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Ann Thorac Surg 2007;84:479-487
© 2007 The Society of Thoracic Surgeons
a Division of Cardiothoracic Surgery, The Center for Diseases of the Thoracic Aorta, Washington University School of Medicine, Barnes Jewish Hospital, St. Louis, Missouri
b Department of Cardiothoracic Surgery, Missouri Baptist Medical Center, St. Louis, Missouri
Accepted for publication March 27, 2007.
* Address correspondence to Dr Moon, Division of Cardiothoracic Surgery, Washington University School of Medicine, 3108 Queeny Tower, #1 Barnes-Jewish Plaza, St. Louis, MO 63110-1013 (Email: moonm{at}wustl.edu).
Presented at the Forty-third Annual Meeting of The Society of Thoracic Surgeons, San Diego, CA, Jan 29–31, 2007.
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Abstract |
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Methods: During a 22-year period, 201 patients underwent repair of acute type A dissection by 25 surgeons. For 168 operative survivors, mean late follow-up for reoperation or death was 6.5 ± 5.5 years and was 100% complete. Late blood pressure and medication history were available for 136 patients. Overall, 412 computed tomography scans were analyzed for segmental diameter and false lumen patency from 69 patients who underwent multiple follow-up imaging studies at our institution.
Results: Freedom from reoperation at 10 years (range, 1 to 170 months) was 74% ± 5% (28 reoperations in 26 patients). A nonresected primary tear (p = 0.05), Marfan syndrome (p < 0. 001), elevated systolic blood pressure at follow-up (p = 0.008), and absence of ß-blocker therapy (p = 0.02) were independent predictors of late reoperation. Aortic growth between consecutive imaging studies was detected in 18% of intervals (62/343) affecting 49% patients (34/69), with mean yearly growth rate of 5.3 ± 4.5 mm. Onset of enlargement was unpredictable and occurred 59 ± 45 months postoperatively (range, 1 to 167 months). Risk factors for growth included aortic diameter (p < 0. 001), elevated systolic blood pressure (p = 0.04), and presence of a patent false lumen (p = 0.05). Maximum aortic diameter of less than 35 mm predicted growth in 11% of intervals, 35 to 49 mm in 22%, and more than 49 mm in 37% (p < 0.001). Different proximal or distal surgical strategies did not affect aortic growth or need for reoperation (p > 0.17).
Conclusions: Optimal long-term outcome of patients with acute type A dissection demands rigorous antihypertensive therapy and lifelong radiographic follow-up because aortic enlargement can begin more than a decade postoperatively.
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Introduction |
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TopAbstractIntroductionMaterial and MethodsResultsCommentDiscussionReferences |
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Clearly, operative survival does not guarantee freedom from subsequent aortic events, as most operative survivors have a persistent, dissected residual aorta, often with a patent false lumen [15]. Halstead and coauthors [16] recently reported that growth of the distal aorta after repair of acute type A dissection is typically slow and linear; however, the factors that impact the natural history of the residual aorta remain incompletely understood. The purpose of the current study was to investigate the incidence, onset, and extent of late distal aortic enlargement in patients who survived the initial repair of an acute type A aortic dissection and to identify factors that may negatively influence aortic growth rates and freedom from reoperation.
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Material and Methods |
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Selected preoperative patient characteristics are summarized in Table 1. The most common underlying medical disorder was hypertension, present in 72% of patients. Eight patients (4%) had previously undergone coronary artery bypass grafting (CABG; n = 5) or aortic valve replacement (n = 3). Marfan syndrome was diagnosed in 10 patients (5%). Sixteen patients (8%) experienced an intraoperative dissection while undergoing either CABG; n = 12 or a valve procedure (aortic, 2; mitral, 2). The location of the primary intimal tear was the ascending aorta in 175 patients (87%), the arch in 17 (8%), and the descending thoracic aorta in 9 (4%).
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Proximally, the aortic valve was preserved in 141 patients (70%), 47 (23%) underwent composite valve graft replacement with reimplantation of the coronary arteries or CABG if the ostia were damaged, and 13 (6%) underwent separate aortic graft and valve replacement. Two patients in the aortic valve preservation group, both with Marfan syndrome presenting in the last year of this series, underwent a valve-sparing root replacement. Aortic valve preservation was more common in the later rather than earlier time periods (p < 0.001; Fig 1A).
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Long-Term Follow-Up
The operative mortality rate was 16% ± 3% (33/201 patients). For operative survivors, mean late follow-up for reoperation or death was 78 ± 65 months and was 100% complete. Clinical records from all operative survivors were reviewed for blood pressure (BP) control at late follow-up and medication history, and patients and their primary care physicians were contacted by mail and telephone during a 3-month closing interval ending June 2006. Follow-up data on BP and medication history were available for 136 patients (81%). Patients and or primary care physicians categorized systolic BP (SBP) at late follow-up as less than 120 mm Hg, between 120 and 140 mm Hg, or greater than 140 mm Hg. Diastolic BP (DBP) was categorized as less than 80 mm Hg or greater than 80 mm Hg.
Postoperative Aortic Imaging
Of 168 operative survivors, 69 underwent two or more follow-up imaging studies (computed tomography [CT] or magnetic resonance imaging [MRI]) at our institution, which provided a review of aortic growth rates. Overall, 412 imaging studies were analyzed for segmental aortic diameter and false lumen patency for an average of 6 ± 5 scans per patient (range, 2 to 25 scans). The mean interval between consecutive scans was 10.6 ± 16.6 months, and the mean time for scanning from the initial dissection was 47.4 ± 44.6 months, with 248 scans (72%) performed more than 1 year postoperatively.
Aortic outer diameter was measured using a caliper method with the reference measurement tool within the scan image. In the case of an elliptical cross section, the minor diameter of the ellipse was measured, regardless of orientation, to avoid convolution effect in an elongated, tortuous aorta [18, 19]. All imaging studies were analyzed retrospectively by one observer who was unaware of the patients’ clinical details.
Aortic diameter was measured at three predetermined segments: (1) descending aorta, (2) aorta at the diaphragmatic hiatus, and (3) abdominal aorta. Measurements in the descending and abdominal aorta were taken at the level of maximum segmental diameter, including both the true and false lumen, if present. A thrombosed false lumen was defined as the presence of a circumferential or crescentic nonenhancing filling defect within the aortic lumen on contrast enhanced scans.
Data Analysis
Study end points were long-term survival and late reoperation for the 168 operative survivors and segmental aortic enlargement for 69 patients with multiple postoperative imaging studies. Operative mortality included any death that occurred during the initial hospitalization or within 30 days of operation for discharged patients. Cumulative survival rates were calculated using Kaplan-Meier analysis, and survival curves were compared using the log-rank test.
Continuous data are reported as mean ± one standard deviation (SD) or median with intraquartile range (IQR), where appropriate, for variables without normal distribution, and compared using analysis of variance. Categoric variables were analyzed using the 
2 test or Fisher exact tests, as appropriate. Odds ratios (OR) are reported with 70% confidence intervals (CI).
Multivariate analysis (stepwise backward regression) was used to determine preoperative, intraoperative, and postoperative risk factors that were significant, independent predictors of impaired long-term survival, increased segmental aortic enlargement, and diminished freedom from late reoperation. SigmaStat 2.03 software (SPSS Inc, Chicago, IL) was used for the analysis. Twenty-nine variables were analyzed: age, year of operation, gender, hypertension, diabetes, coronary artery disease, pulmonary disease, cerebrovascular disease, peripheral vascular disease, chronic renal insufficiency, smoking history, Marfan syndrome, previous cardiac operation, cardiogenic shock, aortic insufficiency, preoperative flow complications, DeBakey classification, HCA, RCP utilization, primary tear location, primary tear resected, aortic valve preservation versus replacement, ascending only versus hemiarch replacement, initial segmental aortic diameter, false lumen patency, SBP (< 120 mm Hg versus 120 to 140 mm Hg versus >140 mm Hg), diastolic BP (
80 mm Hg versus >80 mm Hg), ß-blockers, and any antihypertensive medication. For important, significant factors in the multivariate analyses, standardized (ß) regression coefficients (standardized to dimensionless values) are reported with standard error of the mean. Statistical differences were considered significant at a value of p < 0.05.
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Results |
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For all operative survivors, multivariate regression analysis identified four factors to be independent predictors of late reoperation: (1) Marfan syndrome (p < 0.001; OR, 10.4; 70% CI, 4.3 to 25.0), (2) nonresected primary tear (p = 0.005, OR, 4.0; 70% CI, 2.4 to 6.7), (3) absence of postoperative ß-blocker therapy (p = 0.02, OR, 3.3; 70% CI, 2.1 to 5.3), and (4) elevated SBP at late follow-up (p = 0.008). The impact of each significant predictor was similar, with standardized ß coefficients of 0.18 ± 0.07 for absence of postoperative ß-blocker therapy, 0.21 ± 0.10 for nonresected primary tear, 0.22 ± 0.13 for Marfan syndrome, and 0.24 ± 0.04 for elevated SBP at late follow-up.
Late reoperation was more common with SBP greater than 140 mm Hg (35% ± 11%; 7/20 patients) than with SBP between 120 and 140 mm Hg (22% ± 6%; 12/54 patients) or SBP of less than 120 mm Hg (8% ± 4%; 5/62 patients). Figure 3 demonstrates freedom from reoperation based on SBP at late follow-up. Freedom from reoperation at 10 years and 15 years fell from 83% ± 7% and 83% ± 7% with SBP less than 120 mm Hg to 69% ± 9% and 55% ± 14% with SBP between 120 and 140 mm Hg and 57% ± 15% and 34% ± 15% with SBP greater than 140 mm Hg (p = 0.05).
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Aortic Expansion
Aortic growth between consecutive imaging studies was detected in 18% of the intervals (62/343) affecting 49% patients (34/69). Of the 62 intervals that demonstrated growth, expansion occurred in one isolated aortic segment in 32 intervals (descending only, 20; diaphragmatic, 2; abdominal, 10), expansion occurred in two segments in 19 intervals (descending and diaphragmatic, 12; descending and abdominal, 3; diaphragmatic and abdominal, 4), and expansion occurred in all three segments in 11 intervals. For all intervals, the mean growth rate (± standard error of the mean) was 1.8 ± 0.8 mm for descending, 1.6 ± 2.6 mm for diaphragmatic, and 1.3 ± 0.6 mm for abdominal segments.
Looking specifically at intervals that demonstrated growth, we found expansion occurred in 13% of the descending aorta (46/343 intervals) with a median yearly growth rate of 6.0 mm (IQR, 3.1 to 11.0), in 8% in the diaphragmatic aorta (n = 29) with a median yearly growth rate of 3.8 mm (IQR, 1.9 to 9.6), and in 8% in the abdominal aorta (n = 28) with a median yearly growth rate of 4.1 mm (IQR, 2.5 to 12.1). Expansion was most common in the descending segment (p = 0.04), which also demonstrated the most rapid growth rate (p < 0.001).
The timing of the onset of aortic enlargement was unpredictable and occurred 59 ± 45 months postoperatively (range, 1 to 167 months). Overall, there was a trend for aortic enlargement to begin later than 1 year postoperatively. Growth was detected in 11 (12%) of 95 intervals within the first postoperative year compared with 51 (21%) of 248 intervals in subsequent years (p = 0.07).
Multivariate analysis identified three factors to be independent predictors for segmental growth: (1) aortic diameter (p < 0.001), (2) elevated SBP at late follow-up (p = 0.04), and (3) patent false lumen (p = 0.05, OR, 5.1; 70% CI, 2.8 to 9.5).
Aortic diameter had the greatest impact on late growth, with standardized ß coefficients of 0.21 ± 0.01 compared with 0.07 ± 0.03 for elevated SBP at late follow-up and 0.05 ± 0.04 for patent false lumen. For patients in whom the aortic diameter was less than 35 mm in all segments, growth occurred in 11% ± 2% intervals (20/189). For patients in whom the maximum aortic diameter was between 35 to 49 mm in any segment, growth occurred in 22% ± 4% intervals (23/103). For patients in whom the maximum aortic diameter was 50 mm or greater in any segment, growth occurred in 37% ± 7% intervals (19/51; p < 0.001 versus small-sized or moderate-sized aortas).
SBP of less than 120 mm Hg was associated with growth in 14% ± 3% intervals (16/116). SBP between 120 and 140 mm Hg was associated with growth in 15% ± 3% intervals (23/151). SBP greater than 140 mm was associated with growth in 34% ± 6% (20 of 59) intervals (p = 0.002 versus low or moderate SBP). Different proximal or distal surgical approaches as well as different perfusion strategies used during the initial operation did not affect aortic growth at follow-up (p > 0.17 for all).
The false lumen was patent in 67% patients (46/69). False lumen patency was more common with DeBakey class I dissections (p = 0.01, OR, 5.1; %70 CI, 2.8 to 9.5), but was independent of the location of the primary tear (p = 0.17), resection of the primary tear (p = 0.43), and cross-clamping versus HCA with an open distal anastomosis (p = 0.35). A patent false lumen was associated with growth in 21% ± 3% (46/215), and a thrombosed or absent false lumen was associated with growth in 13% ± 3% (16/128; p = 0.05).
The analysis summarized in Table 4 was undertaken to determine the appropriate time interval to obtain serial imaging studies based on the size of the aorta. For all 343 scan intervals assessed, the time between scans was less than 6 months in 172 (50%), between 6 and 12 months in 92 (27%), and exceeded 1 year in 79 (23%). Overall, 18% of scan intervals demonstrated aortic growth. Small aortas demonstrated growth at an incidence that was below the average in scans that were performed less than 12 months apart. As presented in the table, only 5% of scans performed less than 6 months apart demonstrated growth compared with 21% with an interval exceeding 1 year. Moderate-sized aortas demonstrated growth at an incidence below average in scans performed less than 6 months apart, but scans performed more than 1 year apart commonly demonstrated growth. In contrast, large aortas frequently demonstrated growth at all three time intervals, including 83% of intervals exceeding 1 year.
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Comment |
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Consistent with previous studies of chronic type B aortic dissections [26, 27], the current investigation identified aortic diameter as a strong predictor for subsequent interval enlargement after repair of an acute type A aortic dissection. Table 4 suggested that small aneurysms seldom demonstrate growth at less than 1-year intervals, whereas moderate aneurysms seldom demonstrate growth at less than 6-month intervals. In contrast, large aneurysms frequently demonstrate growth even with intervals of less than 6 months.
On the basis of these findings, our current recommendation for long-term serial imaging after successful repair of an acute type A aortic dissection depends on aortic size. Patients with small aortas can be followed up safely at 12-month intervals, whereas patients with large aneurysms should be monitored at radiographic intervals of 6 months or less.
The onset of enlargement was unpredictable, most often occurring more than 1 year postoperatively and after 10 years or more postoperatively in some patients [28]. The current data do not support the conclusions of a recent report [29] on secondary aortic dilatation after acute type A dissection suggesting that close follow-up is mandatory for only 24 months, after which the interval can be extended up to 2 or 3 years if the false lumen is not patent. This may be appropriate for small atherosclerotic aneurysms not associated with chronic dissection, but we favor a more aggressive approach for chronic dissections. Although contrast imaging may not be necessary at all time points, aortic size should be evaluated with serial imaging every 6 to 12 months based on the size of the residual aorta.
DeBakey and colleagues [30] were the first to suggest a relationship between postoperative BP control and progression of aneurysmal disease long-term. In their classic 1982 series of 527 patients with acute and chronic aortic dissections, the authors noted that aneurysms developed in about 50% of patients with uncontrolled hypertension compared with only 15% with BP control. The findings of the current report statistically support DeBakey’s original contention. In contrast to two recent series [29, 31], the current report demonstrated the relationship of elevated SBP at late follow-up and its management with both aortic enlargement and late reoperation in patients with surgically repaired type A aortic dissections. Ideal BP control not only decreased the incidence of aortic expansion from 34% to 14% but also decreased the incidence of late reoperation from 35% to 8% if the SBP was maintained below 120 mm Hg.
Equally important, we found that the impact of ß-blocker usage was substantial, in that it was an important risk factor for reoperation independent of its impact on BP control. We hypothesize that long-term treatment with ß-adrenergic blockade, by reducing the impulse of left ventricular ejection, may be protective independent of its effects on BP control. A similar mechanism has been identified to protect the aortic root and thoracic aorta in patients with Marfan syndrome [32].
We believe that it is imperative that we reinforce to our patients and their primary care physicians the importance of long-term BP control; that is, maintaining SBP below 120 to 140 mm Hg, and the impact specifically of ß-blocker therapy in the long-term management of patients who survive the repair of an acute type A aortic dissection. We realize that it is often quite difficult to maintain SBP below 120 mm Hg and that attempts to do so may be associated with other undesirable side effects, but when possible, it is an appropriate goal for these patients who are otherwise at a significant disadvantage because of their potential to need major reoperations as they age.
In a large Stanford series of type A dissections complicated by aortic regurgitation, 6-year freedom from proximal reoperation was similar with aortic valve preservation and either separate valve and graft or composite valve graft techniques [8], and the authors were unable to identify any independent risk factors predicting the need for late proximal reoperation. In the current report, freedom from reoperation was also independent of the proximal surgical approach. Kirsch and colleagues [33] reported that severe aortic regurgitation (AI) increased the hazard of reoperation on the proximal aorta by 3.6-fold and recommended more frequent consideration of valve replacement at the time of the initial operation when severe regurgitation is present.
We partly concur given that a severe AI may be a surrogate for more pronounced aortic root disease. However, if the sinuses of Valsalva are not involved, and the regurgitation is secondary to dilatation at the sinotubular ridge, we currently prefer valve repair instead of replacement in both acute and chronic dissections. Freedom from reoperation is acceptable and the risk of a reoperative root surgical procedure appears to be relatively low in experienced hands [34, 35]. We advocate composite valve graft replacement for patients with annuloaortic ectasia, Marfan syndrome, and for patients in whom there is significant cusp pathology, including bicuspid valves.
It has been previously shown that mortality does not increase in patients in whose intimal tear was not resected [14, 15]; however, in the current report, we found that nonresection of the primary tear was an independent predictor of late reoperation. Therefore, our current practice in acute type A dissection is to extend the distal aortic resection using the hemiarch technique if the primary tear resides within the arch. We do not perform total arch replacement in these patients, reserving this technique for chronic dissections with aneurysmal dilatation of the arch or descending aorta [4, 5]. We believe that aggressive hemiarch replacement can accomplish much of the same objective in the acute setting with considerably less risk.
Given the current data as well as findings from previous studies, it is well accepted that late residual false lumen patency plays an important role in determining distal aortic expansion [27, 36–38]. Although multivariate analysis failed to identify late false luminal patency as a predictor of late reoperation in the present series, it becomes eminent that optimal surgical strategy for treatment of acute type A dissection should include measures to optimize operative outcome and also at the same time to reduce the likelihood of a patent false lumen long-term.
Controversy remains, however, about whether specific surgical techniques can help us achieve this goal. Van Arsdell and colleagues [29] noted in an autopsy series of acute type A aortic dissection that unoperated on patients often had only one entry and reentry tear compared with patients operated on with aortic cross-clamping, who generally had multiple tears [39]. The authors speculated that mechanical trauma, applied to the aortic wall during cross-clamping, was responsible for this finding. Consistent with this theory, repair of acute type A dissection with HCA and an open distal aortic repair has been advocated [16]. However, two large series from the Stanford group [40] and Kirsch and associates [33] failed to show a difference in terms of need for late reoperation and false luminal patency with open versus closed distal aortic repair.
Persistence of the false channel does not appear to correlate with successful exclusion of the primary intimal tear, but depends more on the presence of distal fenestrations between the true and false lumens [41]. As a result, during the last half-decade, some surgeons in our group have been more liberal with aortic cross-clamping in patients whose tears are localized to the ascending aorta. Further analyses from our center will surely focus on this potential shift in our philosophical approach to the acute patient who invariably presents in extremes.
The current report is subject to all the limitations of a retrospective, nonrandomized study. We acknowledge that antegrade cerebral perfusion is not routinely used at our center for acute dissections, although we do routinely use antegrade cerebral perfusion for aneurysms and chronic dissections of the ascending aorta and arch. It is important to note however, that satisfactory results have been reported with this technique [42]. We included intraoperative dissections in the current report, and although the iatrogenic etiology is different than a spontaneous dissection, we believe that the treatment strategy is analogous.
We purposely did not include a statistical analysis of the relationship between aortic growth and the incidence of late reoperation. We concluded this would represent a circular analysis because aortic size and growth are clinical indications for reoperation, and therefore, would certainly be related to its incidence.
Finally, as in most natural history studies of aneurysm expansion, the minimum diameter has been reported to avoid the effect of convolution. This approach appears prudent but may lead to under-estimation of effective diameter if the aneurysm is truly elliptical or saccular in cross-section along its long axis at the level of measurement. In addition, there remains the possibility of observer error or bias. However, it has been described that measurements by a single observer appear more reproducible than measurements by different observers [43].
In summary, the current study reveals that modifications in surgical techniques cannot improve most factors associated with aortic enlargement and late reoperation after repair of acute type A aortic dissection. Thus, optimal long-term outcome demands rigorous antihypertensive therapy (SBP ideally less than 120 mm Hg), ß-blocker therapy independent of its effects on BP control, and lifelong radiographic follow-up because aortic enlargement can initially present more than a decade postoperatively.
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Discussion |
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Thank you.
DR ZIERER: The recent trend towards aortic cross clamping in selected patients, including those with DeBakey Type II dissection and patients in whom the intimal tear is isolated to the ascending aorta, was in part based on two large recent series. One was published by the Stanford group (Lai and colleagues) in Circulation in 2002 and the other by a French group (Kirsch and colleagues) in The Journal of Thoracic and Cardiovascular Surgery, also in 2002. Both series showed no difference in long-term survival and freedom from reoperation with aortic cross-clamping versus an open distal technique. We recently (3 months ago), presented our institutional experience with different perfusion strategies at the Fifty-third Annual Meeting of The Southern Thoracic Surgical Association. Our associated manuscript is currently in press in The Annals of Thoracic Surgery. In this study we also failed to demonstrate a difference with an open distal repair during deep hypothermic circulatory arrest compared with aortic cross-clamping in regards to operative mortality and long-term outcome. However, future analysis from our center will surely focus on this potential shift in our philosophical approach to patients suffering from this life-threatening emergency situation.
DR RANDALL B. GRIEPP (New York, NY): I would like to congratulate you on a very nice paper, a well-followed group of patients, a low incidence of necessity for reoperation, and a low operative mortality when the patients needed to be reoperated on. I also think your way of analyzing the results is very interesting, suggesting how frequently one needs to do a follow up CT scan. But I still am concerned that—as we have seen in our series and you have seen in yours, I suspect—a number of patients still die, probably of aortic rupture or dissection, after their initial operation. In our series of survivors of acute type A dissection, there was a twofold increase in mortality above a normal population. So those patients that we send out of the hospital after what we think is a pretty good operation still will die at twice the normal rate.
We have been using, as a criterion for reoperation, a diameter of greater than 5 cm for the dissected descending thoracic aorta. Nevertheless, we are still see sudden death although we are following up the patients carefully and trying to operate on them when we see jumps in the rate of growth. I wonder if you would care to speculate from your series how many of the patients are dying of aortic disease after they go home, and whether you could tell us what your criteria are for suggesting reoperation for the descending thoracic aorta? Once again, I enjoyed the paper.
DR ZIERER: Thank you very much, Dr Griepp, for your nice comments and very interesting question. The focus of our current study was to evaluate and to define risk factors associated with aortic growth and diminished freedom from late reoperation rather than to establish guidelines regarding when to reoperate on these patients. As you know, it is also very difficult to obtain the exact cause of late death in these patients, so it remains very challenging to determine how many patients died due to fatal events related to the downstream aorta.
At this point I would therefore like to refer to groundbreaking work done in this area by you and your colleagues from Mount Sinai and from Dr Elefteriades and his colleagues from Yale regarding the natural history of nondissected thoracic aortic aneurysms. In these landmark studies, it has been shown that the risk for rupture or dissection of the descending aorta dramatically increased at a diameter of 7 cm, and based on this finding, the classic recommendation for prophylactic intervention was a descending aortic diameter of 6.5 cm. Clearly the natural history of a residual dissection in the descending aorta following repair of acute type A aortic dissection may be different. In this context, I would like to refer to a subsequent manuscript you published in 1999 in The Journal of Thoracic and Cardiovascular Surgery regarding the natural history of type B dissections, showing that the last mean diameter of the descending aorta prior to rupture was only 5.4 cm.
Based on these data a more aggressive approach for residual aortic dissections may be warranted. However, the decision to reoperate also depends on individual institutional results regarding the risk of operative morbidity and mortality. I would like to point out that the reoperative mortality rate in our current series was quite reasonable at 7%. Given all of this information, a more aggressive strategy for reoperations on the descending thoracic aorta following repair of acute type A aortic dissection may be justified. Compared to the 5 cm you quoted, we still follow a somewhat more conservative approach recommending reoperation at 5.5 to 6.0 cm.
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