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Remodeling of the aortic valve anulus
Remodeling of the aortic valve anulus Isolated aortic valve regurgitation that results from disease that primarily affects the aortic wall can be repaired by remodeling of the aortic anulus to restore its normal geometry. This involves excision of the aortic wall to within 2 to 3 mm of the leaflet attachments, detachment of the coronary ostia, reshaping of the anulus with the aid of a Dacron graft, and then reimplantation of the coronary arteries. Increases in the surface area of the leaflet that are caused by root dilatation are often present and can be accommodated in the repair procedure. In this study we describe our experience with 10 patients with annuloaortic ectasia who underwent the remodeling procedure at the National Heart Hospital and the Royal Brompton Hospital from 1982 to 1990. (J THORAC CARDIOVASC SURG 1993;105:435-8)
Mazin A. 1. Sarsam, FRCS, and Magdi Yacoub, FRCS,* London. England
Born January 1982 to February 1990, a total of 10 patients (6 male, 4 female, with a mean age of 35.7 years) underwent remodeling of the aortic anulus for the treatment of severe aortic regurgitation (AR) at the National Heart Hospital and Royal Brompton Hospital by one surgeon (MY). Eight patients had fully developed features of Marfan syndrome with symptoms that are associated with chronic severe AR. The other two exhibited AR and type A dissection. In this study we discuss patient selection, anatomic and pathologic considerations, surgical technique, and the potential role of this procedure in the treatment of patients with isolated AR.
Patients and methods Anatomic and physiologic considerations. The aortic valve is a complex structure composed of the leaflets, the aortic sinuses, and the interleaflet triangles.' The leaflets are attached to the aortic wall in a semilunar fashion with the highest point at the commissure and the lowest at the ringlike junction of the aortic wall and the ventricle. The leaflets overlap in the closed position, and the closure line is visible 2 to 3 mm from the edge on the ventricular side of the leaflets. From the Department of Cardiothoracic Surgery, National Heart Hospital and Royal Brompton Hospital, London, England. Received for publication Jan. 20, 1992. Accepted for publication May 25, 1992. Address for reprints: Mazin A. I. Sarsam, FRCS, Consultant Cardiac Surgeon, Royal Victoria Hospital, Belfast BT 12 6BA, United Kingdom. "Present address: Professor Sir M. Yacoub, The National Heart and Lung Institute, Dove House Str. London, England Copyright
1993 by Mosby-Year Book, Inc.
0022-522393 $1.00+ .10
12/1/41624
Reid 2 studied the geometry of the aortic root in five animal species, including human beings.? The measurements depicted the root as a truncated cone; the diameter at the highest point of attachment of the leaflets (commissural diameter) was 15% to 20% less than the diameter at the inlet. A well-defined anatomic ridge that extends at the level of the commissures and forms the upper border of the sinuses is an integral part of the commissural support and marks the sinutubular junction. At this point the wall of the aorta is four to five times thicker than the walls of the sinuses. We measured, in addition to the inlet diameter and the ridge diameter, the sinus height, which is equal to or even larger than the diameter of the aorta at the ridge (Fig. I). We refer to the ringlike junction of the aortic wall and ventricle as the surgical anulus, the measurement used in the sizing of a prosthetic valve. The semilunar attachment of the leaflets is referred to as the anatomic anulus. The term remodeling also refers to the anatomic anulus. In vivo studies that were performed by tagging of radiopaque material to canine aortic valves revealed the dynamic nature of the valve complex.' During systole the diameter at the ridge increases while the inlet diameter decreases, changing the root geometry from conic to cylindric. The reverse occurs in diastole, at which time the leaflets tilt toward the ventricle. Another study," performed in an identical manner, showed that stress and strain are maximal in the region of leaflet attachments. These forces invariably lead to tissue wear and fatigue (notably, senile calcification starts in that area). Living tissues, however, are continuously renewed, and therefore the possibility of valve failure is greatly reduced. Radioautograph studies in which rats were given H 3-proline (a marker for collagen) and H3-glucosamine (a marker of the complex sugar found in connective tissue matrix) showed appreciably higher rates of protein and glycosaminoglycan labeling in the animals' valve leaflets as compared with rates in the skin, intestine, or tail; this indicated a higher rate of tissue renewal." Pathologic considerations. Isolated AR may result from damage to the leaflets, the supporting aortic wall and sinuses, or both. Conditions that spare the leaflet are amenable to repair 435
436
The Journal of Thoracic and Cardiovascular Surgery March 1993
Sarsam and Yacoub
)
v if'i;!':<'~'~·"'y );~. . ,~
"';:" .;.,
Diometer or ridqe
I
,
I
Sinus depth ond width
\ \
\
,
Fig. 2. Excision of dilated aortic segment and harvesting of coronary arteries. (See text for details.) Fig. 1. Aortic root with inlet diameter, ridge diameter, and sinus height. (Reid K. The Anatomy of the Sinus of Valsalva. Thorax 1970;25:79-85, published with permission.)
with the remodeling procedure. These conditions include dissecting aneurysm, atherosclerotic aneurysm, and aneurysm of the sinus of Valsalva. An increasingly recognized cause of isolated AR (accounting for approximately 40%) is noninflammatory aortic root dilatation or annuloaortic ectasia.' The striking feature is the absence of any inflammatory process. There is degeneration of the elastic element of the media, with abnormal organization of the smooth muscle and an increased amount of collagen." A cystic vacuole that contains mucopolysaccharides may be observed in the media; hence the term cystic medial necrosis. It is a feature of the autosomal dominant Marfan syndrome but affects many other patients with no signs of Marfan syndrome." Inflammatory aortitis that produces annular dilatation includes syphilis, with the characteristic opening of the commissures; syphilis rarely extends into the leaflet base. In contrast, aortitis caused by ankylosing spondylitis is more extensive, with fibrosis extending into the base of the leaflets, the interleaflet triangles, the base of the anterior leaflet of the mitral valve, and the membranous septum; this causes varying degrees of heart block' Rheumatoid arthritis, psoriasis, and Reiter's syndrome may create the semblance of ankylosing spondylitis, whereas aortitis that is associated with Takayasu's syndrome and giant cell aortitis characteristically spare the leaflet tissue. We and others?"! have described the condition of myxoid degeneration and floppy aortic valve. On reflection, the thickening of the cusp edge and increased myomatous tissue at the base may be caused by root dilatation. Indeed, 8 of our II patients had annular dilatation, and all had changes of cystic medial necrosis. In one series of 55 patients, 13 experienced such changes, but there was no measurement of aortic root. I I There were no such cases in two large series of 225 12 and 72 13 patients with isolated AR. The condition, however, does exist whereby the leaflet becomes soft and nodular with elongation of the lacunar area and results in leaflet prolapse despite the presence of an aortic root of normal size. Surgical technique. The aim of the procedure is to replace the diseased aortic tissue and, in the process, to reshape the
anulus back to its normal geometry to restore competence and preserve the leaflets. It is essential that the leaflets be thin and pliable. Standard bypass is established with systemic cooling to 25° C, a left ventricular vent is inserted, and the aorta is clamped. An oblique aortotomy is made, and the root is inspected with particular attention paid to the state of the leaflets, the commissural height, the supraannular ridge, and the inlet diameter. If reconstruction is feasible, cardioplegic solution is admiministered directly into the coronary ostia, and the aorta is transected just above the commissure. Supplementary retrograde cardioplegia can be induced with a coronary sinus cannula. The left and right coronary ostia are harvested with a 3 mm button of surrounding aortic wall. The aortic wall is then cut to within 2 to 3 mm from the leaflet and the commissure, thus resembling at this stage a prepared homograft (Fig. 2). A stay suture is put into the aortic rim above each commissural point. When these three sutures are pulled up, the effect will be a restoration of sinus height and a reduction of commissural diameter, with resultant coaptation of the leaflets. A collagen-impregnated Dacron graft, the diameter of which is equal to the inlet diameter, is used. The base of the tube is then divided into three points-a, b, and c. The distances between a and b and between band c equal the tube diameter; the distance between a and c is slightly longer for the noncoronary sinus (circumference = diameter X 3.14). These measurements are only guidelines. Adjustments may be needed for individual cases. A suitable procedure would involve the use of the "Frater stitch" through the nodules of Arantius to help with measurements. Longitudinal incisions are made at these points (a, b and c). The length of the incision is determined by the desired height of the commissure. As in homografts, the commissural point must be stretched up and must never be redundant (Fig. 3). The graft is then cut into the crown shape, which simulates the normal anulus, and after the commissural points are fixed the graft is attached to the aortic rim with 4-0 prolene sutures (Ethicon, Inc., Somervill, Md.). Meticulous suturing is essential because access to this suture line after completion is difficult. A suitable opening is made in the Dacron tube, and the coronaries are anastomosed with 4-0 Prolene sutures. The graft is then sized, and the top end is anastomosed to the aorta with 3-0 Prolene sutures (Fig. 4).
The Journal of Thoracic and Cardiovascular Surgery Volume 105, Number 3
Sarsam and Yacoub
437
Fig. 3. Preparation of graft. (See text for details.)
Results
Of the ten patients, one patient who had acute dissection died of bleeding. In another case aortic incompetence (AI) developed, and the patient underwent valve replacement I year after his original operation. At reoperation there was detachment of the commissure between the right and left coronary cusps. The remaining eight patients were alive and well and had no signs of AI (six patients) or had only mild AI (two patients) after a mean follow-up period of 3.4 years. Discussion
Unlike mitral valve repair, repair of isolated AR has yielded mixed results. Carpentier!" described techniques for the reduction of annular dilatation, repair of leaflet prolapse, and relief of restricted leaflet motion with 13% occurrence of reoperation and 15% occurrence of significant residual regurgitation. 14 He concluded that it is too early to recommend these techniques in adults, although two other techniques with long-term success have been reported. The first is resuspension of the detached commissure in aortic dissection, with 80% freedom from aortic valve replacement at 10 years.'? The second is valvuloplasty for repair of leaflet prolapse in association with ventricular septal defect, with a failure-free rate of 74% at 10 years. 16 Recent early success has been reported with cusp extension with the use of bovine pericardium, but long-term results are lacking.'? With the decline in the prevalence of rheumatic fever, noninflammatory aortic root dilatation is now the most common cause of isolated AR. 12 When the disease causes an aneurysm of the ascending aorta, in addition to AR, the recommended treatment is the composite graft technique as described by Bentall and DeBono l 8 and confirmed by others. 19. 20 Nevertheless, an effective technique for preserving valves would be a superior alternative. The remodeling procedure was initially applied to
Fig. 4. Graft suturedto aorta withreimplantation of coronary arteries.
patients with a dilated aortic root (mean, 6.8 em) and severe AI, diagnosed by echocardiography. The patients were young men who wanted to engage in athletic activities and women of child-bearing age. The procedure was later applied to patients who had type A dissection and were known to have had AI before dissection. The three bases for the repair are resection of pathologic aortic tissue, preservation of viable leaflet, and restoration of root geometry. We chose conduits with the same size as the inlet diameter to accommodate the secondary changes of increased surface area in the leaflets. If a smaller conduit were chosen, the sinus height would have to be adjusted at a higher point. As with homograft aortic valve replacement, there is some flexibility with this repair. In conclusion, the early results from this small series and the larger series at Harefield Hospital (unpublished data) are encouraging indeed. There is, however, a small but definite learning curve, and the long-term results are awaited. The procedure is potentially applicable to other conditions, such as aneurysm of the sinus of Valsalva (where, in a large series, the prevalence of aortic valve replacement in patients with aneurysm of the sinus and AR was 80%21) and other conditions that cause AR but spare the leaflet tissue, as discussed in the section on pathologic consideration. REFERENCES 1. Angelini A, Ho SY, Anderson RH, et al. The morphology ofthe normalaorticvalve as compared withthe aorticvalve having two leaflets. J THORAC CARDIOVASC SURG 1989; 98:362-7.
2. Reid K. The anatomy of the sinus of Valsalva. Thorax 1970;25:79-85.
4 3 8 Sarsam and Yacoub
3. Thubrikar M, Piepgrass WC, Shaner TW, Nolan SP. The design of the normal aortic valve. Am J Physiol 1981; 241:H795-801. 4. Deck JD, Thubrikar M, Schneider PJ, Nolan SP. Structure, stress and tissue repair in aortic valve leaflets. Cardiovase Res 1988;22:7-61. 5. Davis MJ. Pathology of cardiac valves. London: Butterworth & Co., Ltd., 1980:37-61. 6. Roberts WC, Hoing HS. The spectrum of cardiovascular disease in the Marfan syndrome. Am Heart J 1982; 104:115-35. 7. Hirst AE, Gore I. The etiology and pathology of aortic dissection. In: Doroghazi RM, Slater EE, eds. Aortic dissection. New York: McGraw-Hill, 1983:13-54. 8. Koike R, Sasaki S, Takeuchi A, Nakayama Y. Aortic regurgitation caused by giant cell aortitis. J Cardiovasc Surg 1989;30:372-4. 9. McKay R, Yacoub MH. Clinical and pathological findings in patients with "floppy" valves treated surgically. Circulation 1973;48(Pt. 2):IIII163-73. 10. Lakier JB, Copan H, Rosman HS, et al. Idiopathic degeneration of the aortic valve: a common cause of isolated aortic regurgitation. J Am Coli Cardiol 1985;5:347-57. 11. Allen WM, Matlolf JM, Fishbein Me. Myxoid degeneration of the aortic valve and isolated severe aortic regurgitation. Am J Cardiol 1985;55:439-44. 12. Olson LJ, Subramanian R, Edwards W. Surgical pathology of pure aortic insufficiency: a study of 225 cases. Mayo Clin Proc 1984;59:835-41.
The Journal of Thoracic and Cardiovascular Surgery March 1993
13. Guiney TE, Davis MJ, Parker DJ, et al. The etiology and course of isolated severe aortic regurgitation: a clinical, pathological and echocardiographic study. Br Heart J 1987;58:358-68. 14. Carpentier A. Cardiac valve surgery-the "French correction". J THoRAc CARDIOVASC SURG 1983;86:323-37. 15. Crumbly AJ III, Crawford FA Jr. Results of aortic valve replacement. Cardiol Clin 1991;9:353-80. 16. Okita Y, Miki S, Kusuhara K, et al. Long-term results of aortic valvuloplasty for aortic regurgitation associated with ventricular septal defect. J THORAC CARDIOVASC SURG 1988;96:769-74. 17. Al Faigh MR, Al Kassab SM, Ashmeg AI. Aortic valve repair using bovine pericardium for cusp extension. J THORAC CARDIOVASC SURG 1988;96:760-4. 18. Bentall H, DeBono A. A technique for complete replacement of the ascending aorta. Thorax 1968;23:338-9. 19. 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;192:40313. 20. Gott VL, Pyeritz RE, Magovern GJ, et al. Surgical treatment of aneurysm of the ascending aorta in the Marfan syndrome. N Engl J Med 1986;314:1070. 21. Meyer J, Wukasch DC, Hallman GL, Cooley DA. Aneurysm and fistula of the sinus of Valsalva. Ann Thorac Surg 1975;19:170-9.
Mazin A. 1. Sarsam, FRCS, and Magdi Yacoub, FRCS,* London. England
Born January 1982 to February 1990, a total of 10 patients (6 male, 4 female, with a mean age of 35.7 years) underwent remodeling of the aortic anulus for the treatment of severe aortic regurgitation (AR) at the National Heart Hospital and Royal Brompton Hospital by one surgeon (MY). Eight patients had fully developed features of Marfan syndrome with symptoms that are associated with chronic severe AR. The other two exhibited AR and type A dissection. In this study we discuss patient selection, anatomic and pathologic considerations, surgical technique, and the potential role of this procedure in the treatment of patients with isolated AR.
Patients and methods Anatomic and physiologic considerations. The aortic valve is a complex structure composed of the leaflets, the aortic sinuses, and the interleaflet triangles.' The leaflets are attached to the aortic wall in a semilunar fashion with the highest point at the commissure and the lowest at the ringlike junction of the aortic wall and the ventricle. The leaflets overlap in the closed position, and the closure line is visible 2 to 3 mm from the edge on the ventricular side of the leaflets. From the Department of Cardiothoracic Surgery, National Heart Hospital and Royal Brompton Hospital, London, England. Received for publication Jan. 20, 1992. Accepted for publication May 25, 1992. Address for reprints: Mazin A. I. Sarsam, FRCS, Consultant Cardiac Surgeon, Royal Victoria Hospital, Belfast BT 12 6BA, United Kingdom. "Present address: Professor Sir M. Yacoub, The National Heart and Lung Institute, Dove House Str. London, England Copyright
1993 by Mosby-Year Book, Inc.
0022-522393 $1.00+ .10
12/1/41624
Reid 2 studied the geometry of the aortic root in five animal species, including human beings.? The measurements depicted the root as a truncated cone; the diameter at the highest point of attachment of the leaflets (commissural diameter) was 15% to 20% less than the diameter at the inlet. A well-defined anatomic ridge that extends at the level of the commissures and forms the upper border of the sinuses is an integral part of the commissural support and marks the sinutubular junction. At this point the wall of the aorta is four to five times thicker than the walls of the sinuses. We measured, in addition to the inlet diameter and the ridge diameter, the sinus height, which is equal to or even larger than the diameter of the aorta at the ridge (Fig. I). We refer to the ringlike junction of the aortic wall and ventricle as the surgical anulus, the measurement used in the sizing of a prosthetic valve. The semilunar attachment of the leaflets is referred to as the anatomic anulus. The term remodeling also refers to the anatomic anulus. In vivo studies that were performed by tagging of radiopaque material to canine aortic valves revealed the dynamic nature of the valve complex.' During systole the diameter at the ridge increases while the inlet diameter decreases, changing the root geometry from conic to cylindric. The reverse occurs in diastole, at which time the leaflets tilt toward the ventricle. Another study," performed in an identical manner, showed that stress and strain are maximal in the region of leaflet attachments. These forces invariably lead to tissue wear and fatigue (notably, senile calcification starts in that area). Living tissues, however, are continuously renewed, and therefore the possibility of valve failure is greatly reduced. Radioautograph studies in which rats were given H 3-proline (a marker for collagen) and H3-glucosamine (a marker of the complex sugar found in connective tissue matrix) showed appreciably higher rates of protein and glycosaminoglycan labeling in the animals' valve leaflets as compared with rates in the skin, intestine, or tail; this indicated a higher rate of tissue renewal." Pathologic considerations. Isolated AR may result from damage to the leaflets, the supporting aortic wall and sinuses, or both. Conditions that spare the leaflet are amenable to repair 435
436
The Journal of Thoracic and Cardiovascular Surgery March 1993
Sarsam and Yacoub
)
v if'i;!':<'~'~·"'y );~. . ,~
"';:" .;.,
Diometer or ridqe
I
,
I
Sinus depth ond width
\ \
\
,
Fig. 2. Excision of dilated aortic segment and harvesting of coronary arteries. (See text for details.) Fig. 1. Aortic root with inlet diameter, ridge diameter, and sinus height. (Reid K. The Anatomy of the Sinus of Valsalva. Thorax 1970;25:79-85, published with permission.)
with the remodeling procedure. These conditions include dissecting aneurysm, atherosclerotic aneurysm, and aneurysm of the sinus of Valsalva. An increasingly recognized cause of isolated AR (accounting for approximately 40%) is noninflammatory aortic root dilatation or annuloaortic ectasia.' The striking feature is the absence of any inflammatory process. There is degeneration of the elastic element of the media, with abnormal organization of the smooth muscle and an increased amount of collagen." A cystic vacuole that contains mucopolysaccharides may be observed in the media; hence the term cystic medial necrosis. It is a feature of the autosomal dominant Marfan syndrome but affects many other patients with no signs of Marfan syndrome." Inflammatory aortitis that produces annular dilatation includes syphilis, with the characteristic opening of the commissures; syphilis rarely extends into the leaflet base. In contrast, aortitis caused by ankylosing spondylitis is more extensive, with fibrosis extending into the base of the leaflets, the interleaflet triangles, the base of the anterior leaflet of the mitral valve, and the membranous septum; this causes varying degrees of heart block' Rheumatoid arthritis, psoriasis, and Reiter's syndrome may create the semblance of ankylosing spondylitis, whereas aortitis that is associated with Takayasu's syndrome and giant cell aortitis characteristically spare the leaflet tissue. We and others?"! have described the condition of myxoid degeneration and floppy aortic valve. On reflection, the thickening of the cusp edge and increased myomatous tissue at the base may be caused by root dilatation. Indeed, 8 of our II patients had annular dilatation, and all had changes of cystic medial necrosis. In one series of 55 patients, 13 experienced such changes, but there was no measurement of aortic root. I I There were no such cases in two large series of 225 12 and 72 13 patients with isolated AR. The condition, however, does exist whereby the leaflet becomes soft and nodular with elongation of the lacunar area and results in leaflet prolapse despite the presence of an aortic root of normal size. Surgical technique. The aim of the procedure is to replace the diseased aortic tissue and, in the process, to reshape the
anulus back to its normal geometry to restore competence and preserve the leaflets. It is essential that the leaflets be thin and pliable. Standard bypass is established with systemic cooling to 25° C, a left ventricular vent is inserted, and the aorta is clamped. An oblique aortotomy is made, and the root is inspected with particular attention paid to the state of the leaflets, the commissural height, the supraannular ridge, and the inlet diameter. If reconstruction is feasible, cardioplegic solution is admiministered directly into the coronary ostia, and the aorta is transected just above the commissure. Supplementary retrograde cardioplegia can be induced with a coronary sinus cannula. The left and right coronary ostia are harvested with a 3 mm button of surrounding aortic wall. The aortic wall is then cut to within 2 to 3 mm from the leaflet and the commissure, thus resembling at this stage a prepared homograft (Fig. 2). A stay suture is put into the aortic rim above each commissural point. When these three sutures are pulled up, the effect will be a restoration of sinus height and a reduction of commissural diameter, with resultant coaptation of the leaflets. A collagen-impregnated Dacron graft, the diameter of which is equal to the inlet diameter, is used. The base of the tube is then divided into three points-a, b, and c. The distances between a and b and between band c equal the tube diameter; the distance between a and c is slightly longer for the noncoronary sinus (circumference = diameter X 3.14). These measurements are only guidelines. Adjustments may be needed for individual cases. A suitable procedure would involve the use of the "Frater stitch" through the nodules of Arantius to help with measurements. Longitudinal incisions are made at these points (a, b and c). The length of the incision is determined by the desired height of the commissure. As in homografts, the commissural point must be stretched up and must never be redundant (Fig. 3). The graft is then cut into the crown shape, which simulates the normal anulus, and after the commissural points are fixed the graft is attached to the aortic rim with 4-0 prolene sutures (Ethicon, Inc., Somervill, Md.). Meticulous suturing is essential because access to this suture line after completion is difficult. A suitable opening is made in the Dacron tube, and the coronaries are anastomosed with 4-0 Prolene sutures. The graft is then sized, and the top end is anastomosed to the aorta with 3-0 Prolene sutures (Fig. 4).
The Journal of Thoracic and Cardiovascular Surgery Volume 105, Number 3
Sarsam and Yacoub
437
Fig. 3. Preparation of graft. (See text for details.)
Results
Of the ten patients, one patient who had acute dissection died of bleeding. In another case aortic incompetence (AI) developed, and the patient underwent valve replacement I year after his original operation. At reoperation there was detachment of the commissure between the right and left coronary cusps. The remaining eight patients were alive and well and had no signs of AI (six patients) or had only mild AI (two patients) after a mean follow-up period of 3.4 years. Discussion
Unlike mitral valve repair, repair of isolated AR has yielded mixed results. Carpentier!" described techniques for the reduction of annular dilatation, repair of leaflet prolapse, and relief of restricted leaflet motion with 13% occurrence of reoperation and 15% occurrence of significant residual regurgitation. 14 He concluded that it is too early to recommend these techniques in adults, although two other techniques with long-term success have been reported. The first is resuspension of the detached commissure in aortic dissection, with 80% freedom from aortic valve replacement at 10 years.'? The second is valvuloplasty for repair of leaflet prolapse in association with ventricular septal defect, with a failure-free rate of 74% at 10 years. 16 Recent early success has been reported with cusp extension with the use of bovine pericardium, but long-term results are lacking.'? With the decline in the prevalence of rheumatic fever, noninflammatory aortic root dilatation is now the most common cause of isolated AR. 12 When the disease causes an aneurysm of the ascending aorta, in addition to AR, the recommended treatment is the composite graft technique as described by Bentall and DeBono l 8 and confirmed by others. 19. 20 Nevertheless, an effective technique for preserving valves would be a superior alternative. The remodeling procedure was initially applied to
Fig. 4. Graft suturedto aorta withreimplantation of coronary arteries.
patients with a dilated aortic root (mean, 6.8 em) and severe AI, diagnosed by echocardiography. The patients were young men who wanted to engage in athletic activities and women of child-bearing age. The procedure was later applied to patients who had type A dissection and were known to have had AI before dissection. The three bases for the repair are resection of pathologic aortic tissue, preservation of viable leaflet, and restoration of root geometry. We chose conduits with the same size as the inlet diameter to accommodate the secondary changes of increased surface area in the leaflets. If a smaller conduit were chosen, the sinus height would have to be adjusted at a higher point. As with homograft aortic valve replacement, there is some flexibility with this repair. In conclusion, the early results from this small series and the larger series at Harefield Hospital (unpublished data) are encouraging indeed. There is, however, a small but definite learning curve, and the long-term results are awaited. The procedure is potentially applicable to other conditions, such as aneurysm of the sinus of Valsalva (where, in a large series, the prevalence of aortic valve replacement in patients with aneurysm of the sinus and AR was 80%21) and other conditions that cause AR but spare the leaflet tissue, as discussed in the section on pathologic consideration. REFERENCES 1. Angelini A, Ho SY, Anderson RH, et al. The morphology ofthe normalaorticvalve as compared withthe aorticvalve having two leaflets. J THORAC CARDIOVASC SURG 1989; 98:362-7.
2. Reid K. The anatomy of the sinus of Valsalva. Thorax 1970;25:79-85.
4 3 8 Sarsam and Yacoub
3. Thubrikar M, Piepgrass WC, Shaner TW, Nolan SP. The design of the normal aortic valve. Am J Physiol 1981; 241:H795-801. 4. Deck JD, Thubrikar M, Schneider PJ, Nolan SP. Structure, stress and tissue repair in aortic valve leaflets. Cardiovase Res 1988;22:7-61. 5. Davis MJ. Pathology of cardiac valves. London: Butterworth & Co., Ltd., 1980:37-61. 6. Roberts WC, Hoing HS. The spectrum of cardiovascular disease in the Marfan syndrome. Am Heart J 1982; 104:115-35. 7. Hirst AE, Gore I. The etiology and pathology of aortic dissection. In: Doroghazi RM, Slater EE, eds. Aortic dissection. New York: McGraw-Hill, 1983:13-54. 8. Koike R, Sasaki S, Takeuchi A, Nakayama Y. Aortic regurgitation caused by giant cell aortitis. J Cardiovasc Surg 1989;30:372-4. 9. McKay R, Yacoub MH. Clinical and pathological findings in patients with "floppy" valves treated surgically. Circulation 1973;48(Pt. 2):IIII163-73. 10. Lakier JB, Copan H, Rosman HS, et al. Idiopathic degeneration of the aortic valve: a common cause of isolated aortic regurgitation. J Am Coli Cardiol 1985;5:347-57. 11. Allen WM, Matlolf JM, Fishbein Me. Myxoid degeneration of the aortic valve and isolated severe aortic regurgitation. Am J Cardiol 1985;55:439-44. 12. Olson LJ, Subramanian R, Edwards W. Surgical pathology of pure aortic insufficiency: a study of 225 cases. Mayo Clin Proc 1984;59:835-41.
The Journal of Thoracic and Cardiovascular Surgery March 1993
13. Guiney TE, Davis MJ, Parker DJ, et al. The etiology and course of isolated severe aortic regurgitation: a clinical, pathological and echocardiographic study. Br Heart J 1987;58:358-68. 14. Carpentier A. Cardiac valve surgery-the "French correction". J THoRAc CARDIOVASC SURG 1983;86:323-37. 15. Crumbly AJ III, Crawford FA Jr. Results of aortic valve replacement. Cardiol Clin 1991;9:353-80. 16. Okita Y, Miki S, Kusuhara K, et al. Long-term results of aortic valvuloplasty for aortic regurgitation associated with ventricular septal defect. J THORAC CARDIOVASC SURG 1988;96:769-74. 17. Al Faigh MR, Al Kassab SM, Ashmeg AI. Aortic valve repair using bovine pericardium for cusp extension. J THORAC CARDIOVASC SURG 1988;96:760-4. 18. Bentall H, DeBono A. A technique for complete replacement of the ascending aorta. Thorax 1968;23:338-9. 19. 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;192:40313. 20. Gott VL, Pyeritz RE, Magovern GJ, et al. Surgical treatment of aneurysm of the ascending aorta in the Marfan syndrome. N Engl J Med 1986;314:1070. 21. Meyer J, Wukasch DC, Hallman GL, Cooley DA. Aneurysm and fistula of the sinus of Valsalva. Ann Thorac Surg 1975;19:170-9.