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Ann Thorac Surg 1997;63:762-766
© 1997 The Society of Thoracic Surgeons
Department of Cardiovascular Surgery and Institute of Pathology, Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland
Accepted for publication October 21, 1996.
| Abstract |
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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 |
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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 |
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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 Verhoeffvan 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 |
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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 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.
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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 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.
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| Comment |
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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 thenespecially the increased experience with titrable intravenous antihypertensive agents and parenteral drug therapy for ß-adrenergic blockadehave 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 survivorsand 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 |
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| References |
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