doi: 10.1161/01.cir.0000032890.55215.27
(Circulation. 2002;106:I-218.)
© 2002 American Heart Association, Inc.
Aortic and Peripheral Vascular Surgery |
Does Profound Hypothermic Circulatory Arrest Improve Survival in Patients With Acute Type A Aortic Dissection?
From the Department of Cardiovascular and Thoracic Surgery, Stanford University School of Medicine, Stanford, Calif.
Correspondence to D. Craig Miller, MD, Department of Cardiothoracic Surgery, Falk Cardiovascular Research Center, Stanford University School of Medicine, Stanford, California 94305-5247. E-mail dcm{at}stanford.edu
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Abstract |
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Objective No evidence exists that profound hypothermic circulatory arrest (PHCA) improves survival or reduces the likelihood of distal aortic reoperation in patients with acute type A aortic dissection.
Methods Records of 307 patients with acute type A aortic dissection from 1967 to 1999 were retrospectively reviewed. The influence of repair using PHCA (n=121) versus without PHCA (n=186) on death and freedom from distal aortic reoperation was analyzed using multivariable Cox regression models. Propensity score analysis identified a subset of 152 comparable patients in 3 quintiles (QIII–V) in which the effects of PHCA (n=113) versus no PHCA (n=39) were further compared.
Results For all patients, 30-day, 1-year, and 5-year survival estimates were 81±2%, 74±3%, and 63±3% (±1 SE). Survival rates and actual freedom from distal aortic reoperation was not significantly different between treatment methods in the entire patient cohort nor in the matched patients in quintiles III–V. Treatment method was not associated with differences in early major complications, late survival, or distal aortic reoperation rates in the entire patient sample or in quintiles III–V.
Conclusions Aortic repair with or without circulatory arrest was associated with comparable early complications, survival, and distal aortic reoperation rates in patients with acute type A aortic dissection. Despite the lack of concrete evidence favoring the use of PHCA, it does no harm, and most of our group uses PHCA regularly because of its practical technical advantages and theoretical potential merit.
Key Words: aortic dissection • ascending thoracic aorta • profound hypothermic circulatory arrest • cardiopulmonary bypass • thoracic aortic aneurysm
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Introduction |
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In 1975, Griepp from Stanford described the technique of profound hypothermic circulatory arrest (PHCA) for replacement of the aortic arch.1 Recently, PHCA has been used increasingly in patients with acute type A aortic dissection to construct an "open distal anastomosis."2–4 Inspection of the arch during PHCA also avoids the possibility of leaving unrecognized intimal tears in the arch, which are present in some 20% to 30% of patients5–7 and may predispose to late distal aortic reoperation.8 No evidence exists that PHCA improves survival or reduces the rate of downstream aortic reoperations, however, despite the technical and theoretical advantages it affords. Furthermore, operative mortality even in centers with special interest and expertise in thoracic aortic surgery still remains discouragingly high (approximately 15% to 35%).9–13 To address the question of whether aortic repair under PHCA confers benefits over repair without PHCA in patients with acute type A aortic dissection, a propensity-matched analysis was performed to neutralize statistically patient selection and treatment choice biases inherent in a retrospective 32-year database.
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Methods |
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Patient Population
The records of 307 patients who underwent surgical repair of spontaneous acute type A aortic dissection at Stanford University Medical Center, Stanford, CA, from January 1967 to July 1999 were reviewed. Two treatment groups were defined (Figure 1A) one group consisted of 121 patients surgically repaired using PHCA (1986–1999) and the other group consisted of 186 patients repaired without PHCA (1967–1999). Clinical characteristics of the patients are presented in Appendix, Table 5. The PHCA patients were older than the non-PHCA patients and had been operated on more recently. Renal dysfunction, congestive heart failure, aortic rupture, and cardiac tamponade occurred more frequently in the PHCA patients.
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Definitions
The dissection was classified according to the Stanford system,14 and all patients were diagnosed within 14 days of onset of symptoms (mean time=46±65 hours [Appendix, Table 5]). Ten patients with type A intramural hematoma were also included. The known distal extent of aortic dissection was established by preoperative imaging and at operation. Documented extension of the dissection into the aortic arch—defined as arch involvement—occurred more frequently in PHCA patients.
Operative Methods
The operative techniques in the PHCA cohort evolved over time. The present approach15 was aimed at resecting all of the tubular portion of the ascending aorta, the undersurface of the transverse arch, and, if identified, the primary intimal tear. Patients are systemically cooled toward 15 to 25°C bladder temperature. In earlier years, a brief period of retrograde cerebral perfusion was used when completing the distal aortic anastomosis. When the circulatory arrest period is anticipated to be longer than 30 minutes, selective antegrade cerebral perfusion was used. The right axillary artery has become the preferred site for arterial cannulation and used for simplified selective antegrade cerebral perfusion as well as antegrade cardiopulmonary bypass cooling and reperfusion/warming.16 In the non-PHCA patients, only the ascending aorta was resected. With either approach, the distal aorta was routinely reinforced with a Teflon felt "sandwich"15 to form a multilayered cuff, or, more recently, Bioglue (Cryolife, Inc., North West Kennesaw, GA). The extent of aortic resection in PHCA patients, management of the aortic root, and distribution of the location of the primary intimal tear (PIT) are listed in Appendix Table 5; resection of the PIT was similar in both groups.
Follow-Up
Current follow-up was obtained by telephone and/or written communication. Follow-up was 97% complete (n=297), extended to a maximum of 30.7 years, and totaled 1778 patient-years. Follow-up was significantly longer in the non-PHCA patients.
Postoperative Care
Negative inotropic drug treatment was advised indefinitely, even in normotensive patients, in order to minimize the incidence of late redissection, aortic rupture, and false lumen enlargement.17,18 After discharge, it was recommended that all patients receive serial aortic surveillance with annual CT or MRI scans, but compliance with this recommendation could not be assured because most patients were referred from long geographical distances and were covered by a wide variety of different health care providers.
Statistical Methods
Outcomes
Freedom from death at any time after operation and reoperation for distal aortic complications were estimated using the nonparametric method of Kaplan and Meier. In the case of freedom from reoperation, which is a nonfatal event, actual (or observed cumulative frequency) probabilities of reoperation were also calculated. Analyses stratified according to treatment method were compared using the log-rank test. Early mortality was defined as death within 30 days of treatment or during the same hospitalization, regardless of time. Variability of continuous data are expressed as mean±1 SD, that of important fractions or ratios as ±70% confidence levels (CL), and the variability of actuarial or actual estimates as ±1 SEM, roughly equivalent to ±70% CL.
Identification of Predictors of Outcome
The influence of 25 preoperative characteristics or dissection-related complications (the independent variables) on time-related outcome (dependent variables) was analyzed. These preoperative independent variables included age, gender, duration of symptoms, year of operation, surgeon, shock, acute aortic insufficiency, paraplegia, visceral ischemia, renal dysfunction, peripheral pulse deficit, arch involvement, stroke, coronary artery disease, congestive heart failure, pulmonary disease, liver disease, diabetes mellitus, prior stroke, Marfan syndrome (MFS), hypertension, previous dissection, previous sternotomy, tamponade, and rupture. The independent variables chosen were not influenced by treatment type. The predictors of time-related outcome were identified and their hazard ratios (eB, or HR) and 95% CLs were determined from Cox proportional hazards analysis.
Propensity Score Analysis
To neutralize the patient selection and choice of treatment biases present in this retrospective series, the patients were matched by developing a propensity model for PHCA versus no circulatory arrest based on multivariable logistic regression in which operative year, cardiac tamponade, and arch involvement emerged as significant predictors of treatment method. This propensity score was calculated from the logistic equation for each patient. The patients were then divided into 5 propensity-matched quintiles (Appendix, Table 6). Patients in quintiles I and II (n=155) were not analyzed because they had a very low propensity to undergo PHCA. Because of the small patient numbers in each strata in quintiles III–V, the 152 patients in quintiles III–V (39 non-PHCA and 113 PHCA patients), representing 49% of the total patient population, were combined for further analysis to determine whether there was any difference in outcome between the 2 treatment approaches (Appendix, Table 6). The PHCA and non-PHCA subsets in quintiles III–V were well matched in terms of risk factors; thus, this approach allowed us to asses the impact of PHCA versus no PHCA on overall outcome in a cohort of comparable patients.
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Results |
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Survival
For all patients, the 30-day, 1-year, and 5-year actuarial survival estimates were 82±2%, 74±3%, and 63±3% [± 1 SEM]. There was no significant difference in overall survival between treatment methods (P=NS, Figure 2A). Risk factors for death at any time in all patients include previous sternotomy, prior stroke, liver disease, cardiac tamponade, aortic arch involvement, hypertension, older age, and earlier year of operation (hazard ratios [HR] listed in Table 1A). In the combined patient subset in quintiles III–V, 30-day, 1-year, and 5-year survival estimates were 84±3%, 77±3%, and 66±4%, respectively; there was no significant difference in survival between treatment methods (P=NS; Figure 2B). Risk factors for death at any time in the 152 propensity-matched patients include prior stroke, renal dysfunction, previous sternotomy, and older age (HR listed in Table 1B), and again treatment method was not associated with any difference in survival.
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Early Death
The 30-day mortality rate using either treatment method tended to fall in the more recent operative era (Figure 1B). The risk of death was highest immediately after operation (Figure 2A and 2B). In all patients, as well as the patients from quintiles III–V, there was no difference in early death rate between treatment types (Appendix, Tables 5 and 6). A logistic regression model showed that renal dysfunction, cardiac tamponade, older age, and earlier operative year predicted a higher probability of early death in the entire patient cohort (HR listed in Table 2A). In the 152 propensity-matched patients (Table 2B), renal dysfunction, cardiac tamponade, and older age predicted early mortality. Again, treatment method was not associated with a difference in early death rate.
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Late Death
The causes of late death are listed in Table 3. Combining late deaths as a result of progression of dissection and/or rupture, those deaths that were sudden and unexplained (because they possibly could have been due to aortic rupture), and those in which a cause was unknown, 28% of the non-PHCA and 50% of the PHCA patients theoretically could have possibly died because of an aortic complication. Comorbidities such as CHF, renal failure, cancer, and stroke accounted for 45% of the deaths in the non-PHCA subset, compared with 30% in PHCA patients. These fractional numbers are misleading, however, because the follow-up period was much shorter for the PHCA patients.
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Distal Aortic Reoperation
In all patients, the 30-day, 1-year, and 5-year actuarial freedom estimates from distal aortic reoperation were 97±1%. 94±2%, and 87±2%. The actual freedom from distal aortic reoperation was 98±1%, 95±1%, and 90±2%, respectively, at 30 days, 1 year, and 5 years. The actual freedom from distal aortic reoperation was not significantly different between treatment types in the entire patient cohort (P=NS; Figure 3A) or among the 152 matched patients in quintiles III–V (P=NS; Figure 3B). Risk factors for distal aortic reoperation in all patients include arch involvement, MFS, peripheral pulse deficit, male gender, and coronary artery disease (HR listed in Table 4A). In patients from quintiles III–V, peripheral pulse deficit was the only risk factor indicating a higher likelihood of distal aortic reoperation (Table 4B).
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Major Morbidity
There was no statistically significant difference in the prevalence of early postoperative bleeding or neurological complications between treatment methods in all patients and the propensity-matched patients from quintiles III–V (Appendix, Tables 5 and 6).
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Discussion |
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The technique of "open distal aortic anastomosis" introduced by the Texas Heart Institute group2 has since been embraced by many others,4,19–23 including our institution,3 for patients with acute type A aortic dissection. Using the open distal aortic anastomosis approach, a sounder and more hemostatic anastomosis can be constructed by avoiding the crowding and distortion induced by the aortic clamp, clamp injuries to the aorta are avoided, and the friable, dissected aorta under the innominate artery is not left behind. Additionally, inspection of the arch during PHCA allows identification and treatment of intimal tears in the arch and distal ascending aorta, which were present in 12±6% (±1 SEM) of PHCA patients compared with 5±3% in the non-PHCA (P=0.02) cohort. The lower number of arch tears in the non-PHCA group probably indicates that many arch tears were not appreciated when a cross-clamp was used. Although a PIT in the arch portends poorer long-term survival relative to tears in other locations,7 there is no evidence that resection of arch tears lowers the risk of early death.17,24 Furthermore, there are no data indicating that using an open distal anastomosis confers any long-term survival benefit,4 with the exception of 1 study by Niederhauser et al19 who reported that 8-year survival improved from 55±6% using noncirculatory arrest and graft wrap-inclusion techniques to 62±4% when PHCA and open anastomoses were employed. This putative survival benefit using open techniques19 could also have been due to minimizing the incidence of false aneurysms associated with use of the wrap-inclusion technique,25 which was employed frequently in the non-PHCA group; anastomotic false aneurysms occur less frequently if an open end-to-end anastomosis to the completely transected distal aorta is constructed.25 It is also possible that the improved short21,22,26 and long-term survival19 reported in patients who underwent aortic repair using PHCA may have been confounded by a "recent era" effect, whereby the apparent improved survival rate may actually be more attributable to surgical and other advances that occurred over time. Such a "recent era" effect was apparent in our series, in which more recent operative year decreased the hazard of early death and of all deaths. Propensity matching is a useful statistical tool to adjust for these biases in patient selection and treatment choice.
Surprisingly, there was no difference in long-term survival or need for reoperation following repair with or without PHCA after propensity matching to neutralize the differences between patient cohorts and other confounding factors. One possible reason for this lack of survival benefit may have been a result of the nonelective need to resort to PHCA to "bail out" patients in certain untoward circumstances (eg, when the arch was disintegrating or the need for total arch replacement arose unexpectedly or when the initial distal anastomosis performed using a cross-clamp did not hold, mandating redoing the anastomosis using PHCA) in the earlier years of this study. Perhaps the crossover of these very high risk patients from planned non-PHCA to the PHCA group masked some potential survival benefit in the PHCA group, despite the propensity score matching process. Although the number of patients who crossed over cannot be determined in this retrospective analysis, we know that such events did occur during the 1985 to 1994 time period (Figure 1A).
Overall, it would appear that patient substrate and not treatment method was the main determinant of outcome. Reported predictors of short-term24,27 and long-term survival and in our series were patient-related and disease-related factors, which for the most part cannot readily be modified. Even after propensity matching, these patient-related factors (ie, prior stroke, renal dysfunction, previous sternotomy, and older age) emerged as independent predictive variables of death. In fact, Neri and associates28 urged that patient-related factors, including age, should be used as criteria to deny patients operation in view of an 83±8% operative mortality rate in very ill patients over 80 years of age. Several other groups, however, have reported operative mortalities under 20% in the elderly.12,29,30 In general, the survival rates in our series were comparable with most reported series,8,13,23,24,26,31–33 despite the advent of a LifeFlight Medi Evac system whereby moribund patients otherwise not destined to survive have been transported expeditiously from as far as a 400-km radius.
Because little extra surgical effort is necessary and no apparent additional risk is imposed by hemiarch repair,8,23,24 we believe that formal hemiarch distal repair under PHCA is better than simple end-to-end anastomosis in the distal ascending aorta even if there is no tear in the aortic arch. The 5-year survival rate was 69±6% (n=60) following replacement of only the ascending aorta under PHCA versus 62±7% (n=61) following hemiarch repair (P=NS). This more aggressive approach results in more resection of the friable dissected aorta and should theoretically lead to fewer late false aneurysms in the distal ascending aorta and proximal arch.22 Indeed, Kazui and associates34 have reported a remarkable 5-year survival rate of 73±6% after total arch replacement in selected patients with acute type A aortic dissection. In Kazui’s report,34 however, resection of more distal aorta (total arch replacement) did not translate into fewer reoperations, because only 77±8% of patients were free from reoperation after 5 years.34
A persistently patent distal aortic false lumen portends more late mortality and morbidity due to progressive aneurysmal dilatation of the false lumen in the distal aorta based on trends showing a lower 5-year survival rate (95±5% with closed versus 76±15% with a patent false lumen) and event-free survival (84±8% with closed versus 63±14% with a patent false lumen).20 The literature suggests that the open technique may reduce the prevalence of persistently patent false lumen from 90% following closed repair to 59% after open repair,4 and from 40% at 5 years following closed repair to 8% at 5 years after open repair.22 Conversely, it is disappointing that the reduction in the false lumen patency rate in David’s series4 after open repair did not improve survival.
Nguyen et al35 reported a reduction in the rate of persistent false lumen from 85% following closed anastomosis using Teflon felt to 55% using open distal anastomosis and biological glues, which lowered the incidence of downstream aortic reoperation from 30% following closed repair to 6% after open repair. Pugliese and associates36 also reported fewer downstream aortic reoperations (24% following closed repair versus 8% after open repair). Both of these studies, however, were statistically lacking in that only crude fractions (and not actuarial or actual data, ie, rates of aortic reoperations over time) were reported. In our series, treatment method had no discernible influence on the rate of downstream aortic reoperation, but the need for reoperation was low: 90±2% of patients were free from distal aortic reoperation in actual terms at 5 years. Lack of assiduous radiological surveillance imaging beyond our control may have been responsible for fewer reoperations, because some patients with expanding or large, but asymptomatic, aortic false lumens may not have been detected. Thus, we cannot comment conclusively on the rate of progression of residual downstream aortic disease. The higher prevalence of late deaths resulting from dissection in the non-PHCA group does suggest, nonetheless, that the use of PHCA might reduce the number of late deaths related to aortic dissection. This observation may have been confounded, however, by the shorter follow-up period and incomplete data regarding the cause of late death in the PHCA group (Table 3). The determinants of distal aortic reoperation were patient-related and disease-related factors. Arch involvement, MFS, peripheral pulse deficit, male gender, and coronary artery disease emerged as risk factors for distal aortic reoperation in the entire patient cohort, and only peripheral pulse deficit was a significant predictor in the propensity-matched patients. Postoperative complications were not analyzed in detail in this study, but there was no significant difference in postoperative bleeding or neurological complications between treatment methods in propensity-matched patients. Use of retrospective data are the main limitation inherent in this analysis because we can only statistically adjust for observed covariates, unlike prospective randomized trials that can account for both observed and unobserved factors.
In conclusion, both treatment methods provided comparable survival for patients with acute type A aortic dissection. No evidence favoring the use of PHCA in terms of early major complication rates, overall patient survival, or late distal aortic reoperation was found. Nevertheless, most of our group continues to use this technical option because of the practical technical advantages it affords and its theoretical potential merit. Demonstrable patient benefit in terms of fewer early postoperative complications, improved survival, and freedom from downstream late aortic reoperation may in time become clear when larger numbers of patients and longer follow-up become available.
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Footnotes |
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Dr Lai is a Carl and Leah McConnell Cardiovascular Surgical Research Fellow
Guest editor Richard D. Weisel, MD, Toronto General Hospital, Toronto, Canada
Presented in part at the American Heart Association Scientific Sessions
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Appendix |
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References |
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1. Griepp RB, Stinson EB, Hollingsworth JF. Prosthetic replacement of the aortic arch. J Thorac Cardiovasc Surg. 1975; 70: 1051–1063.[Abstract]
2. Livesay JJ, Cooley DA, Duncan JM, et al. Open aortic anastomosis: improved results in the treatment of aneurysms of the aortic arch. Circulation. 1982; 66 (2 Pt 2):I122–I127.
3. Yun KL, Glower DD, Miller DC, et al. Aortic dissection resulting from tear of transverse arch: is concomitant arch repair warranted? J Thorac Cardiovasc Surg. 1991; 102: 355–368.[Abstract]
4. David TE, Armstrong S, Ivanov J, et al. Surgery for acute type A aortic dissection. Ann Thorac Surg. 1999; 67: 1999–2001.
5. Roberts WC. Aortic dissection: anatomy, consequences, and causes. Am Heart J. 1981; 101: 195–214.[CrossRef][Medline] [Order article via Infotrieve]
6. Van Arsdell GS, David TE, Butany J. Autopsies in acute type A aortic dissection. Surgical implications. Circulation. 1998; 98 (19 suppl):II299–II302.
7. Lansman SL, McCullough JN, Nguyen KH, et al. Subtypes of acute aortic dissection. Ann Thorac Surg. 1999; 67: 1975–1978.
8. Moon MR, Sundt TM,III, Pasque MK et al. Does the extent of proximal or distal resection influence outcome for type A dissections Ann Thorac Surg. 2001; 71: 1244–1249.
9. Pansini S, Gagliardotto PV, Pompei E, et al. Early and late risk factors in surgical treatment of acute type A aortic dissection. Ann Thorac Surg. 1998; 66: 779–784.
10. Fann JI, Smith JA, Miller DC, et al. Surgical management of aortic dissection during a 30-year period. Circulation. 1995; 92 (9 suppl):II113–II121.
11. Kawahito K, Adachi H, Yamaguchi A, et al. Preoperative risk factors for hospital mortality in acute type A aortic dissection. Ann Thorac Surg. 2001; 71: 1239–1243.
12. Kawahito K, Adachi H, Yamaguchi A, et al. Early and late surgical outcomes of acute type A aortic dissection in patients aged 75 years and older. Ann Thorac Surg. 2000; 70: 1455–1459.
13. Hagan PG, Nienaber CA, Isselbacher EM, et al. The International Registry of Acute Aortic Dissection (IRAD): new insights into an old disease. JAMA. 2000; 283: 897–903.
14. Daily PO, Trueblood HW, Stinson EB, et al. Management of acute aortic dissections. Ann Thorac Surg. 1970; 10: 237–247.[Medline] [Order article via Infotrieve]
15. Moon MR, Miller DC. Aortic arch replacement for dissection. Operative Tech Thorac Cardiovasc Surg. 1999; 4: 33–57.
16. Sabik JF, Lytle BW, McCarthy PM, et al. Axillary artery: an alternative site of arterial cannulation for patients with extensive aortic and peripheral vascular disease. J Thorac Cardiovasc Surg. 1995; 109: 885–890.[Abstract]
17. Miller DC, Mitchell RS, Oyer PE, et al. Independent determinants of operative mortality for patients with aortic dissections. Circulation. 1984; 70 (3 Pt 2):I153–I164.
18. Svensson LG, Crawford ES, Hess KR, et al. Variables predictive of outcome in 832 patients undergoing repairs of the descending thoracic aorta. Chest. 1993; 104: 1248–1253.
19. Niederhauser U, Rudiger H, Kunzli A, et al. Surgery for acute type a aortic dissection: comparison of techniques. Eur J Cardiothorac Surg. 2000; 18: 307–312.
20. Ergin MA, Phillips RA, Galla JD, et al. Significance of distal false lumen after type A dissection repair. Ann Thorac Surg. 1994; 57: 820–824.[Abstract]
21. Svensson LG, Crawford ES, Hess KR, et al. Dissection of the aorta and dissecting aortic aneurysms. Improving early and long-term surgical results. Circulation. 1990; 82 (5 suppl):IV24–IV38.
22. Bernard Y, Zimmermann H, Chocron S, et al. False lumen patency as a predictor of late outcome in aortic dissection. Am J Cardiol. 2001; 87: 1378–1382.[CrossRef][Medline] [Order article via Infotrieve]
23. Sabik JF, Lytle BW, Blackstone EH, et al. Long-term effectiveness of operations for ascending aortic dissections. J Thorac Cardiovasc Surg. 2000; 119: 946–962.
24. Ehrlich MP, Ergin MA, McCullough JN, et al. Results of immediate surgical treatment of all acute type A dissections. Circulation. 2000; 102 (19 suppl 3):III248–III252.
25. Carrel T, Pasic M, Jenni R, et al. Reoperations after operation on the thoracic aorta: etiology, surgical techniques, and prevention. Ann Thorac Surg. 1993; 56: 259–268.[Abstract]
26. Crawford ES, Kirklin JW, Naftel DC, et al. Surgery for acute dissection of ascending aorta. Should the arch be included? J Thorac Cardiovasc Surg. 1992; 104: 46–59.[Abstract]
27. Svensson LG, Crawford ES, Hess KR, et al. Deep hypothermia with circulatory arrest. Determinants of stroke and early mortality in 656 patients. J Thorac Cardiovasc Surg. 1993; 106: 19–28.[Abstract]
28. Neri E, Toscano T, Massetti M, et al. Operation for acute type A aortic dissection in octogenarians: is it justified? J Thorac Cardiovasc Surg. 2001; 121: 259–267.
29. Hagl C, Griepp RB. Acute type A dissection in octogenarians. J Thorac Cardiovasc Surg. 2001; 122: 1050–1051.
30. Hagl C, Galla JD, Spielvogel D, et al. Is aortic surgery using hypothermic circulatory arrest in octogenarians justifiable? Eur J Cardiothorac Surg. 2001; 19: 417–422.
31. Casselman FP, Tan ES, Vermeulen FE, et al. Durability of aortic valve preservation and root reconstruction in acute type A aortic dissection. Ann Thorac Surg. 2000; 70: 1227–1233.
32. Bachet J, Goudot B, Dreyfus GD, et al. Surgery for acute type A aortic dissection: the H"pital Foch experience (1977–1998). Ann Thorac Surg. 1999; 67: 2006–2009.
33. Ehrlich M, Fang WC, Grabenwoger M, et al. Perioperative risk factors for mortality in patients with acute type A aortic dissection. Circulation. 1998; 98 (19 suppl):II294–II298.
34. Kazui T, Washiyama N, Muhammad BA, et al. Extended total arch replacement for acute type a aortic dissection: experience with seventy patients. J Thorac Cardiovasc Surg. 2000; 119: 558–565.
35. Nguyen B, Muller M, Kipfer B, et al. Different techniques of distal aortic repair in acute type A dissection: impact on late aortic morphology and reoperation. Eur J Cardiothorac Surg. 1999; 15: 496–500.
36. Pugliese P, Pessotto R, Santini F, et al. Risk of late reoperations in patients with acute type A aortic dissection: impact of a more radical surgical approach. Eur J Cardiothorac Surg. 1998; 13: 576–580.
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