 belonged to the patent group.
Actuarial survival, with in-hospital deaths counted for all patients including those with DeBakey type II aortic dissection (n = 243), was 89.5% ± 2.0% at 1 year, 79.5% ± 3.0% at 5 years, and 71.3% ± 4.3% at 10 years (Figure E1, B). Actuarial survival for the patent group (n = 124) was 96.7% ± 1.6%, 87.9% ± 3.4%, and 79.0% ± 5.3% at 1, 5, and 10 years, respectively, and that for the thrombosed group (n = 69) was 96.8% ± 2.2%, 87.9% ± 4.8%, and 75.0% ± 8.4% at 1, 5, and 10 years, respectively. Long-term survival between groups was similar and without significant difference (Figure 2, B).
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Discussion |
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TopAbstractIntroductionPatients and MethodsResultsDiscussionConclusionsFigure E1Table E1Table E2References |
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A residual patent false lumen is considered to be the cause of unresected or secondary entry in the distal aorta. Although complete resection of all entry sites is required for thrombosis of the residual false lumen, initial surgery for AAAD fails to achieve this objective, particularly in patients with primary or secondary entry located in the descending thoracic or abdominal aorta. To decrease the incidence of residual patent false lumen, some authors recommend systematic extended or total arch replacement for the initial surgical management of AAAD, irrespective of the site of entry.2,10-12 The main benefit of this approach is complete resection of a small, invisible entry site located in the aortic arch.12 The incidence of residual patent false lumen was 64.2% (124/193) in our series of patients. This was in accordance with results of previous studies (43%–78%) in which aortic arch replacement was performed in selected patients8,9,15-17; however, it was higher than the 27% to 46% incidence of residual patent false lumen reported by other groups that used aortic arch grafting in all patients with AAAD extending to the descending aorta.2,11,12 It is possible that the low percentage of aortic arch replacements in the present series (14.0%, 27/193) led to the relatively high rate of residual false lumen patency. Other reported risk factors for residual patent false lumen after surgery for AAAD include Marfan syndrome, preoperative extension of the false lumen, male sex, and increased aortic diameter.2,7 In the present study, age less than 70 years was identified as an independent risk factor for residual patent false lumen after surgery for AAAD. This finding was similar to that of Tsai and associates.18 It has been reported that younger age is associated with late aortic enlargement in patients with type B aortic dissection.14,19 The elasticity and distensibility of the aorta decline with age. Sueyoshi and colleagues.14 hypothesized that loss of elasticity might limit enlargement of the aorta in patients with aortic dissection. However, the reason why age less than 70 years was associated with residual patent false lumen in our study is unknown, and further investigation is needed.
The major finding of the present study was that the residual patent false lumen strongly influences aortic growth rate after surgery for AAAD. Our finding confirms the findings of previous studies showing that the residual patent false lumen is a risk factor for faster aortic growth in patients with aortic dissection.7-9,14,17,19,20 A new finding is that about 50% of the patients with residual patent false lumen showed an aortic growth rate of less than 1 mm per year at all aortic segments, indicating that the residual patent false lumen is not necessarily associated with secondary enlargement of the distal aorta. Although the distal aorta with a residual patent false lumen tends to enlarge, the aortic growth rate is generally slow, and it takes a relatively long time for a large aneurysm requiring surgical intervention to develop. In the present study, freedom from distal aortic reoperation and long-term survival were similar in patients with and without residual patent false lumen; the findings of Sabik and coworkers21 were similar.
We observed a relatively low incidence of distal reoperation (89.5% freedom from reoperation at 10 years), similar to incidences reported by other groups who performed aortic arch replacement in selected patients (77%–91% freedom from distal reoperation at 10 years).21,22 Although reoperation-free rates reported by groups adopting routine aortic arch replacement for AAAD were also satisfactory (77%–93% freedom from reoperation at 10 years),10,12 reoperation-free rates were similar between groups. We agree that extended aortic arch replacement can decrease the incidence of residual patent false lumen. However, it remains unclear whether this approach can decrease the need for reoperation in the distal aorta and improve late survival. We believe that surgical technique alone is not the main determinant of the natural history of the distal aorta after surgery for AAAD. Crawford and associates23 recommended replacing the aortic arch only when it is aneurysmal and there is excessive enlargement and impending or actual rupture of the false lumen, but not treating a false lumen in the aortic arch. Recently, some groups that routinely use extended aortic arch replacement have reported excellent operative outcomes, with mortality ranging from 4.7% to 10%.2,11,12 However, such an aggressive approach might increase the already high operative risk. In the present study, in-hospital mortality for patients who underwent total or partial arch replacement was higher than that for patients who underwent ascending aorta or hemiarch replacement (10% [3/30] vs 6.9% [13/188]; P = .82). The difference was not significant, but we consider that this risk largely outweighs the relatively low incidence of reoperation in the distal aorta and its associated operative risk. As noted earlier, elderly patients tend to have a thrombosed false lumen after initial surgery for AAAD. Therefore, especially when a patient is elderly or has at least one of various preoperative complications, our relatively conservative operative approach seems to be reasonable.
Another finding of the present study was that some patients with a patent false lumen can show unusually rapid aortic enlargement. Enlarged aorta is reported to be related to a faster growth rate in patients with aortic dissection.7,9,20,24 In the present study, significant differences were found in the initial aortic diameter at the proximal and distal descending thoracic aorta. This suggests that not only patency of the residual false lumen but also initial aortic diameter has some influence on late aortic growth. The other reported risk factors for aortic enlargement or distal reoperation after surgery for AAAD include nonresection of the entry site, distal extension of a dissection, and Marfan syndrome22,24-26 We think that when young patients who are in stable condition show such risk factors, extended arch replacement is a preferable operative approach and can decrease the need for late reoperation in the distal aorta. Zierer and colleagues24 recently reported that uncontrolled hypertension is a risk factor for late aortic enlargement. Careful antihypertensive therapy seems to be important for prevention of later aortic enlargement.
Reported 10-year survivals with in-hospital deaths counted ranged from 37% to 71%.15,21,22,25,26 Although patient characteristics are not comparable, the 71% survival at 10 years in our series was acceptable. DeBakey and colleagues27 reported that rupture of the distal aorta was the most common cause of death in patients with AAAD, accounting for 29.3% of 205 late deaths. In this series, the most common cause of late death was malignancy. However, despite close surveillance, 4 patients died of rupture of the distal aorta, and all 4 had a residual patent false lumen. Although careful follow-up is mandatory to prevent rupture of the distal aorta, the decision to perform repeat surgical intervention in a stable, asymptomatic patient is another important issue. For timely reoperation, we must take into account not only comorbidities and the aortic diameter but also the status of the residual false lumen. As mentioned earlier, results of reoperation in the distal aorta were satisfactory (no perioperative deaths among 8 patients who underwent reoperation). Therefore, we consider distal reoperation to be necessary when the aortic diameter reaches 55 mm in otherwise healthy young patients with a patent false lumen. Favorable results of endovascular treatment for acute or chronic aortic dissection were recently reported, with high rates of success with false lumen thrombosis.28 Endovascular treatment can be an effective approach even for elderly or severely compromised patients.
Study Limitations
The present study had several limitations. For assessment of aortic growth rate, follow-up CT examinations were performed in only 139 (72%) of the 193 patients who underwent initial postoperative enhanced CT scan and were discharged from the hospital. An important question was whether the patients who contributed serial CT scans were representative of the entire cohort of patients who survived the initial operation for AAAD. However, there was no significant difference between these groups in perioperative characteristics or long-term outcomes.
Another limitation is related to the CT scanning. Since 2002, we have routinely performed an initial postoperative enhanced CT examination, both early and delayed phase. However, before 2002, some CT examinations were performed only in the early phase. Therefore, we might have underestimated the actual incidence of residual patent false lumen owing to misclassification of the false lumen. Moreover, enhanced CT scanning was not routinely performed in all patients who were included in the growth rate assessment. This is because follow-up CT examinations after discharge were not standardized between our hospital and the neighboring hospitals. Therefore, we were unable to evaluate long-term changes in the diameter of the true and false lumina.
The third limitation was the relatively short follow-up period. The mean follow-up period was 4.3 years, which was shorter than the 10- to 20-year follow-up periods of previous studies on long-term survival after surgery for AAAD.15,21,22,25-27 With a longer follow-up period, a significant difference in the distal reoperation-free rate may become evident between patients with and without a residual patent false lumen, and patients with patent false lumina may be shown to have poorer late outcomes. Further studies involving larger numbers of patients with a longer follow-up period are required.
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Conclusions |
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TopAbstractIntroductionPatients and MethodsResultsDiscussionConclusionsFigure E1Table E1Table E2References |
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Figure E1 |
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TopAbstractIntroductionPatients and MethodsResultsDiscussionConclusionsFigure E1Table E1Table E2References |
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Table E1 |
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TopAbstractIntroductionPatients and MethodsResultsDiscussionConclusionsFigure E1Table E1Table E2References |
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CAD, coronary artery disease; CVD, cerebrovascular disease; COPD, chronic obstructive pulmonary disease; TIA, transient ischemic attack; CABG, coronary artery bypass grafting; NS, not significant.
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Table E2 |
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TopAbstractIntroductionPatients and MethodsResultsDiscussionConclusionsFigure E1Table E1Table E2References |
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Number and percentage of patients are shown. Differences were not significant.
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References |
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TopAbstractIntroductionPatients and MethodsResultsDiscussionConclusionsFigure E1Table E1Table E2References |
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