The need to deal with an associated ascending aortic

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, and Ludwig K. von Segesser, MD Department of Cardiovascular Surgery and Institute of Pathology, Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland 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. (Ann Thorac Surg 1997;63:762 7) 1997 by The Society of Thoracic Surgeons 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 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 Accepted for publication Oct 21, 1996. Address reprint requests to Dr Mueller, Department of Cardiovascular Surgery, CHUV, CH-1011 Lausanne, Switzerland. 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 1997 by The Society of Thoracic Surgeons 0003-4975/97/$17.00 Published by Elsevier Science Inc PII S0003-4975(97)00008-8

Ann Thorac Surg MUELLER ET AL 1997;63:762 7 AORTOPLASTY FOR ASCENDING AORTA ANEURYSM 763 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. Fig 1. Kaplan-Meier actuarial survival curve of hospital survivors. (N number of patients; SD 1 standard deviation [%].) 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 1. All surviving patients were in New York Heart Association functional class I (8 patients) or II (5 patients) at the time of follow-up. 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 2. 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 Results 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 Fig 2. Kaplan-Meier actuarial analysis of freedom from aneurysm recurrence after unsupported aortoplasty. (N number of patients; SD 1 standard deviation [%].)

764 MUELLER ET AL Ann Thorac Surg AORTOPLASTY FOR ASCENDING AORTA ANEURYSM 1997;63:762 7 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. 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 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 -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 [15 17]. 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

Ann Thorac Surg MUELLER ET AL 1997;63:762 7 AORTOPLASTY FOR ASCENDING AORTA ANEURYSM 765 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. 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. 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. 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. 5. Schlatmann TJ, Becker AE. Histologic changes in the normal aging aorta: implications for dissecting aortic aneurysm. Am J Cardiol 1977;39:13 20. 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. 7. Klima T, Spjut HJ, Coelho A, et al. The morphology of ascending aortic aneurysms. Hum Pathol 1983;14:810 7. 8. McCready RA, Pluth JR. Surgical treatment of ascending aortic aneurysms associated with aortic valve insufficiency. Ann Thorac Surg 1979;28:307 16. 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. 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.

766 MUELLER ET AL Ann Thorac Surg AORTOPLASTY FOR ASCENDING AORTA ANEURYSM 1997;63:762 7 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. 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. 13. Robicsek F. Post-stenotic dilatation of the great vessels. Acta Med Scand 1955;151:481 5. 14. Lindsay J. Coarctation of the aorta, bicuspid aortic valve and abnormal ascending aortic wall. Am J Cardiol 1988;61:182 4. 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. 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. 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. 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. 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. INVITED COMMENTARY When, in 1982, the procedure of ascending aortoplasty was first recommended for the treatment of selected patients with ascending aortic aneurysms, we emphasized that the operation should consist of two equally important components: (1) an axial tailoring aortoplasty with the aortotomy beginning at the bottom of the noncoronary sinus and extending throughout the entire dilated portion of the ascending aorta, with excision of an oval portion of the anterior aortic wall to bring the aortic diameter down to normal and linear closure; and (2) inclusion of the entire involved aortic segment in a well-fitted Dacron vascular prosthesis anchored proximally to the aortic annulus and distally to the anterior aortic wall. The procedure may be supplemented with aortic valve replacement if indicated. In my opinion, the above procedure fulfills Laplace s criteria of mural wall stress reduction by restoring both normal aortic diameter and aortic wall strength, thus making the development of dissection extremely unlikely and rupture nearly impossible. The procedure is especially well suited in cases in which the aortic valve requires replacement as well. Using this operation, our experience, as well as that of others, was gratifying. To me, therefore, it is somewhat surprising that, contrary to both clinical experience and theoretic considerations, there are continued efforts such as those of Mueller and associates that, although appropriately addressing the issue of mural stress reduction by decreasing the aortic diameter, leave unattended the other, probably even more important, anatomic feature, ie, the weakened condition of the aortic wall. These aortas have already proved themselves prone to dilatation because of their defective wall structure. After the aneurysm is formed, the aortic wall is not only structurally defective, but also thinner (for example, if an aorta with a diameter of 3 cm and a wall thickness of 3 mm doubles in diameter, the wall thickness will decrease to about 1.5 mm). Even if the mural stress is decreased by reducing the aortic diameter by aortoplasty, the patient will still be left with an aorta that is likely to dilate again, with a much higher potential for rupture; its wall is now not only structurally abnormal, but also abnormally thinned because of the initial dilatation. For these reasons, I find it highly advisable, if not mandatory, that whenever one chooses ascending aortoplasty, the procedure should be supplemented with wall reinforcement using a tailored Dacron vascular prosthesis. This point is well emphasized in the above article, in which patients who did not have external support after aortoplasty had an unacceptably high rate of recurrence. Francis Robicsek, MD, PhD Department of Thoracic and Cardiovascular Surgery The Carolinas Heart Institute PO Box 32861 Charlotte, NC 28232-2861 INVITED COMMENTARY I believe the surgeon evaluating an abnormal aorta has to make a distinction between ectasia and an aorta that is unquestionably aneurysmal. If the aorta is considered dilated, but not aneurysmal (less than twice the diameter of a normal aorta), and in addition it is of good quality with normal vaso vasorum, thickness, texture, and resiliency but has become enlarged because of long-standing severe aortic regurgitation (secondary aortic changes), one might want to perform aortoplasty with or without reinforcement. I have done this on rare occasions with satisfactory long-term results. The second situation in which one might want to compromise is in a high-risk patient, particularly in a very old patient who requires a long operation that includes management of dilated or 1997 by The Society of Thoracic Surgeons 0003-4975/97/$17.00 Published by Elsevier Science Inc PII S0003-4975(97)00009-X

Ann Thorac Surg MUELLER ET AL 1997;63:762 7 AORTOPLASTY FOR ASCENDING AORTA ANEURYSM 767 aneurysmal ascending aorta. Aneurysmorrhaphy adds substantially less to the magnitude of the operation than resection and graft replacement. The aneurysmal ascending aorta (localized aortic enlargement 2 or more times greater than normal diameter) should be managed by resection and graft interposition. If the sinuses of Valsalva are normal and the coronary orifices are not displaced, the proximal anastomosis should be at the commissural attachments. The exception is a patient with Marfan syndrome, who should undergo insertion of a conduit to avoid the need for reoperation on the proximal aortic root later. Finally, I believe when we consider a 5- to 6-cm aneurysm we should take the size of the patient and the diameter of the normal aorta proximal and distal to the aneurysm into consideration. A 6-cm aneurysm in a little woman weighing 45 kg with an otherwise normal thoracic aorta (2 to 2 1 2 cm) is a large aneurysm, whereas the same lesion in an unusually large, but not necessarily obese man (1.9 m weighing 122 kg) with an otherwise normal 3.5-cm aorta may not be a definitive surgical target by itself. It has been my habit to finalize my decision as to the ultimate mode of surgical reconstruction of an abnormal aorta during the operation. It is then that the patient s history and objective findings on noninvasive studies plus angiography and intraoperative assessments together lead the surgeon to the most appropriate decision regarding the management of the enlarged aorta. Hassan Najafi, MD Department of Cardiovascular-Thoracic Surgery Rush-Presbyterian-St. Luke s Medical Center 1653 W Congress Pkwy Chicago, IL 60612-3833 Bound volumes available to subscribers Bound volumes of the 1996 issues of The Annals of Thoracic Surgery are available only to subscribers from the Publisher. The cost is $105.00 (outside US add $27.00 for postage) for volumes 61 and 62. Each bound volume contains a subject and author index, and all advertising is removed. The binding is durable buckram with the name of the journal, volume number, and year stamped on the spine. Payment must accompany all orders. Contact Elsevier Science Inc, 655 Avenue of the Americas, New York, NY 10010; or telephone (212) 633-3950 (facsimile: (212) 633-3990). 1997 by The Society of Thoracic Surgeons 0003-4975/97/$17.00 Published by Elsevier Science Inc PII S0003-4975(97)00059-3