ATS
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


This Article
Right arrow Abstract Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to Personal Folders
Right arrow Download to citation manager
Right arrow Author home page(s):
Xavier M. Mueller
Hendrik T. Tevaearai
Patrick Ruchat
Right arrow Permission Requests
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Mueller, X. M.
Right arrow Articles by von Segesser, L. K.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Mueller, X. M.
Right arrow Articles by von Segesser, L. K.
Related Collections
Right arrowRelated Articles

Ann Thorac Surg 1997;63:762-766
© 1997 The Society of Thoracic Surgeons


Original Article: Cardiovascular

Drawback of Aortoplasty for Aneurysm of the Ascending Aorta Associated With Aortic Valve Disease

Xavier M. Mueller, MD, Hendrik T. Tevaearai, MD, Claude Y. Genton, MD, Michel Hurni, MD, Patrick Ruchat, MD, Adam P. Fischer, MD, Frank Stumpe, MD, Ludwig K. von Segesser, MD

Department of Cardiovascular Surgery and Institute of Pathology, Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland

Accepted for publication October 21, 1996.


    Abstract
 Top
 Footnotes
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 References
 
Background. Aortoplasty has been advocated for moderate dilatation of the ascending aorta associated with aortic valve disease. We report our results with this conservative approach.

Methods. Seventeen consecutive patients with unsupported aortoplasty were reviewed. Twelve patients had aortic valve regurgitation and 5 had stenosis. The aortic wall was analyzed histologically in 14 patients. Follow-up was complete, with a mean time of 6 years (range, 2.3 to 10.5 years).

Results. Two patients among the 15 hospital survivors died during follow-up of causes unrelated to aortic pathology. Survival at 7 years was 86.7% (±8.8%). Recurring aortic aneurysms developed in 4 patients after a mean time of 63 months, with an event-free survival at 7 years of 41% (±21%). All of these 4 patients had aortic valve regurgitation and cystic medial necrosis.

Conclusions. The recurrence rate of aneurysms after unsupported aortoplasty and aortic valve replacement is high in patients with aortic regurgitation. This strongly suggests that in these patients, the aortic dilatation is related to an underlying wall deficiency, associated with the aortic valve pathology, rather than to the hemodynamic stress imposed by the aortic valve disease.


    Introduction
 Top
 Footnotes
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 References
 
See also page 766a.

The need to deal with an associated ascending aortic aneurysm during aortic valve replacement is frequently encountered by the surgeon. Controversy exists as to whether these aortic changes are the result of turbulent flow related to valvular pathology, underlying intrinsic wall weakness, or both [1, 2]. Dacron (Du Pont Pharma GmbH) graft replacement is the most commonly used method for repair of the ascending aortic aneurysm. However, less radical treatment has been advocated for moderate dilatation of the ascending aorta, sparing the sinus of Valsalva [3, 4]. In these selected patients, we performed an unsupported aortoplasty with excision of a segment of the aortic wall to decrease the diameter of the aneurysm and remodel the ascending aorta. This study evaluates the results of this conservative approach specifically in terms of aneurysm recurrence.


    Patients and Methods
 Top
 Footnotes
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 References
 
We reviewed the medical records of 17 consecutive patients in our institution who underwent an unsupported aortoplasty of an aneurysm of the ascending aorta associated with aortic valve disease between January 1984 and December 1992. There were 13 men and 4 women, with a median age of 68 years (range, 30 to 78 years). None had undergone previous cardiac or aortic operations. Symptoms included congestive heart failure in 13 patients and angina pectoris in 1. Two patients were in New York Heart Association functional class I, 7 in class II, 6 in class III, and 2 in class IV. Ten patients were known to have hypertension. Twelve patients had predominantly regurgitation of the aortic valve, and 5 patients had stenosis. All of the patients with stenosis were found to have congenitally bicuspid valves. In the aortic valve regurgitation group, seven valves showed features of myxoid degeneration, two valves were bicuspid, one valve was fibrosed, and two valves were ultrastructurally normal. Most of the ascending aortas ranged from 5 to 5.5 cm in diameter. In 6 elderly patients, the aorta was between 5.5 and 6 cm in diameter. Although this is a borderline size for aortoplasty, we believed that this procedure was warranted, as a short aortic cross-clamp time could be advantageous in these high-risk patients. Routine postoperative echocardiography was performed at 7 days.

Operative Method
The ascending aorta was approached through the usual median sternotomy. An aortic cannula was placed in the proximal transverse aortic arch in 15 patients, and femoral arterial cannulation was used in 2 patients. The aorta was then cross-clamped distal to the aneurysm, and the aortic valve was exposed through an oblique or longitudinal aortotomy, which was carried into the noncoronary sinus. Myocardial protection was achieved with intermittent cold crystalloid cardioplegia into the exposed coronary orifices. The aortic valve was excised and replaced with a St. Jude mechanical prosthesis in 15 patients and a Carpentier-Edwards bioprosthesis in 2. Four patients underwent concomitant coronary artery bypass grafting. An aortoplasty was performed by removing an oval portion of the aortic wall. The aortotomy was closed in two layers using 4/0 polypropylene sutures. Two patients required Teflon (Du Pont Pharma) felt reinforcement of the suture line. No aortic external wall support with a Mersilene (Johnson and Johnson, Spreitenbach, Switzerland) net or a piece of graft was performed.

Histopathologic Studies
The histologic slides of the resected aortic wall, stained with hematoxylin and eosin and combined Verhoeff–van Gieson, were reviewed and analyzed according to the system proposed by Schlatmann and Becker [5, 6]. These investigators identified four categories of changes in the media of the aorta: (1) cystic medial necrosis, defined as pooling of mucoid material; (2) elastin fragmentation, characterized by disruption of elastin lamellae; (3) fibrosis, defined as an increase in collagen at the expense of smooth muscle cells; and (4) medionecrosis, defined as areas with apparent loss of nuclei. Each feature was divided into three grades. Atherosclerotic features were also sought and graded according to the criteria of Klima and associates [7].

Follow-up
Mortality and aneurysm recurrence were analyzed. The patients were interviewed by telephone. If death had occurred, the cause of death was established by contacting the general practitioner. Follow-up was complete in all patients, with a mean time of 6 years (range, 2.2 to 10.5 years). All surviving patients had control echocardiographic studies during follow-up.

Statistical Method
Actuarial survival and event-free curves were plotted by the Kaplan-Meier method. Results were expressed with 1 standard deviation.


    Results
 Top
 Footnotes
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 References
 
Early Results
Fifteen patients were discharged from the hospital. One patient had bronchoaspiration on the sixth postoperative day, with a subsequently intractable acute respiratory distress syndrome, and died on the 14th postoperative day. Another patient had postoperative bleeding because of consumptive coagulopathy, with reexploration on the first postoperative day. Multiple organ failure developed, and she died on the 20th postoperative day. No other major complications occurred.

Late Results
There were two late deaths. One patient presented in a septic state at 2 months, which was recognized at autopsy to be related to an acute endocarditis of the aortic valve bioprosthesis. The other patient, known to have carotid artery disease, had a massive stroke at 6 months. Thirteen patients were alive at follow-up. The Kaplan-Meier patient actuarial survival curve is shown in Figure 1Go. All surviving patients were in New York Heart Association functional class I (8 patients) or II (5 patients) at the time of follow-up.



View larger version (13K):
[in this window]
[in a new window]
 
Fig 1. . Kaplan-Meier actuarial survival curve of hospital survivors. ( N = number of patients; SD = ± 1 standard deviation [%].)

 
One patient had a growing paravalvular leak postoperatively shown on echocardiography, requiring reoperation at 3 months.

Aortic enlargement recurred in 4 patients. The recurrence-free curve is shown in Figure 2Go. Their median age at the first operation was 53 years (range, 46 to 62 years). All initially had aortic valve regurgitation; morphologic analysis showed myxoid changes in 2 patients, bicuspid configuration in 1, and fibrosis in 1. Three patients had their enlargement established by routine control echocardiographic studies, and 1 had echocardiography because of a superior vena cava syndrome. Two patients had chronic aortic dissection. The aneurysm recurrences were diagnosed 45, 59, 67, and 81 months after the initial operation (mean, 63 months). Two patients underwent ascending aorta prosthetic replacement, and the 2 patients with dissection had a Bentall procedure. One of the latter suffered three major complications after the second operation: a perioperative myocardial infarction with transient low output syndrome, a severe streptococcal lung infection requiring 10 days of mechanical ventilation, and an acute tubular necrosis not requiring dialysis. This patient recovered and is now in New York Heart Association functional class II.



View larger version (14K):
[in this window]
[in a new window]
 
Fig 2. . Kaplan-Meier actuarial analysis of freedom from aneurysm recurrence after unsupported aortoplasty. ( N = number of patients; SD = ± 1 standard deviation [%].)

 
Histopathologic Features
The histologic slides of 14 patients were available. A striking finding in these morphologic examinations was the marked variation in lesion severity from one area to another. Cystic medial necrosis was present in all of the patients with aneurysm recurrence, but no reliable predictive morphologic index for risk of recurrence could be identified.


    Comment
 Top
 Footnotes
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 References
 
An aneurysm of the ascending aorta encountered during an aortic valve operation may be of limited size. It is tempting under these conditions to use a less radical operation than graft replacement, such as reduction aortoplasty, especially in high-risk elderly patients in whom a decreased aortic cross-clamp time is advantageous. Series of patients operated on using this procedure are scarce in the literature [4, 8, 9], and the results are conflicting. We therefore reviewed our experience to analyze the hospital and long-term results.

Our 12% hospital mortality rate is comparable to that in current large series of ascending aneurysms treated by ascending aorta graft replacement: 30-day mortality was 7.6% in the 339 patients of Jault and colleagues [10] and 13.8% in the 225 patients of Lytle and co-workers [11]. One of our patients died of postoperative bleeding related to consumptive coagulopathy, with no identifiable operative source. This contrasts with the series of aortoplasties by McCready and Pluth [8] and Egloff and colleagues [9], performed in the 1970s, which reported early mortality rates of 19% (4/21 patients) and 29% (9/31 patients) with two postoperative deaths each, due to suture line bleeding. These results can be related in part to the inclusion of 6 and 7 patients, respectively, with aortic dissection, which is known to be associated with more friable wall. Moreover, improvements in perioperative care since then—especially the increased experience with titrable intravenous antihypertensive agents and parenteral drug therapy for ß-adrenergic blockade—have permitted precise control of the hemodynamic condition and minimized the risk of postoperative bleeding.

The survival at 7 years of 86.7% (±8.8%) is higher than those of the aortoplasty series [8, 9]. In the latter, 10 and 4 patients, among 22 and 16 hospital survivors, respectively, had died at a median follow-up of 54 and 52 months. These results may be explained by a high mortality rate after reoperation for recurrent aneurysms, and by rupture of undetected recurrent aneurysms, in the absence of routine follow-up echocardiography.

We found a high rate of recurrence of aneurysms among the long-term survivors; the percentage of patients who were event free and alive was 41% (±21%) at 7 years. This is in keeping with the findings of McCready and Pluth [8]—three recurrences in 22 hospital survivors—and of Egloff and colleagues [9]—five recurrences in 16 hospital survivors. On the other hand, Barnett and associates [4] found no recurrences among 12 hospital survivors in their recent report. Several features of their study design may explain this result. First, nearly half of their patients had aortoplasties including wall reinforcement with Dacron wrap of the ascending aorta, leaving only 9 patients with aortoplasty alone for analysis. Second, their follow-up extended from 2 to 120 months (average, 4.4 years). Considering that the average interval from operation to recurrence was 65 months in the group of McCready and Pluth [8] and 63 months in our group, with the shortest intervals of 32 and 45 months, respectively, the follow-up of Barnett and associates [4] is too short to detect recurrent aneurysms. Finally, they relied on chest roentgenograms for diagnosis of recurrence, in contrast to routine control echocardiographic studies performed in our patients. The latter diagnosed three of the four recurrent aneurysms. We stress again the need to perform this control at regular intervals after unsupported aortoplasty.

Whether congenital aortic wall weakness, hemodynamic stress imposed by the associated aortic valve disease, or both, is the primary factor in the development of ascending aorta dilatation is still debatable.

In stenotic aortic lesions, hemodynamic stress has been implicated as the primary factor in the development of poststenotic dilatation [2, 12, 13]. However, the recognized association of ascending aortic dilatation with a stenotic aortic bicuspid valve suggests that wall weakness may also play an etiologic role [14]. In our experience, no recurrence was found in the 5 patients with aortic stenosis, suggesting that in this subgroup, hemodynamic factors play a predominant role in the development of aortic dilatation. However, the limited number of patients prevents us from drawing definite conclusions.

Recent clinical and pathologic studies have pointed out that idiopathic aortic root dilatation is currently the most common cause of aortic valve regurgitation in western countries [1517]. In particular, a striking association has been found between aortic valve regurgitation of bicuspid valves and root dilatation [14, 16, 17], suggesting that abnormal structural integrity of the ascending aorta predisposes to aortic root dilatation. Hahn and associates [1] also demonstrated a high prevalence of aortic root enlargement in patients with a bicuspid aortic valve regardless of altered valvular hemodynamic indices. In our group, most of the insufficient valves were morphologically abnormal, supporting the hypothesis that abnormalities of both the aortic wall and valve may be manifestations of a common underlying process. Our four recurrences, two with chronic dissection, all occurred among the 9 patients with aortic valve regurgitation. This high recurrence rate after elimination of the source of hemodynamic turbulence further supports intrinsic wall weakness as the primary cause of ascending aortic dilatation in patients with aortic valve regurgitation. In keeping with this finding, Crawford and colleagues [18] reported a series of patients reoperated on for recurrent aneurysmal disease after previous operations involving the ascending aorta and transverse aortic arch. Aortic valve regurgitation was present in 11 of 18 patients, who presented initially with a nondissecting aneurysm due to non-Marfan's medial degenerative disease.

In the report of Barnett and associates [4], only 30% of the patients had severe aortic valve regurgitation, suggesting an additional reason for the nonrecurrence of their disease. Neither McCready and Pluth [8] nor Egloff and colleagues [9] mentioned the type of aortic valve pathology in their patients with recurrence. However, in the early Zürich experience, Egloff and colleagues [9] already concluded that a tissue factor must be important and at least partly responsible for recurrent dilatation and dissection, as they occurred in patients with all types of aortic wall disease and after all types of repair or replacement procedures. More recently, in the same institution, Carrel and co-workers [3] confirmed this view, reporting dilatation and dissection pathology in further segments in the ascending arch or descending or abdominal aorta after operations on the ascending aorta.

Morphologic analysis showed a uniform prevalence of cystic medial necrosis in the patients with recurrence of aneurysm. Klima and associates [7] found that cystic medial change was inversely correlated with increasing age in patients with ascending aortic aneurysms, especially in patients without clinical evidence of Marfan's syndrome. This suggests the existence of undetected connective tissue disorder in the general population. However, no specific histologic feature was found to be predictive of recurrence in our group. This can be explained in part by the variability of the lesions from one area to another within the same specimen. Schlatmann and Becker [5, 6] found only quantitative differences of these histologic features between normal aging aorta and aneurysmal or dissecting aorta. Thus, they concluded that these findings merely represent the morphologic substrate of traumatizing and reparative processes, occurring earlier in life in patients with connective tissue disorder.

Our results have changed our attitude toward aneurysm of the ascending aorta associated with aortic valve disease and have led us to a few recommendations.

(1) In our experience, the aneurysm recurrence rate is high after unsupported aortoplasty for aortic aneurysm associated with aortic valve regurgitation. There is strong evidence that this tendency is related to an underlying intrinsic wall deficiency. As underlined by Robicsek [19]: Although aortoplasty addresses one of the principal components of increased wall stress, ie, the aortic diameter, it leaves the second equally important contributor, wall thickness and strength, unattended. In other words, aortoplasty eliminates the aneurysm, but it does not prevent recurrence. We have definitively abandoned unsupported aortoplasty in patients with aortic valve regurgitation. Moreover, our results present indirect evidence for wrapping the ascending aorta after aortoplasty [20], as further emphasized by Robicsek [19]: The normal aortic geometry, thus restored, should be further secured by external application of a well fitted Dacron vascular graft anchored proximally either to the commissure or, if a prosthetic valve was implanted, to the prosthetic valve itself. However, in view of the low morbidity and mortality in large series of ascending aortic graft replacements [10, 11], we now perform this radical procedure routinely in patients with aortic aneurysm associated with aortic valve regurgitation, and we keep aortic wall support as an adjunct to aortoplasty for older or high-risk patients in whom a short aortic cross-clamp time is advantageous.

(2) In patients with aortic stenosis, aortoplasty is likely to suffice, especially in the elderly. We add an aortic wall support, as our experience is too limited to assess definitively the reliability of unsupported aortoplasty with this condition.

(3) The lack of any specific histologic features predictive of aneurysm recurrence and the variability of the morphologic lesions within the same specimen preclude any value of perioperative frozen section for deciding whether the aortic wall itself is the cause of the dilatation.

(4) In all patients who have undergone aortoplasty without wall support, we strongly advise yearly echocardiographic follow-up to detect aneurysm recurrences early enough to treat them operatively.


    Footnotes
 Top
 Footnotes
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 References
 
Address reprint requests to Dr Mueller, Department of Cardiovascular Surgery, CHUV, CH-1011 Lausanne, Switzerland.


    References
 Top
 Footnotes
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 References
 

  1. Hahn RT, Roman MJ, Mogtader AH, Devereux RB. Association of aortic dilation with regurgitant, stenotic and functionally normal bicuspid aortic valves. J Am Coll Cardiol 1992;19:283–8.[Abstract]
  2. Holman E. The obscure physiology of poststenotic dilatation: its relation to the development of aneurysms. J Thorac Surg 1954;28:109–33.
  3. Carrel T, von Segesser L, Jenni R, et al. Dealing with dilated ascending aorta during aortic valve replacement: advantages of conservative surgical approach. Eur J Cardiothorac Surg 1991;5:137–43.[Abstract/Free Full Text]
  4. Barnett MG, Fiore AC, Vaca KJ, Milligan TW, Barner HB. Tailoring aortoplasty for repair of fusiform ascending aortic aneurysms. Ann Thorac Surg 1995;59:497–501.[Abstract/Free Full Text]
  5. Schlatmann TJ, Becker AE. Histologic changes in the normal aging aorta: implications for dissecting aortic aneurysm. Am J Cardiol 1977;39:13–20.[Medline]
  6. Schlatmann TJ, Becker AE. Pathogenesis of dissecting aneurysm of aorta. Comparative histopathologic study of significance of medial changes. Am J Cardiol 1977;39:21–6.[Medline]
  7. Klima T, Spjut HJ, Coelho A, et al. The morphology of ascending aortic aneurysms. Hum Pathol 1983;14:810–7.[Medline]
  8. McCready RA, Pluth JR. Surgical treatment of ascending aortic aneurysms associated with aortic valve insufficiency. Ann Thorac Surg 1979;28:307–16.[Abstract/Free Full Text]
  9. Egloff L, Rothlin M, Kugelmeier J, Senning A, Turina M. The ascending aortic aneurysm: replacement or repair? Ann Thorac Surg 1982;34:117–24.[Abstract/Free Full Text]
  10. Jault F, Nataf P, Rama A, et al. Chronic disease of the ascending aorta. Surgical treatment and long-term results. J Thorac Cardiovasc Surg 1994;108:747–54.[Abstract/Free Full Text]
  11. Lytle BW, Mahfood SS, Cosgrove DM, Loop FD. Replacement of the ascending aorta. Early and late results. J Thorac Cardiovasc Surg 1990;99:651–8.[Abstract]
  12. Jarchow BH, Kincaid OW. Poststenotic dilatation of the ascending aorta: its occurrence and significance as a roentgenologic sign of aortic stenosis. Proc Staff Meet Mayo Clin 1961;36:23–33.[Medline]
  13. Robicsek F. Post-stenotic dilatation of the great vessels. Acta Med Scand 1955;151:481–5.[Medline]
  14. Lindsay J. Coarctation of the aorta, bicuspid aortic valve and abnormal ascending aortic wall. Am J Cardiol 1988;61:182–4.[Medline]
  15. Guiney TE, Davies MJ, Parker DJ, Leech GJ, Leatham A. The aetiology and course of isolated severe aortic regurgitation: a clinical, pathological, and echocardiographic study. Br Heart J 1987;58:358–68.[Abstract/Free Full Text]
  16. Roman MJ, Devereux RB, Niles NW, et al. Aortic root dilatation as a cause of isolated, severe aortic regurgitation. Prevalence, clinical and echocardiographic patterns, and relation to left ventricular hypertrophy and function. Ann Intern Med 1987;106:800–7.[Abstract/Free Full Text]
  17. Olson LJ, Subramanian R, Edward WD. Surgical pathology of pure aortic insufficiency: a study of 225 cases. Mayo Clin Proc 1984;59:835–41.[Medline]
  18. Crawford ES, Crawford JL, Safi HJ, Coselli JS. Redo operations for recurrent aneurysmal disease of the ascending aorta and transverse aortic arch. Ann Thorac Surg 1985;40:439–55.[Abstract/Free Full Text]
  19. Robicsek F. Invited commentary on: Barnett MG, Fiore AC, Vaca KJ, Milligan TW, Barner HB. Tailoring aortoplasty for repair of fusiform ascending aneurysms. Ann Thorac Surg 1995;59:501.
  20. Robicsek F. A new method to treat fusiform aneurysms of the ascending aorta associated with aortic valve disease: an alternative to radical resection. Ann Thorac Surg 1982;34:91–4.

Related Articles

Francis Robicsek
Ann. Thorac. Surg. 1997 63: 766. [Extract] [Full Text]

Hassan Najafi
Ann. Thorac. Surg. 1997 63: 766-767. [Extract] [Full Text]



This article has been cited by other articles:


Home page
Interact CardioVasc Thorac SurgHome page
S. J. Park, J. B. Kim, and C. H. Chung
Isolated aortic root dilatation following sinotubular junction reduction using prosthetic rings
Interact CardioVasc Thorac Surg, January 31, 2012; (2012) ivr170v1.
[Abstract] [Full Text] [PDF]


Home page
J. Thorac. Cardiovasc. Surg.Home page
H. Zhang, F. Lu, D. Qu, L. Han, J. Xu, G. Ji, and Z. Xu
Treatment of fusiform ascending aortic aneurysms: A comparative study with 2 options
J. Thorac. Cardiovasc. Surg., March 1, 2011; 141(3): 738 - 743.
[Abstract] [Full Text] [PDF]


Home page
Ann. Thorac. Surg.Home page
S. Akgun, N. Atalan, O. Fazliogullari, A. T. Kunt, C. Basaran, and S. Arsan
Aortic Root Aneurysm After Off-Pump Reduction Aortoplasty
Ann. Thorac. Surg., November 1, 2010; 90(5): e69 - e70.
[Abstract] [Full Text] [PDF]


Home page
Interact CardioVasc Thorac SurgHome page
M. Gill and J. Dunning
Is reduction aortoplasty (with or without external wrap) an acceptable alternative to replacement of the dilated ascending aorta?
Interact CardioVasc Thorac Surg, October 1, 2009; 9(4): 693 - 697.
[Abstract] [Full Text] [PDF]


Home page
Ann. Thorac. Surg.Home page
T. Walker, D. H.L. Bail, M. Gruler, R. Vonthein, V. Steger, and G. Ziemer
Unsupported Reduction Ascending Aortoplasty: Fate of Diameter and of Windkessel Function
Ann. Thorac. Surg., March 1, 2007; 83(3): 1047 - 1053.
[Abstract] [Full Text] [PDF]


Home page
Ann. Thorac. Surg.Home page
G. Polvani, F. Barili, L. Dainese, V. K. Topkara, F. H. Cheema, E. Penza, S. Ferrarese, A. Parolari, F. Alamanni, and P. Biglioli
Reduction Ascending Aortoplasty: Midterm Follow-Up and Predictors of Redilatation
Ann. Thorac. Surg., August 1, 2006; 82(2): 586 - 591.
[Abstract] [Full Text] [PDF]


Home page
Ann. Thorac. Surg.Home page
C. Banfi, M. Rinaldi, A. M. D'Armini, and M. Vigano
End-to-End Anastomosis for Ascending Aortic Aneurysm
Ann. Thorac. Surg., July 1, 2005; 80(1): 385 - 386.
[Full Text] [PDF]


Home page
J. Thorac. Cardiovasc. Surg.Home page
M. A. Borger, M. Preston, J. Ivanov, P. W.M. Fedak, P. Davierwala, S. Armstrong, and T. E. David
Should the ascending aorta be replaced more frequently in patients with bicuspid aortic valve disease?
J. Thorac. Cardiovasc. Surg., November 1, 2004; 128(5): 677 - 683.
[Abstract] [Full Text] [PDF]


Home page
J. Thorac. Cardiovasc. Surg.Home page
F. Robicsek, J. W. Cook, M. K. Reames Sr, and E. R. Skipper
Size reduction ascending aortoplasty: Is it dead or alive?
J. Thorac. Cardiovasc. Surg., October 1, 2004; 128(4): 562 - 570.
[Abstract] [Full Text] [PDF]


Home page
Ann. Thorac. Surg.Home page
S. Arsan, S. Akgun, N. Kurtoglu, T. Yildirim, and B. Tekinsoy
Reduction aortoplasty and external wrapping for moderately sized tubular ascending aortic aneurysm with concomitant operations
Ann. Thorac. Surg., September 1, 2004; 78(3): 858 - 861.
[Abstract] [Full Text] [PDF]


Home page
J. Thorac. Cardiovasc. Surg.Home page
M. Massetti, S. Veron, E. Neri, O. Coffin, O. le Page, G. Babatasi, D. Buklas, D. Maiza, J. L. Gerard, and A. Khayat
Long-term durability of resection and end-to-end anastomosis for ascending aortic aneurysms
J. Thorac. Cardiovasc. Surg., May 1, 2004; 127(5): 1381 - 1387.
[Abstract] [Full Text] [PDF]


Home page
Eur J Cardiothorac SurgHome page
L. Agozzino, F. Ferraraccio, S. Esposito, A. Trocciola, A. Parente, A. Della Corte, M. De Feo, and M. Cotrufo
Medial degeneration does not involve uniformly the whole ascending aorta: morphological, biochemical and clinical correlations
Eur J Cardiothorac Surg, April 1, 2002; 21(4): 675 - 682.
[Abstract] [Full Text] [PDF]


Home page
Ann. Thorac. Surg.Home page
M. Bauer, M. Pasic, R. Schaffarzyk, H. Siniawski, F. Knollmann, R. Meyer, and R. Hetzer
Reduction aortoplasty for dilatation of the ascending aorta in patients with bicuspid aortic valve
Ann. Thorac. Surg., March 1, 2002; 73(3): 720 - 723.
[Abstract] [Full Text] [PDF]


Home page
J. Thorac. Cardiovasc. Surg.Home page
E. Neri, M. Massetti, P. Tanganelli, G. Capannini, E. Carone, A. Tripodi, E. Tucci, and C. Sassi
IS IT ONLY A MECHANICAL MATTER? HISTOLOGIC MODIFICATIONS OF THE AORTA UNDERLYING EXTERNAL BANDING
J. Thorac. Cardiovasc. Surg., December 1, 1999; 118(6): 1116 - 1118.
[Full Text] [PDF]


Home page
Ann. Thorac. Surg.Home page
R. P. Siebenmann
Implantation of the Toronto SPV Stentless Porcine Bioprosthesis in Dilated Ascending Aorta
Ann. Thorac. Surg., October 1, 1997; 64(4): 1197 - 1200.
[Abstract] [Full Text]


This Article
Right arrow Abstract Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to Personal Folders
Right arrow Download to citation manager
Right arrow Author home page(s):
Xavier M. Mueller
Hendrik T. Tevaearai
Patrick Ruchat
Right arrow Permission Requests
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Mueller, X. M.
Right arrow Articles by von Segesser, L. K.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Mueller, X. M.
Right arrow Articles by von Segesser, L. K.
Related Collections
Right arrowRelated Articles


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