|
|
||||||||
Ann Thorac Surg 2007;83:1047-1053
© 2007 The Society of Thoracic Surgeons
a Department of Thoracic, Cardiac and Vascular Surgery, Tuebingen University Hospital, Tuebingen, Germany
b Department of Medical Biometry, Tuebingen University Hospital, Tuebingen, Germany
Accepted for publication October 11, 2006.
* Address correspondence to Dr Walker, Department of Thoracic, Cardiac and Vascular Surgery, Tuebingen University Hospital, Hoppe-Seyler-Strasse 3, 72076 Tuebingen, Germany (Email: tobias.walker{at}med.uni-tuebingen.de).
| Abstract |
|---|
|
|
|---|
Methods: From 1996 to 2003, 97 patients (mean age, 67 years) underwent RAA without external stabilization in our institution as a concomitant procedure during cardiac surgery. The diameter of the ascending aorta was measured before and directly after surgery, as well as postoperatively from 10 to 96 months (median, 32 months).
Results: The mean preoperative diameter was 4.55 ± 0.43 cm, while the early postoperative diameter measured 3.53 ± 0.44 cm. Fifty-four of the 97 patients were available for follow-up. The mean diameter measured at follow-up was 3.68 ± 0.41 cm. The mean increase was 0.17 ± 0.27 cm. There was no relevant difference in redilatation between patients with follow-up of more than 60 months or less. Furthermore, the aortic wall demonstrated a near normal diastolic-systolic augmentation assessed by echocardiography.
Conclusions: Reduction ascending aortoplasty without external stabilization is a reliable treatment for patients suffering from a moderately enlarged ascending aorta who require cardiac surgery for other indications. In these cases, with the technique described, a redilatation can be prevented and the Windkessel function of the ascending aorta remains preserved.
| Introduction |
|---|
|
|
|---|
|
We hypothesize that RAA without external reinforcement, in a moderately enlarged ascending aorta of up to 5.0 cm in diameter, is a safe and reliable technique for size reduction and reliably prevents redilatation of the vessel. We investigated the postoperative stability and preservation of the physiologic elasticity of the reconstructed ascending aorta (Windkessel function). In the case of the unsupported RAA, the absence of a rigid sleeve allows for a systolic diameter expansion of the ascending aorta. For this reason we evaluated the diastolic-systolic changes in the vessel diameter by using transthoracic echocardiography.
| Patients and Methods |
|---|
|
|
|---|
Keeping in mind the data published by Roman and colleagues [5], a diameter of greater than 4.0 cm in a normal sized patient was considered to be pathologic, 5.0 cm was the upper limit to apply RAA, and in exceptional cases 5.5 cm. If a bicuspid valve was suspected preoperatively or detected intraoperatively, RAA was not performed because of concerns of a connective tissue disorder of the ascending aorta. The Ethics Committee of Tuebingen University waived the need for patients consent and approved this study.
Reduction ascending aortoplasty without external wrapping was performed in 97 patients between June 1996 and December 2003 as a concomitant cardiac procedure. The different primary cardiac procedures employed and their frequencies are indicated in Table 1. Reoperation was not considered a contraindication for RAA.
|
|
Recurrence of an ascending aortic dilatation was defined as any increase in aortic diameter. Windkessel function was defined as the difference of aortic diameter during systole minus aortic diameter during diastole.
CT Measurements
A contrast-enhanced helical CT scan of the chest was performed using a single slice scanner or a four-row multidetector CT unit. A preoperative CT-scan (Fig 3) was done in 87 patients, including all 54 patients seen at follow-up. Forty-six postoperative CT scans were available.
|
Echocardiography
To determine the Windkessel function, the patients were examined using a two-dimensional echocardiogram. End-systolic and end-diastolic diameters of the ascending aorta were assessed using the parasternal long and short axis views and additionally by a suprasternal view when necessary. These echocardiographic measurements were determined only at follow-up investigation. Therefore, no statement can be made about the elastic properties of the preoperative ectatic aorta, early postoperative augmentation, or postoperative development of the Windkessel function.
Statistical Analysis
All analyses were performed using the statistical software package JMP IN 5.1 (SAS Institute Inc, Cary, NC). Aortic diameter was analyzed by 95% confidence intervals (CI) for differences in expected values and summarized by mean ± SD. For the aortic augmentation, cross-clamp time, cardiopulmonary bypass time, intensive care stay, and hospitalization time without intensive care stay, assumed lognormal distributions, geometric means, coefficients of variation (CV), and CIs for the ratio of geometric means as a percentage of the duration in the aortic replacement group were computed. Distributional assumptions were verified by quantile-quantile plots.
| Results |
|---|
|
|
|---|
Five to ten hours postoperatively, six of 97 RAA patients (6%) had to be reopened because of persistent bleeding. Only one patient bled at the suture line of the longitudinal plication. In the other five of six cases, the bleeding was not RAA-related.
Hospital mortality after RAA was 3% (three of 97 cases). A 70-year-old female patient died on the seventh postoperative day as a result of ventricular fibrillation, occurring after an uneventful postoperative course. Autopsy could not find any conclusive cause. Another 75-year-old female died on the seventh postoperative day in the intensive care unit as a result of progressive cardiac failure and untreatable cardiac arrhythmias. The death of a 67-year-old male was attributable to a multiorgan failure after generalized sepsis. Therefore, 94 of 97 patients were discharged from the hospital (Table 2).
|
The study group consisted of 43 males and 11 females with a mean age at investigation of 69 ± 10 years (range, 36 to 83). Geometric mean time of follow-up was 32 months (CV 56%; range, 10 to 96 months). The mean preoperative diameter was 4.55 cm (±0.36 cm). Early postoperative measurements showed a decrease to 3.54 cm (±0.44 cm), and at follow-up measured 3.68 cm (±0.41 cm). Mean dilatation during the time from early postoperative measurement to follow-up was 0.17 cm (±0.27 cm; CI 0.09 to 0.25 cm) in 45 patients with both early and late postoperative measurements (Table 4).
|
|
|
Follow-up revealed redilatation of the aorta in a 59-year-old patient who was operated on 15 months previously because of aortic regurgitation (5.1 cm preoperatively and 3.2 cm postoperatively). Follow-up CT demonstrated an increased diameter at the level of the sinus of Valsalva. At the level of the RAA, the diameter remained relatively stable with 0.3 cm difference compared with the early postoperative value. He was operated on again and underwent a successful tube graft replacement of the entire ascending aorta with reimplantation of the coronary arteries.
| Comment |
|---|
|
|
|---|
Neri and colleagues [7] were able to investigate aortic wall specimens from covered and uncovered aorta. They observed extremely thin aortic walls under the reinforcement cuff but not in the regions without wrap. This atrophy possibly could be followed by a dissection at the border zone between the native aorta and the wrap leading to aortic rupture [8].
For a smooth and snug fit of the wrap, the aorta has to be dissected circumferentially in the entire length of its ascending segment. By doing this, the majority of the native vasa vasorum is probably destroyed leading to a nutritive disorder of the vessel, at least in its subadventitial layers. Furthermore, the reduced wall stress might be an important stimulus for aortic wall degeneration. Both triggers are avoided when an unsupported reduction ascending aortoplasty is employed. The vasa vasorum remain conserved as the aorta has to be prepared only to the extent necessary for cross-clamping. Additionally, the unaltered wall stress seems to contribute to the preservation of the structural integrity of the aortic wall.
But does the unsupported aortoplasty securely prevent a significant redilatation and in which patients? We performed unsupported aortoplasty in 97 patients; 54 were available for follow-up. Mean follow-up was 32 months (range, 10 to 96). Moderate ascending aneurysms could be reduced to near normal diameters with unsupported RAA. Notably, the diameter remained stable during follow-up. Although a slight diameter progression was observed, this augmentation cannot be considered as a relevant increase as a bias of this magnitude in CT could be introduced by the systole-diastolic fluctuations of the aorta during scanning. The mean enlargement of 0.17 cm during 37 months (range, 10 to 96 months) of follow-up was almost equal to that seen by Carrel and colleagues [9]. They observed an increase of 0.21 cm during a mean follow-up of 6.5 years in a population with aortoplasty with the additional applied wall support.
Mueller and colleagues [10] published their experiences with unsupported aortoplasty in 1997. In four out of 13 patients, redilatation was observed and all of them occurred in patients whose primary condition was aortic valve regurgitation. Therefore, they abandoned unsupported RAA associated to aortic valve replacement performed for valvular regurgitation. These results are not supported by our investigation. We could not demonstrate any difference in the postoperative outcome between the groups having aortic stenosis and regurgitation as the leading operative diagnosis (Table 5). One reason could be that they enrolled patients with truly aneurysmic aortas up to diameters of 6.0 cm. We excluded these patients because we believe in a remaining wall thickness as a guarantor for postoperative stability. This assumption was confirmed most recently by Polvani and colleagues [11] who identified a diameter greater than 5.5 cm as the main predictive factor leading to a redilatation after unsupported RAA. Furthermore, they included patients with a bicuspid aortic valve. Considering the data published by Fedak and colleagues [12], a bicuspid aortic valve seems to be associated with various enzymatic disorders and therefore might be associated with an unstable aortic wall [13]. This criterion is supported by an observation of Nistri and colleagues [14]. He demonstrated, in young men with bicuspid aortic valves that despite no valvular disorder, the annulus of the aortic valve and the sinus of Valsalva are enlarged in comparison with healthy volunteers with tricuspid aortic valves [15]. Therefore, patients with bicuspid valves seem to be inappropriate for an unsupported aortoplasty and we excluded them from RAA, although satisfying results could also be achieved by others with these patients [16].
Consent exists about the importance of a close follow-up. In the population examined by Mueller and colleagues [10], an aortic reenlargement recurred in four patients after a mean time of 63 months. Therefore, we investigated patients separately with a follow-up of at least 60 months. According to our results described above, the diameter of these eight patients remained stable in the follow-up and they did not differ significantly from the patients with a follow-up of less than 60 months.
Follow-up examinations revealed only one patient who had to be reoperated because of a progressive dilatation of the aortic root beneath the reduction. There are two probable causes leading to failure in this case. First, on the basis of a retrospective review of the preoperative CT, the aortic annulus and sinus region were dilated making the indication for operation incorrect. Second was the imperfect application of the technique by ending the incision proximally at the level of the sinotubular junction instead of carrying it down to the acoronary sinus, and a composite graft or a valve sparing technique should have been employed instead.
Unfortunately, we have limited information about the causes of the deaths in five patients (all female) which occurred after hospital discharge. A 49-year-old woman died two years after surgery from a terminal malignancy and therefore an association with the aortoplasty cannot be excluded. However, given the stability of the RAA technique demonstrated in this investigation we believe it to be unlikely. Furthermore, the majority of patients were old and had other serious comorbidities, increasing the probability of death related to other factors other than the applied operative technique.
If the RAA is performed as a complementary procedure to a CABG, anastomosis of the proximal graft to an unsupported aorta is easier to perform as the side-biting clamp can be easily positioned without interfering with the longitudinal suture line. In a sleeve-supported RAA, the graft has to be anastomosed directly over the wrap and the sutures have to penetrate both the native aortic wall and the fabric. The quality of such a wrap-graft anastomosis could be impaired by the compliance mismatch between the elastic venous graft and the relatively rigid wrap contributing to a diminished patency of the graft [17, 18]. Alternatively, the graft can be placed either proximally or distally to the wrap using the innominate artery.
We were able to demonstrate that the elasticity of the aortic wall, the Windkessel function, remains preserved after unsupported RAA. It enables the ascending aorta to store energy and volume during systole and release it during diastole, leading to a near continuous blood flow in the small peripheral vessels. Additionally, volume and energy storage not only decrease the afterload influencing the peripheral circulation, but also increase coronary perfusion and improve left ventricular function. This conclusion can be drawn from the increased afterload and a possible reduction in subendocardial coronary perfusion during diastole when the elasticity of the ascending aorta is lost [19]. Being largely underestimated in the past, this storage function of the ascending aorta seems important and we speculate (although no hard evidence is currently available) that an elastic ascending aorta, as is found after an unsupported RAA, might contribute to the postoperative regression of left ventricular hypertrophy.
Our results prove that the main goal of significantly reducing a moderately enlarged ascending aorta to near normal values with acceptable stability over a midterm follow-up period can be achieved by the unsupported RAA technique. In comparison with the external wall reinforcement, the unsupported aortoplasty may provide additional advantages in terms of easier access to the ascending aorta, as in the case of associated CABG. Furthermore, the preserved Windkessel function may ameliorate the structural and functional recovery of the myocardium after the operation.
According to the appeal of Sievers [20], the method of unsupported RAA needs to be confirmed by prospective studies with strict inclusion criteria. Until this is the case, we would like to answer the poetical question of the esteemed Robicsek and colleagues [21] concerning the current status of size reduction aortoplasty: "Is it dead or alive?" with "Yes sir, we believe the unsupported RAA is alive."
| Acknowledgments |
|---|
|
|
|---|
| Footnotes |
|---|
|
|
|---|
| References |
|---|
|
|
|---|
Related Article
This article has been cited by other articles:
![]() |
M. Gill and J. Dunning Is reduction aortoplasty (with or without external wrap) an acceptable alternative to replacement of the dilated ascending aorta? Interactive CardioVascular and Thoracic Surgery, October 1, 2009; 9(4): 693 - 697. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. Litmathe and P. Feindt Reply to Yavuz Eur. J. Cardiothorac. Surg., September 1, 2007; 32(3): 555 - 555. [Full Text] [PDF] |
||||
![]() |
S. Yavuz Reduction ascending aortoplasty: how safe is it? Eur. J. Cardiothorac. Surg., September 1, 2007; 32(3): 554 - 555. [Full Text] [PDF] |
||||
![]() |
T. Sundt III Invited commentary Ann. Thorac. Surg., March 1, 2007; 83(3): 1053 - 1054. [Full Text] [PDF] |
||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| ANN THORAC SURG | ASIAN CARDIOVASC THORAC ANN | EUR J CARDIOTHORAC SURG |
| J THORAC CARDIOVASC SURG | ICVTS | ALL CTSNet JOURNALS |