CLINICAL STUDY
Transesophageal echocardiographic description of the mechanisms of aortic regurgitation in acute type A aortic dissection: implications for aortic valve repair
Herman D. Movsowitz, MDa,
Robert A. Levine, MD, FACCa,
Alan D. Hilgenberg, MD, FACCb and
Eric M. Isselbacher, MD, FACCa
a Cardiac Ultrasound Laboratory, Massachusetts General Hospital, Boston, Massachusetts, USA
b Thoracic Aortic Center, Massachusetts General Hospital, Boston, Massachusetts, USA
Manuscript received June 21, 1999;
revised manuscript received March 15, 2000,
accepted April 14, 2000.
Reprint requests and correspondence: Dr. Eric M. Isselbacher, Massachusetts General Hospital, 15 Parkman St, ACC 469, Boston, Massachusetts 02114
isselbacher.eric{at}mgh.harvard.edu
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Abstract
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OBJECTIVES
The purpose of this study was to use transesophageal echocardiography (TEE) to define the mechanisms of aortic regurgitation (AR) in acute type A aortic dissection so as to assist the surgeon in identifying patients with mechanisms of AR suitable for valve preservation.
BACKGROUND
Significant AR frequently complicates acute type A aortic dissection necessitating either aortic valve repair or replacement at the time of aortic surgery. Although direct surgical inspection can identify intrinsically normal leaflets suitable for repair, it is preferable for the surgeon to correlate aortic valve function with the anatomy prior to thoracotomy.
METHODS
We studied 50 consecutive patients with acute type A aortic dissection in whom preoperative TEE findings were considered by the surgeons in planning aortic valve surgery. Six patients did not undergo surgery (noncandidacy or refusal) and one patient had had a prior aortic valve replacement and therefore was excluded from the analysis.
RESULTS
Twenty-seven patients had no or minimal AR and 22 had moderate or severe AR. In all, there were 16 with intrinsically normal leaflets who had AR due to one or more correctable aortic valve lesion: incomplete leaflet closure due to leaflet tethering in a dilated aortic root in 7; leaflet prolapse due to disrupted leaflet attachments in 8; and dissection flap prolapse through the aortic valve orifice in 5. Of these 16 patients, 15 had successful aortic valve repair whereas just 1 underwent aortic valve replacement after a complicated intraoperative course (unrelated to the aortic valve). Nine patients underwent aortic valve replacement for nonrepairable abnormalities, including Marfan’s syndrome in four, bicuspid aortic valve in four, and aortitis in one. In patients undergoing aortic valve repair, follow-up transthoracic echocardiography at a median of three months revealed no or minimal residual AR, and clinical follow-up at a median of 23 months showed that none required aortic valve replacement.
CONCLUSIONS
When significant AR complicates acute type A aortic dissection, TEE can define the severity and mechanisms of AR and can assist the surgeon in identifying patients in whom valve repair is likely to be successful.
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Abbreviations and Acronyms
| | AR | = aortic regurgitation | | TEE | = transesophageal echocardiography | | TTE | = transthoracic echocardiography |
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The optimal management of significant aortic regurgitation (AR) complicating acute type A aortic dissection is controversial. While in the past there was a trend favoring aortic valve replacement (1–4), more recently, several investigators have described aortic valve sparing surgery as an alternative approach in selected patients (5–16). To assess the aortic valve abnormality in such cases, surgeons have traditionally relied on direct inspection of the aortic valve leaflets and aortic root anatomy with the heart and aorta empty and flaccid. In principle, however, it would be preferable for the surgeon to be able to assess the aortic valve in its physiologic state with the aorta full and the heart beating. Transesophageal echocardiography (TEE), performed preoperatively or intraoperatively, produces such a detailed anatomic view of the functioning aortic valve, and should therefore provide the surgeon with valuable information prior to thoracotomy.
Previous echocardiographic studies of aortic dissection have documented the ability of TEE to detect aortic dissection accurately and to define its anatomic features, such as the extent of dissection, sites of intimal tear, presence of pericardial effusion, and presence and severity of AR (17–23). To date and to our knowledge, however, no study has systematically addressed the role of TEE in defining the mechanisms of AR in acute aortic dissection. We hypothesized that TEE performed in patients with acute type A aortic dissection can, in addition to assessing the severity of AR, assist the surgeon in identifying those patients with mechanisms of AR suitable for aortic valve repair as opposed to those with fixed abnormalities (e.g., bicuspid aortic valve, aortic stenosis, marfanoid aortic root) requiring aortic valve replacement.
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Methods
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Patients.
We studied 50 consecutive patients with acute aortic dissection admitted to Massachusetts General Hospital between January 1995 and October 1998 who underwent preoperative or intraoperative TEE to evaluate the aorta and aortic valve. Five other patients with acute type A aortic dissection admitted to the hospital during this period who did not undergo TEE were excluded from the study. Aortic dissection was defined as acute when the diagnosis was made within 14 days of the onset of symptoms; in fact, all study patients presented within 72 h of symptom onset.
Echocardiography.
All patients underwent preoperative or intraoperative TEE. The studies were performed with a standard two-dimensional and color-coded Doppler flow ultrasound system (Hewlett Packard Sonos 1500 / 2500 / 5500) equipped with a flexible 5-MHz multiplane transesophageal probe. The probe was passed after sedation and/or administration of anesthesia, and before the thoracic cavity was opened. The clinical purpose of the TEE examination was to confirm the diagnosis of aortic dissection, determine its location and extent and evaluate the severity and specific mechanisms of AR when present. Two echocardiographers interpreted the TEE findings, which were in turn considered by the surgeons in planning aortic valve surgery. The severity of AR was assessed by a semiquantitative method based on the ratio of the proximal jet height to annular diameter (<0.25 = trace; 0.25 to 0.46 = mild; 0.47 to 0.64 = moderate;  0.65 = severe) (24) measured in a long-axis view obtained at approximately 120° by multiplane TEE; this method has been validated in vitro and correlates well with angiographic grading (25). We defined five potential mechanisms of AR in this population, the first three of which were considered repairable without need for valve replacement: 1) incomplete closure of intrinsically normal leaflets due to leaflet tethering by a dilated sinotubular junction (Figs. 1 and 2); 2) leaflet prolapse due to disruption of leaflet attachments by a dissection flap that extends below the sinotubular junction and into the aortic root (Figs. 1 and 3); 3) prolapse of the dissection flap through intrinsically normal leaflets that disrupts leaflet coaptation (Figs. 1 and 4); 4) a bicuspid aortic valve with associated leaflet prolapse unrelated to the dissection process; and 5) degenerative leaflet thickening resulting in abnormal leaflet coaptation. Some patients had more than one mechanism of AR. Follow-up transthoracic echocardiograms—the timing of which was based on clinical factors—were performed in all patients who underwent aortic valve repair.
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Figure 1 Mechanisms of functional aortic regurgitation in type A aortic dissection: Panel A is a schematic of normal aortic valve anatomy in the short-axis view (left) and long-axis view (right). The dotted lines represent the attachment of the leaflet tips to the sinotubular junction. Note that the leaflet tips coapt fully in diastole (short-axis view) and that the diameter of the sinotubular junction is similar to that at the base of the annulus. Panel B shows incomplete leaflet closure that occurs when the sinotubular junction dilates (arrows) relative to the aortic annulus resulting in leaflet tethering and a persistent diastolic orifice. This is usually best visualized in the short-axis view but may also be seen in the long-axis view if it is optimally aligned. Panel C shows aortic leaflet prolapse that occurs when the dissection extends into the aortic root and disrupts normal leaflet attachments to the aortic wall, thereby resulting in abnormal leaflet coaptation and eccentric AR. This is usually best visualized in the long-axis view where one or more leaflets are seen prolapsing into the left ventricular outflow tract in diastole. Panel D shows dissection flap prolapse that occurs when a redundant dissection flap prolapses through intrinsically normal aortic leaflets resulting in AR that is often short-lived and may be intermittent. The regurgitant flow occurs through the funnel shaped by the dissection flap.
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Figure 2 Incomplete leaflet closure is characterized by a persistent diastolic orifice that is best visualized in the short-axis view of the aortic leaflets, usually obtained at approximately 45° by multiplane TEE. It is important to find the short-axis plane in which the diastolic orifice appears smallest so as to avoid overestimation of the size of the persistent diastolic orifice. The top panel shows the short-axis view of the aortic valve leaflets in systole; the bottom panel shows the persistent valve orifice in diastole. It should be noted that a persistent diastolic orifice can be visualized in the long-axis view when it is optimally aligned. However, off-axis views in the longitudinal plane can falsely create the appearance of incomplete leaflet closure. We therefore recommend the more reliable short-axis view.
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Figure 3 Aortic leaflet prolapse is best visualized in a long-axis view of the aortic valve, aortic root and ascending aorta, which is usually obtained at approximately 120° by multiplane TEE. The top panel shows a long-axis view of the aortic valve and aortic root. The long narrow gray arrows point to an intimal dissection flap that extends into the aortic root. The broad white arrow points to right coronary cusp that is prolapsing into the left ventricular outflow tract behind the noncoronary cusp, seen above. The bottom panel shows an eccentric jet of severe AR that is directed posteriorly into the left ventricular outflow tract. AO = aorta; LA = left atrium; LVOT = left ventricular outflow tract.
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Figure 4 Dissection flap prolapse can be visualized by mutiplane TEE in the short-axis and long-axis views at 45° and 120°, respectively. The top panel is a short-axis view of the aortic valve at the onset of diastole. The arrows point to the three aortic leaflets; a dissection flap is seen prolapsing through the center of the aortic leaflets. The bottom panel is a long-axis view of the aorta showing the dissection flap prolapsing through the plane of the aortic valve.
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Operative technique.
Those patients who underwent surgery did so emergently upon confirmation of the diagnosis. Median sternotomy was performed. Cardiopulmonary bypass was instituted and systemic temperature was lowered to 14° to 18°C. A cross clamp was applied to the ascending aorta in an area that would later be resected. The aorta was opened.
In patients whose valves were preserved, the proximal aorta was completely transected at the sinotubular junction and blood clot was removed from the false lumen. Leaflet prolapse was corrected by suturing together a sandwich of the aortic layers immediately distal to the aortic valve commissures, thereby resuspending the aortic leaflets in the aortic root. Incomplete leaflet closure due to leaflet tethering by a dilated aorta was corrected by reducing the diameter of the sinotubular junction, thereby restoring normal aortic leaflet coaptation.
Under hypothermic arrest, the cross clamp was removed and the aorta was completely transected distally at the junction of the ascending aorta and arch. The ascending aorta, including the intimal tear (if evident), was resected, which corrected dissection flap prolapse when present. A collagen-impregnated Dacron graft, sized to match the diameter of the reconstituted sinotubular junction, was anastomosed to the distal ascending aorta. Bypass was reinstituted and the anastomosis of the graft to the proximal aorta was made while the patient was being rewarmed.
Composite aortic root replacement was performed in all patients with Marfan’s syndrome or a preexisting aortic root aneurysm in order to avoid retaining any portion of the diseased aortic sinuses that might be prone to subsequent dilatation and rupture. All patients with bicuspid aortic valves and significant AR due to leaflet prolapse (unrelated to the dissection process) underwent aortic valve replacement. A valve-graft composite prosthesis was sutured to the aortic valve annulus after valve excision, and the coronary arteries were implanted directly into the Dacron graft as previously described. The distal aorta was managed with circulatory arrest in the manner described above.
Statistical analysis.
Statistical analysis was performed with software (SPSS 8.0; SPSS, Inc.). Normally distributed continuous variables were expressed as the mean ± 1 SD. Nonparametric continuous variables were expressed as the median and range.
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Results
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Patients.
Demographic data for the 50 patients with acute type A aortic dissection undergoing emergent preoperative or intraoperative TEE are listed in Table 1. The mean age was 62 ± 16 years. Seventy percent had a history of systemic hypertension, 14% had a previously documented thoracic aortic aneurysm, 8% had morphologic features of Marfan’s syndrome, and 12% had bicuspid aortic valves (previously known in two patients and diagnosed by TEE at the time of presentation in four patients). All patients presented within 72 h of the onset of symptoms. Clinical features on admission to the hospital are listed in Table 2. Chest pain was present in two thirds of patients. Only 3 of 22 (14%) patients with moderate or severe AR by TEE presented with pulmonary edema.
Transesophageal echocardiography.
An intimal dissection flap was identified in all patients. Thirty-nine (78%) patients had a DeBakey type I dissection and 11 (22%) had a type II dissection. One patient had a prior aortic valve replacement and was therefore excluded from further analysis. Five (10%) patients had no AR, 11 (22%) had trace AR, 11 (22%) had mild AR, 10 (20%) had moderate AR, and 12 (24%) had severe AR. Table 3 compares the mechanisms of AR among patients with no or minimal (trace/mild) AR versus those with moderate or severe AR. A number of patients had AR due to more than one mechanism. The presence of incomplete leaflet closure due to leaflet tethering was associated with moderate or severe AR in all cases. Leaflet prolapse also resulted in moderate or severe AR, except in two patients who had concomitant intimal flap prolapse, with part of the dissection flap resting on the aortic leaflets during diastole and occluding the regurgitant orifice. The presence of degenerative leaflet thickening alone was associated with only trace or mild AR. Examples of incomplete leaflet closure, leaflet prolapse and intimal flap prolapse are shown in Figures 2 through 4, respectively.
Management and operative procedure.
The surgeons considered the severity and mechanisms of AR as defined by TEE in planning the surgical approach. One patient who had a prior St. Jude aortic valve replacement underwent ascending aortic replacement with an interposition graft and was excluded from further analysis. Of the remaining 49 patients with native aortic valves, 27 (55%) had no, trace or mild AR and 22 (45%) had moderate or severe AR.
Five of the 27 patients with no, trace or mild AR were treated medically: 2 refused surgery; 1 had cold agglutinins that were considered a contraindication to deep hypothermic arrest; 1 had a very localized catheter-induced dissection that remained stable; and 1 had several comorbid conditions and mesenteric ischemia and was therefore treated with percutaneous fenestration of the abdominal aortic intimal flap only. The remaining 22 patients underwent aortic surgery: 18 had isolated replacement of the ascending aorta with an interposition graft; 2 required aortic valve replacement with a composite graft because of either Marfan’s syndrome or a bicuspid aortic valve with significant stenosis; and 2 underwent aortic valve repair in addition to ascending aortic replacement with an interposition graft. These latter two cases had echocardiographic evidence of significant aortic leaflet prolapse that necessitated valve repair, but neither had more than mild AR due to prolapse of the intimal flap that occluded the valve orifice in diastole.
Twenty-two patients had moderate or severe AR. All but one patient—who had comorbid massive hemoptysis and mesenteric infarction—underwent aortic surgery. Eight patients required a composite aortic graft with aortic valve replacement: three patients had Marfan’s syndrome; three had a bicuspid aortic valve and severe AR; one had active aortitis; and one underwent valve replacement at the surgeon’s discretion after a prolonged complicated intraoperative course (unrelated to the aortic valve disease). The remaining 13 patients underwent aortic valve repair and replacement of the ascending aorta with an interposition graft. Among those undergoing aortic valve repair, the following mechanisms of AR were identified by TEE, with some patients having more than one mechanism present: seven had incomplete aortic leaflet closure; six had aortic leaflet prolapse; three had prolapse of the intimal flap through the valve; and five had degenerative leaflet thickening. No patient undergoing aortic valve repair proceeded to aortic valve replacement for an inadequate repair.
In summary, of the 43 patients who underwent aortic surgery, 33 (77%) did not require aortic valve replacement. The severity of AR, mechanisms of AR and management strategies for all patients undergoing aortic valve procedures are presented in Table 4.
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Table 4 Case Analysis of Patients Undergoing Aortic Valve Repair or Replacement: The Mechanisms and Severity of Aortic Regurgitation Correlated With the Type of Aortic Valve Surgery
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Hospital course.
The median duration of hospitalization was 11 days (range, 5 to 126 days). The 30-day mortality rate for the full study population (i.e., all 49 patients) was 10%. Of the five patients who died within 30 days, one died on the first postoperative day of an acute inferior and right ventricular infarction complicated by ventricular asystole, two died >3 weeks after surgery of multiorgan failure, and two who did not undergo surgery died of mesenteric infarction.
Follow-up of aortic valve repair.
Follow-up transthoracic echocardiography (TTE) was performed in all 15 patients who underwent aortic valve repair. The median time to follow-up TTE was three months (range, 4 days to 22 months). One patient had no residual AR, six had trace AR and six had mild AR. None had moderate or severe AR and none had required reoperation at a median of 23 months of clinical follow-up (range, 1 to 38 months).
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Discussion
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Aortic regurgitation frequently complicates acute type A aortic dissection, occurring in 41% to 76% of patients (6,8,10,11,13,15,26). While the need for early aortic surgery is well established (6,27,28), the optimal management of associated AR is controversial. For many years, aortic valve replacement was preferred (1–4), but more recently several investigators have reported favorable short- and long-term results with aortic valve preservation (5–8,10,11,13–16). A few studies have assessed the severity of AR by color Doppler echocardiography (13–16); however, to date and to our knowledge, no study has systematically defined the mechanisms of AR by TEE.
TEE assessment of the mechanisms of AR.
This study shows that TEE can define the mechanisms and severity of AR that complicate acute type A aortic dissection, and that these TEE findings may help the surgeon to distinguish valves with geometric distortion amenable to repair from those with fixed abnormalities that require replacement. Although the severity of AR is certainly a consideration, it is the mechanism responsible for the AR that weighs more heavily in the decision to repair versus replace the aortic valve in such patients. Although in many cases a potentially repairable aortic valve can be identified by direct intraoperative inspection, in the setting of acute aortic dissection complicated by significant AR, many surgeons opt for valve replacement rather than repair because of the emergent nature of the surgery and the instability of the patients. In such situations, employing TEE to identify those mechanisms of AR amenable to repair may make the surgeon more confident that an attempt at aortic valve repair is likely to be successful.
Five different mechanisms of AR were identified by TEE in this study population. Three of these mechanisms—leaflet thickening, bicuspid aortic valve disease and incomplete leaflet closure in a dilated aortic root—may also be observed in patients without aortic dissection. Multiple mechanisms of AR were present in some patients. When aortic valve repair was performed, the surgeons made certain to correct all reversible mechanisms of AR identified by TEE and direct surgical inspection: for incomplete aortic leaflet closure, valve repair involved narrowing the diameter of the dilated sinotubular junction to relieve tension on the aortic leaflets, thereby restoring normal leaflet coaptation; for aortic leaflet prolapse, repair involved resuspending the aortic leaflets by reapposing the aortic layers at the commissures; for prolapse of the dissection flap through the valve orifice, repair involved resecting the ascending aorta including the redundant dissection flap. Importantly, in this study, TEE also identified two patients in whom AR was only mild but repair was nevertheless indicated because of severe anatomic distortions—incomplete leaflet closure or leaflet prolapse with concomitant dissection flap prolapse. Finally, intraoperative TEE provided confirmation of successful valve repair prior to closing of the chest.
In this study, the aortic valve was spared in 77% of the 43 patients undergoing aortic surgery, which is consistent with prior series that have reported aortic valve preservation in 56% to 89% of patients (6–8,10,11,13,15). Of the 16 patients determined by TEE to have potentially repairable mechanisms of AR, 15 did, in fact, undergo successful aortic valve repair with no, trace or at most mild residual AR; none needed subsequent aortic valve surgery at a median follow-up of 23 months. Only one patient underwent aortic valve replacement, this being at the surgeon’s discretion following a prolonged intraoperative course with complications unrelated to the aortic valve disease.
Study limitations.
Although AR volume may decline in sedated or hypotensive patients (due to decreased diastolic aortic pressure), in this study, the assessment of AR was based on proximal jet dimension, a method that is relatively independent of driving pressure for a given orifice size at clinically relevant flow rates (25,29). Moreover, for the purposes of analysis, we broadly grouped patients into those with minimal AR (no, trace or mild AR) and with significant AR (moderate or severe AR), thereby diminishing the potential for error in categorization.
In this study, the mechanisms of AR were determined by two-dimensional echocardiography with color-flow Doppler. This technique has inherent limitations, however, because using standard two-dimensional imaging, it may be difficult to appreciate the true three-dimensional anatomy of the aortic valve. In future studies, therefore, it may be worthwhile to utilize recently developed techniques in three-dimensional echocardiography to define in more detail the anatomic and geometric abnormalities of the aortic valve that result in AR in patients with aortic dissection.
Aortic valve repair was not attempted in patients with Marfan’s syndrome, preexisting aortic root aneurysm or bicuspid aortic valve with significant AR. While this conservative approach has support in the aortic dissection literature (4,6,10,11,16,30), it should be noted that there are a growing number of reports of successful valve-sparing operations among these patients groups (31–34); however, to date these series have been limited to a few centers and have included few patients with acute type A aortic dissection. Nevertheless, the future dissemination of such valve-sparing operations should serve only to increase the potential value of TEE to identify repairable mechanisms of AR.
Finally, the follow-up period in this study was relatively short. Although echocardiographic follow-up was obtained at a median of only three months, clinical follow-up was obtained at a median of 23 months. More importantly, the clinical follow-up showed that patients who underwent aortic valve repair did not require reoperation for progressive AR.
Conclusions and clinical implications.
In summary, when significant AR complicates acute type A aortic dissection, TEE can define the severity and mechanisms of AR. The TEE findings may help the surgeon to distinguish those mechanisms of AR suitable for repair from the chronic fixed abnormalities requiring aortic valve replacement. While the highly experienced surgeon may feel comfortable making such a determination by direct surgical inspection alone, other surgeons may well appreciate the ability of TEE to define the aortic abnormality preoperatively and/or to confirm their own intraoperative impressions. Based on the results of this study, TEE may play an increasingly important role in patients with acute type A aortic dissection as cardiologists and cardiac surgeons work together to determine the optimal management of any consequent AR.
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Footnotes
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Dr. Movsowitz is supported in part by a grant from the William A. Schreyer Cardiology Fellowship Fund, Boston, Massachusetts.
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References
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|---|
1. Seybold-Epting W, Meyer J, Hallman GL, Cooley DA. Surgical treatment of acute dissecting aneurysm of the ascending aorta. J Cardiovasc Surg. 1977;18:43–48[Medline]
2. Kouchoukos NT, Karp RB, Blackstone EH, et al. Replacement of the ascending aorta and aortic valve with a composite graft: results in 86 patients. Ann Surg. 1980;192:403–413[Medline]
3. DeBakey ME, McCollum CH, Crawford ES, et al. Dissection and dissecting aneurysms of the aorta: twenty-year follow-up of five hundred twenty-seven patients treated surgically. Surgery. 1982;92:1118–1134[Medline]
4. Kouchoukos NT, Marshall WG, Wedige-Stecher TA. Eleven-year experience with composite graft replacement of the ascending aorta and aortic valve. J Thorac Cardiovasc Surg. 1986;92:691–705[Abstract]
5. Najafi H, Dye WS, Javid H, et al. Acute aortic regurgitation secondary to aortic dissection: surgical management without valve replacement. Ann Thorac Surg. 1972;14:474–482[Medline]
6. Miller DC, Stinson EB, Oyer PE, et al. Operative treatment of aortic dissections: experience with 125 patients over a sixteen-year period. J Thorac Cardiovasc Surg. 1979;78:365–382[Abstract]
7. Meng RL, Najafi H, Javid H, et al. Acute ascending aortic dissection: surgical management. Circulation 1981;64 Suppl II:II–231–II–234.
8. Cachera J, Vouhe P, Loisance D, et al. Surgical management of acute dissections involving the ascending aorta: early and late results in 38 patients. J Thorac Cardiovasc Surg. 1981;82:576–584[Abstract]
9. Wolfe WG, Oldham HN, Rankin JS, Moran JF. Surgical treatment of acute ascending aortic dissection. Ann Surg. 1983;197:738–742[Medline]
10. Jex RK, Schaff HV, Piehler JM, et al. Repair of ascending aortic dissection: influence of associated aortic valve insufficiency on early and late results. J Thorac Cardiovasc Surg. 1987;93:375–384[Abstract]
11. Fann JI, Glower DD, Miller DC, et al. Preservation of aortic valve in type A aortic dissection complicated by aortic regurgitation. J Thorac Cardiovasc Surg. 1991;102:62–75[Abstract]
12. Weinschelbaum EE, Schamun C, Caramutti V, et al. Surgical treatment of acute type A dissecting aneurysms, with preservation of the native aortic valve and the use of biologic glue: follow-up for 6 years. J Thorac Cardiovasc Surg. 1992;103:369–374[Abstract]
13. Mazzucotelli JP, Deleuze PH, Baufreton C, et al. Preservation of the aortic valve in acute aortic dissection: long-term echocardiographic assessment and clinical outcome. Ann Thorac Surg. 1993;55:1513–1517[Abstract]
14. Seguin JR, Picard E, Frapier J, Chaptal P. Aortic valve repair with fibrin glue for type A acute aortic dissection. Ann Thorac Surg. 1994;58:304–307[Abstract]
15. Von Segesser LK, Lorenzetti E, Lachat M, et al. Aortic valve preservation in acute type A dissection: is it sound? J Thorac Cardiovasc Surg. 1996;111:381–391[Abstract/Free Full Text]
16. Westaby S, Katsumata T, Freitas E. Aortic valve conservation in acute type A dissection. Ann Thorac Surg. 1997;64:1108–1112[Abstract/Free Full Text]
17. Erbel R, Engberding R, Daniel W, et al. Echocardiography in the diagnosis of aortic dissection. Lancet. 1989;1:457–461[Medline]
18. Hashimoto S, Kumada T, Osakada G, et al. Assessment of transesophageal Doppler echocardiography in dissecting aortic aneurysm. J Am Coll Cardiol. 1989;14:1253–1262[Abstract]
19. Ballal R, Nanda N, Gatewood R, et al. Usefulness of transesophageal echocardiography in assessment of aortic dissection. Circulation. 1991;84:1903–1914[Abstract/Free Full Text]
20. Simon P, Owen AN, Havel M, et al. Transesophageal echocardiography in the emergency surgical management of patients with aortic dissection. J Thorac Cardiovasc Surg. 1992;103:1113–1118[Abstract]
21. Nienaber CA, Kodolitsch Y, Nicolas V, et al. The diagnosis of thoracic aortic dissection by noninvasive imaging procedures. N Engl J Med. 1993;328:1–9[Abstract/Free Full Text]
22. Epperlein S, Mohr-Kahaly S, Erbel R, et al. Aortic and aortic valve morphologies predisposing to aortic dissection: an in vivo assessment with transesophageal echocardiography. Eur Heart J. 1994;15:1520–1527[Abstract/Free Full Text]
23. Keren A, Kim CB, Hu BS, et al. Accuracy of biplane and multiplane transesophageal echocardiography in diagnosis of typical acute aortic dissection and intramural hematoma. J Am Coll Cardiol. 1996;28:627–636[Abstract]
24. Perry GJ, Helmcke F, Nanda NC, et al. Evaluation of aortic insufficiency by Doppler color flow mapping. J Am Coll Cardiol. 1987;9:952–959[Abstract]
25. Switzer DF, Yoganathan AP, Nanda NC, et al. Calibration of color Doppler flow mapping during extreme hemodynamic conditions in vitro: a foundation for a reliable quantitative grading system for aortic incompetence. Circulation. 1987;75:837–846[Abstract/Free Full Text]
26. Massimo CG, Presenti LF, Marranci P, et al. Extended and total aortic resection in the surgical treatment of acute type A aortic dissection: experience with 54 patients. Ann Thorac Surg. 1998;46:420–424
27. Miller DC, Mitchell RS, Oyer PE, et al. Independent determinants of operative mortality for patients with aortic dissections. Circulation 1984;70 Suppl I:I–153–I–164.
28. DeSanctis RW, Doroghazi RM, Austen WG, Buckley MJ. Aortic dissection. N Engl J Med. 1987;317:1060–1067[Medline]
29. Baumgartner H, Schima H, Kuhn P. Value and limitations of proximal jet dimensions for the quantification of valvular regurgitation: an in vitro study using Doppler flow imaging. J Am Soc Echocardiogr. 1991;4:57–66[Medline]
30. Gott VL, Peyritz RE, Macgovern GJ, et al. Surgical treatment of aneurysms of the ascending aorta in Marfan syndrome: results of composite-graft repair in 50 patients. N Engl J Med. 1986;314:1070–1074[Abstract]
31. David TE. Aortic valve repair in patients with Marfan syndrome and ascending aorta aneurysms due to degenerative disease. J Card Surg. 1994;9(Suppl):182–187[Medline]
32. David TE, Feindel CM, Bos J. Repair of the aortic valve in patients with aortic insufficiency and aortic root aneurysm. J Thorac Cardiovasc Surg. 1995;109:345–352[Abstract/Free Full Text]
33. Cosgrove DM, Rosenkranz ER, Hendren WG, et al. Valvuloplasty for aortic insufficiency. J Thorac Cardiovasc Surg. 1991;102:571–577[Abstract]
34. Fraser CD, Wang N, Mee RBB, et al. Repair of insufficient bicuspid aortic valves. Ann Thorac Surg. 1994;58:386–390[Abstract]
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S. L. Rao and S. R. Auerbach
Severe Acute Aortic Regurgitation due to Aortic Dissection
Anesth. Analg.,
March 1, 2007;
104(3):
500 - 501.
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F. A. Flachskampf
Assessment of Aortic Dissection and Hematoma
Seminars in Cardiothoracic and Vascular Anesthesia,
March 1, 2006;
10(1):
83 - 88.
[Abstract]
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A. E. Newcomb and M. A. Rowland
Nontraumatic localized dehiscence of the proximal ascending aorta through an aortic valve commissure
Ann. Thorac. Surg.,
July 1, 2004;
78(1):
321 - 323.
[Abstract]
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R. A. Hopkins
Aortic valve leaflet sparing and salvage surgery: evolution of techniques for aortic root reconstruction
Eur. J. Cardiothorac. Surg.,
December 1, 2003;
24(6):
886 - 897.
[Abstract]
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J. A. Fox, V. Formanek, A. Friedrich, and S. K. Shernan
Intraoperative Echocardiography
Card. Surg. Adult,
January 1, 2003;
2(2003):
283 - 314.
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T. E. David
Aortic Valve Repair and Aortic Valve-Sparing Operations
Card. Surg. Adult,
January 1, 2003;
2(2003):
811 - 824.
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I. A. Khan and C. K. Nair
Clinical, Diagnostic, and Management Perspectives of Aortic Dissection*
Chest,
July 1, 2002;
122(1):
311 - 328.
[Abstract]
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T. Murashita, T. Kunihara, N. Shiiya, H. Aoki, K. Myojin, and K. Yasuda
Is preservation of the aortic valve different between acute and chronic type A aortic dissections?
Eur. J. Cardiothorac. Surg.,
November 1, 2001;
20(5):
967 - 972.
[Abstract]
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