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Repair of ventricular septal defect with aortic insufficiency
Repair of ventricular septal defect with aortic insufficiency G. A. Trusler, M.D., C. A. F. Moes, M.D. (by invitation), and
B. S. L. Kidd, M.D. (by invitation), Toronto, Ontario, Canada
Aortic insufficiency, secondary to ventricular septal defect, is usually caused by prolapse of an aortic valve leaflet with elongation of its free margin. Since the problem is essentially mechanical it is surprising that valvuloplasty has not been more successful in solving it. Both Garamella' and Starrand their colleagues shortened the free margin of the prolapsed cusp with some success. Similarly, Spencer and his associates" by taking a tuck in the elongated free margin of the prolapsed cusp, achieved almost complete aortic competence in 2 patients. Plauth and co-workers,' emphasizing the importance of accurate measurement, used sutures in the corpora Arantii as a guideline to making the length of the free margin of the prolapsed cusp equal to that of the adjacent normal cusps by plication. Frater? described a simple technique for comparing the length of the aortic leaflets by suspending the three corpora Arantii in a single suture. He showed by experiment that to maintain valve competence the free margin of each cusp should be equal to that of the opposing cusps. Recently Spencer and his colleagues" rekindled optimism in
valvuloplasty by presenting their largely successful experience with a combined group of 20 patients from three different centers. Valvuloplasty, accurately measured and carefully performed, should be effective. Perhaps some of the past failures were caused by breakdown of the repair. While accurately adjusting the size of the defective cusp to that of the other cusps, our technique emphasizes the security of the repair by reducing the possibility of later dehiscence. Our experience with 16 children treated over the past 4th years is the subject of this paper.
Clinical material Sixteen children, 10 girls and 6 boys ranging in age from 3 to 12 years, were operated upon for repair of ventricular septal defect and aortic insufficiency. The aortic insufficiency varied from mild to severe as graded by the intensity of the aortic diastolic murmur, the width of the pulse pressure, and the heart size (Table I). The severity of the aortic insufficiency was graded, by the appearance on the angiocardiogram, as mild in 2 children, moderate in 9, and severe in 5. The calculated pulmonaryIsystemic flow ratio varied from LOll to 2.0/1 in 15 children but was 2,8/1 in the sixteenth.
From the Departments of Surgery, Radiology. and Pediatrics, The Hospital for Sick Children, Toronto. and the University of Toronto. Toronto, Ontario, Canada. Read at the Fifty-third Annual Meeting of The American Association for Thoracic Surgery, Dallas, Texas, April 16, 17, and 18, 1973.
Operative findings
Address for reprints: Dr. G. A. Trusler, Department of Surgery, The Hospital for Sick Children, 555 University Ave., Toronto, Ontario, M5G lX8, Canada
The essential lesion causing aortic insufficiency in 13 of the 16 children was elonga-
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Fig. 1. Diagram of aortic valve repair showing the folIowing: A, Elongated free margin of prolapsed right leaflet. B, Sutures in corpora Arantii alIowing accurate comparison with opposing leaflets to determine extent of plication. C, Suture at commissure to maintain correct leaflet length. D, Fold of excess valve securely sandwiched against aortic wall by pledgetted mattress sutures. E, Commissure reinforced with hood of fine Dacron.
tion of the free margin of one aortic valve leaflet with prolapse of that leaflet into the left ventricle and adjacent ventricular septal defect. In 10 of the 13 children with this typical prolapsed aortic cusp, the ventricular septal defect was situated below the crista supraventricularis (subcristal) (Table I). Three had associated infundibular stenosis. The ventricular septal defect ranged from 8 to 15 mm. in diameter and, in 8 children, was situated directly below the right coronary leaflet which prolapsed, partly filling the defect. In 1 child the ventricular septal defect lay below the right commissure with some extension under the prolapsed right leaflet. In the tenth child the ventricular septal defect was situated below the right commissure of the aortic valve with prolapse of the adjacent posterior leaflet. In 3 of the 13 children with a prolapsed
aortic cusp the ventricular septal defect was situated above the crista supraventricularis (supracristal). These defects tended to be larger, ranging from 10 to 18 mm. in diameter. In 2 the defect lay immediately below a prolapsing right coronary leaflet. In the third child the defect was beneath the anterior commissure of the aortic valve. The adjacent part of the left coronary leaflet was prolapsed; its margin was thin, elongated, and attached slightly below the right coronary leaflet at the anterior commissure. In the other 3 children the aortic valve problem was atypical, with malformation of one or more commissures rather than a simple prolapse of one aortic leaflet. In 2 the ventricular septal defect was small, 2 and 5 mm. in diameter, and unrelated to the aortic insufficiency. From the right ventricular aspect, one was below and the other on the lower edge of the crista supraventric-
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Table I. Operative findings
Ventricular septal defect Case No.
1 2 3
4 5 6 7
8
9 10
Relation to aortic leaflet
Size (mm.)
5 8 4 9 6
10 9 7 3
12 8 8 12 8 12 9
5
15 8 8
7
14
Leaflet prolapsed
Subcristal ventricular septal defect Right Right Right Right Right Right Right Right Right Right Right and right commissure Right Right Right Right Right Right Right Posterior Right commissure
10
Supracristal ventricular septal defect Right Right Anterior commissure Left
10
18
Right
14
12
5
*
Right Commissure malformation Bicuspid leaflet
15
12
2
*
Bicuspid leaflet
16
12
10
Right commissure
Right and posterior
11
12
5
13
Other defects None None None None None None None Infundibular stenosis Infundibular stenosis Infundibular stenosis, slight fusion of right and posterior leaflet None Left coronary leaflet attachment low at anterior commissure None Bicuspid valve (right and posterior), infundibular stenosis Bicuspid valve (right and posterior) Abnormal formation of right commissure
*Not identified. tNd, Not done. ularis. The position relative to the aortic valve was not recorded. In both children the right and posterior leaflets were fused to form a single bicuspid leaflet which had a longer free margin than the third aortic leaflet and prolapsed into the ventricle, causing insufficiency. In the third child the subscristal ventricular septal defect, 10 mm. in diameter, was situated below the right commissure of the aortic valve. The adjacent right and posterior leaflets were shallow and poorly formed in the region of this commissure. Though the free margin was elongated the prolapse was not typical. The aortic valve ring seemed dilated but was not measured. Operation
Details of the operations included a median sternotomy incision, cardiopulmonary
bypass, left ventricular drainage, either normothermia or moderate hypothermia, and cardiac arrest without coronary perfusion. The aortic valve, repaired before the ventricular septal defect, was exposed by a curved transverse aortic incision which could be extended into the posterior sinus. The prolapsed leaflet, usually the right, was inspected and measured with particular regard to the length and appearance of the free margin and the formation and competence at each commissure. If the prolapse was severe and the free margin greatly elongated, the valve leaflet was plicated at both commissures (Fig. I). If the prolapse was less severe the valve was plicated at one commissure, usually the shallower and less well formed or where the valve leaflet was thin and weak. Plication at this site deepened the commissure and eliminated
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Results
allow-up (mo.)
54 38 30 25 18 17 10 39 30
Aortic diastolic murmur: Grade o to VI Before
25
II II III III II III III II II III
19 16
III III
12
II
30
III
14
III
6
II
I
After
Pulse pressure (mm. Hg)
Before
After
Before
75 90 80 85
40 35 30 35 30 35 30 30 35 40
Before
68 53 58 59 55 63 60 61 60 50
54 47 52 52 48 55 53 56 50 44
Moderate Moderate Severe Moderate Moderate Severe Severe Mild Moderate Moderate
110 88
40 40
54 58
51 53
Severe Mild
Nd Trace
70
40
56
51
Severe
Nd
70
50
50
46
Moderate
Mild
60
62
49
52
Moderate
Nd
50
52
53
54
Moderate
Nd
70 45 60 45 40
I I II
72
I
0 I
II
I
I
A ngiocardiographic estimate of insufficiency
After
0 0 0 0 0
0
I
Cardiothoracic ratio (per cent)
the weak portion of the leaflet. After the part of the valve to be taken up in the plication had been identified, small stay sutures were placed in the corpora Arantii of the two normal valve leaflets and at the future center point of the redundant right leaflet. The length of the free margin of the leaflet was adjusted to that of the other leaflets so that all three would be identical. When the amount of excess leaflet to be plicated had been determined, the appropriate point on the margin was tacked to the adjacent leaflet at the commissure with a fine silk suture. The excess leaflet tissue, folded at the commissure, was then secured to the aortic wall with two or three mattress sutures. These sutures were reinforced by Teflon felt pledgets, one within the aortic sinus and one on the outside of the aortic wall. This,
I
Aftert
0 Nd
0 0 0
Trace Nd Nd Nd Trace
in effect, sandwiched the folded valve tissue against the aortic wall. The pledget within the sinus extended over the free margin of the valve tissue to prevent blood dissecting the repair away from the aortic wall. Finally, the commissure was reinforced with a tiny patch of thin Dacron held with a mattress suture, the outer limb of which passed through the aortic wall into the external pledget and then back into the lumen of the aorta to secure the new commissure to the aortic wall. By forming a hood over the commissure and adjacent leaflets, the Dacron patch prevented blood from separating the two valve leaflets at this point. The aortotomy incision was then closed, the aortic clamp removed, and the right ventricle opened. Inspection of the aortic valve through the ventricular septal defect
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Fig. 2. A. Preoperative roentgenogram demonstrating cardiomegaly and moderate pulmonary plethora. B. At follow-up 4 112 years after the operation, the heart is much smaller and pulmonary vascularity is norm al.
revealed any remaining valve incompetence. Infundibular obstruction was relieved when present. The ventricular septal defect was closed with a patch of Dacron in all but 2 patients, whose defects were small enough to be closed directly. As an index of improvement, we compared the severity of the aortic diastolic murmur, the pulse pressure, the heart size (cardiothoracic ratio), and in 8 children the aortic root angiogram with the same parameters before the operation. Results No child died or had major complications such as heart block or recurrence of the ventricular septal defect. Results are summarized in Table 1. The status of all 10 children with subcristal ventricular septal defects and prolapsed leaflets is improved regardless of the presence or absence of associated infundibular stenosis. Four still have aortic diastolic murmurs, but the aortic pulse pressure is 40 mm. Hg or less in all, and heart size is significantly diminished except in 1 child (Fig. 2, A and B) . In this child (Case 2) , who had a subcristal ventricular septal defect and a severe infundibular stenosis similar to that found in tetralogy of Fallot, the redundant valve margin
had become thin and attenuated. The valvuloplasty in this patient did not include a Dacron hood to reinforce the commissures. The valve repair broke down soon after operation and a secondary repair was necessary 6 months later. Although clinically better than before operation and fully active, he still has a Grade 2 aortic diastolic murmur and a cardiothoracic ratio of 56 per cent. Operative results are good in the 3 children with supracristal ventricular septal defects. One has no aortic diastolic murmur and the other 2 have Grade 1 murmurs. In all 3 the pulse pressure is reduced to 40 mm. Hg and the heart size is decreased. One child (Case 12) was found by angiography to have poor left ventricular contraction before operation. This has not changed since repair although he has only a trivial degree of aortic incompetence. Seven children with a prolapsed leaflet have been restudied recently by cardiac catheterization including aortic root and left ventricular angiography. Four have completely competent aortic valves, while 3 have a barely visible degree of insufficiency (Fig. 3, A and B) and a Grade 1 diastolic murmur. In 3 children the angiographic appearance suggests some restric-
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Fig. 3. A, Preoperative aortic root angiogram showing moderate aortic valve regurgitation. B, Postoperatively, a barely visible degree of regurgitation is present.
tion of movement of the repaired right coronary cusp, and in 2 of these the cusp appears slightly thickened, but there is no pressure gradient across the aortic valve. The length of the follow-up period varies from 6 months to 4 112 years. In 1 child a diastolic murmur, present soon after the operation, disappeared over the next few months. No child has any evidence of late recurrence or increase in aortic insufficiency. Of the 3 children with commissure malformation, I is improved; the pulse pressure and cardiothoracic ratio are reduced, and postoperative angiography shows only mild residual aortic insufficiency. The other 2 children still have aortic insufficiency and are not improved. Discussion Nadas and colleagues' classified their cases of ventricular septal defect with aortic insufficiency into two groups according to the position of the defect, subcristal and supracristal. Van Praagh and MeNamara" further divided the subcristal defects into those with associated pulmonary infundibular stenosis and those without. They pointed out that major commissural malformations occur frequently in those patients with subcristal ventricular septal defect, thus rendering them inappropriate for valvuloplasty. Indeed, we encountered 3
children with major commissural malformations which were not really amenable to valvuloplasty, although 1 patient was improved by that procedure. All 3 had essentially subcristal defects. However, the presence of a subcristal defect is not as important as the exact mechanism of the aortic insufficiency. All 13 children with insufficiency from a redundant prolapsed aortic valve leaflet were improved by valvuloplasty, whether the defect was supracristal or subcristal. Six have no evidence of aortic insufficiency at this time and 6 are left with only trivial insufficiency, normal pulse pressure, and a Grade 1 diastolic murmur. One child has moderate aortic insufficiency due to an inadequate repair. The presence or absence of infundibular stenosis does not affect the result. A number of authors including Keck" and Nadas' and their co-workers mention some degree of dextrorotation of the aortic root. We noticed this on a number of occasions in both subcristal and supracristal ventricular septal defects. While this rotation suggests the malformation is complex and related to formation of the conus, further study is necessary to make clear the exact relationship of the conal abnormality and ventricular septal defect to the aortic insufficiency. The remarkable experience of Tatsuno
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Fig. 4. Lateral aortogram in diastole and systole. A, Diastole, showing moderate aortic valve regurgitation with downward protrusion of the inferior portion of the right coronary sinus (~). B, Systole, showing a "tear drop" protrusion of the right coronary sinus (~) .
Fig. 5. Aortic root angiogram showing a bicuspid aortic valve. The anterior sinus is large while the other is of normal size. An eccentric jet of contrast material is seen regurgitating into the left ventricle.
and his associates: " with angiographic identification of this malformation is valuable. Our retrospective study confirms their finding that the angiogram correlates well with the anatomic findings at operation. The position of the ventricular septal defect can usually be determined and the exact portion of aortic valve involved in the defect can be ascertained (Fig. 4). It is most important to identify those patients whose defect is not amenable to repair, such as the 3
children in our series whose malformations were primarily of the commissure. In retrospect, the 2 children whose bicuspid aortic valves represented a different entity could have been so identified. On angiography the valve appeared bicuspid (Fig. 5) and the usual cusp prolapse was not present. The ventricular septal defect in these 2 children was small. A small ventricular septal defect is an unreliable guide, because a prolapsing leaflet will often partially cover the defect. In the third child, three valve leaflets could be seen and there appeared to be slight prolapse of the posterior leaflet. We are still uncertain how to distinguish this child from the 13 who are good candidates for the repair. What mechanism produces the aortic insufficiency? In the typical case, the affected leaflet is situated directly over the ventricular septal defect. The usual explanation is that the valve leaflet lacks support; this causes prolapse and eventually leads to stretching and elongation of the free margin of the cusp, which slips below the support of other two leaflets and spills blood back into the ventricle . The prolapsed leaflet bulges down into and through the ventricular septal defect, sometimes extending into the right ventricular outflow tract. However, in some forms of transposition, tetralogy of Fallot, and double-outlet right
Volume 66 Number 3 September, 1973
Ventricular septal defect with aortic insufficiency
ventricle, relatively unsupported aortic valves may be seen but rarely do they prolapse, More that mere lack of support must be necessary to create the insufficiency. Perhaps a dynamic factor related to blood flow acts on the aortic cusp so intimately related to the ventricular septal defect. Starr and his colleagues" suggested the prolapse was due to the high-velocity jet of blood passing through the ventricular septal defect and pulling the leaflet downward. Blood flowing through the defect from the left to right ventricle could pull or drag on the belly of the leaflet in accordance with the Bernoulli principle, in much the same way that the negative pressure from the side arm of a laboratory water tap produces suction (Fig. 6). In the early stages the pull of this blood flowing across the ventricular septal defect may be just enough to stretch the valve leaflet, causing it to prolapse slightly to produce mild aortic insufficiency. Merely repairing the ventricular septal defect and stopping the flow before the valve leaflet has developed an elongated free margin would then stop the insufficiency, as has been advocated by Treasure and his co-workers. 11 In later stages, when the free margin of the ventricular septal defect is permanently elongated so that it can no longer maintain its position, a valvuloplasty is necessary. The essence of successful valvuloplasty is to measure the prolapsing leaflet precisely and then reduce the length of its free margin until it matches that of the adjacent normal leaflets. The excess free margin is taken up by some method of plication secure enough to prohibit recurrence. Weldon" plicates the abnormal leaflet with an ingenious running suture technique. Although it is simple and rapid, we feel that this technique may not be sufficiently secure to avoid recurrences. Spencer? advocates plication near, but not at, the commissure, and in a relatively mobile portion of the aortic valve, suggesting that a plicated segment anchored to a fixed point is more likely to dehisce. On the contrary we feel that, by placing pledgets
40 1
Fig. 6. Diagram illustrating hemodynamic forces on the aortic cusp adjacent to the ventricular septal defect. In accordance with the BernoulIi principle, blood flow through the defect produces forces that tend to pull the cusp down into the defect.
on both sides of the aortic wall, the plicated segment can be securely held and will be less likely to come apart than will a repair in a mobile segment of the valve leaflet. The mobile portion of the leaflet is then unencumbered by sutures or pledgets which might well form the nidus for degenerative change. In addition, by plicating the valve leaflet at one or both commissures, we are able to refashion and improve the shape of the valve at the commissure, deepening it where it is shallow or raising it where it is low. A small hood of Dacron binding the abnormal valve leaflet to the adjacent normal leaflet at the commissure ensures competence at this site and further reduces the possibility of recurrence. The early results in children to whom
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this technique was applied are good. The only child with more than minute aortic insufficiency was one in whom the original repair was incomplete. The follow-up period is now as long as 4yz years with no evidence of increasing insufficiency in any child. Although both mild and severe aortic insufficiency were relieved, the results of the operation appear to justify early rather than late repair of the ventricular septal defect and aortic insufficiency to avoid the deleterious effects of prolonged insufficiency on the aortic valve and left ventricle. Summary
Sixteen children with ventricular septal defect and aortic insufficiency have been treated by repair of the ventricular septal defect and valvuloplasty of the affected valve leaflet. The valvuloplasty involves precise measurement of the elongated free margin of the prolapsed leaflet, secure fixation of the excess to the aortic wall, and reconstruction of the adjacent commissure. Rather than the typical prolapsed leaflet abnormality, 3 of the 16 children had a malformation of one or more aortic valve commissures, 2 with bicuspid valves. These cases should be identified before operation because for them valvuloplasty is of little benefit. The other I 3 children had a typical prolapsed leaflet. The ventricular septal defect was subcristal in 10 children and supracristal in 3. One child operated upon early in the series, in whom repair was less complete, still has moderate aortic insufficiency. The other 12 are much improved with normal pulse pressures and decreasing heart size. In 7 the diastolic murmur disappeared and in 5 it was of Grade 1 intensity. Late postoperative aortic root angiography in 7 of these children indicated residual aortic insufficiency ranging from nil to a trace. The longest follow-up period was 4yz years with no evidence of increasing aortic insufficiency in any child. Aortic insufficiency secondary to the presence of ventricular
Thoracic and Cardiovascular Surgery
septal defect with a typical prolapsed aortic valve leaflet can be safely and effectively repaired by this technique. We are grateful to Dr. W. T. Mustard for assistance in the preparation of this paper and Dr. A. M. Albisser for advice about the hemodynamic forces acting on the aortic cusp. REFERENCES
2
3
4
5 6
7
8
9
10 11
Garamella, J. J., Cruz, A. B., Jr., Heupel, W. H., Dahl, 1. c., Jensen, N. K., and Berman, R.: Ventricular Septal Defect With Aortic Insufficiency: Successful Surgical Correction of Both Defects by the Transaortic Approach, Am. J. Cardio!. 5: 266, 1960. Starr, A., Menashe, V., and Dotter, C.: Surgical Correction of Aortic Insufficiency Associated With Ventricular Septal Defect, Surg. Gynecol, Obstet. 111: 71, 1960. Spencer, F. c., Bahnson, H. T., and Neil\, C. A.: The Treatment of Aortic Regurgitation Associated With a Ventricular Septal Defect, J. THoRAc. CARDIOVASC. SURG. 43: 222, 1962. Plauth, W. H., Braunwald, E., Rockoff, S. D., Mason, D. T., and Morrow, A. G.: Ventricular Septal Defect and Aortic Regurgitation: Clinical, Hemodynamic and Surgical Considerations, Am. J. Med. 39: 552, 1965. Frater, R. W. M.: The Prolapsing Aortic Cusp: Experimental and Clinical Observations, Ann. Thorac. Surg. 3: 63, 1967. Spencer, F. c., Doyle, E. F., Danilowicz, D. A., Bahnson, H. T., and Weldon, C. S.: Long-Term Evaluation of Aortic Valvuloplasty for Aortic Insufficiency and Ventricular Septal Defect, 1. THORAc. CARDIOVASC. SURG. 65: 15, 1973. Nadas, A. S., Thilenius, O. G., LaFarge, C. G., and Hauck, A. J.: Ventricular Septal Defect With Aortic Regurgitation: Medical and Pathologic Aspects, Circulation 29: 862, 1964. Van Praagh, R., and McNamara, J. J.: Anatomic Types of Ventricular Septal Defect With Aortic Insufficiency, Am. Heart J. 75: 604, 1968. Keck, E. W.O., Ongley, P. A., Kincaid, O. W., and Swan, H. J. C.: Ventricular Septal Defect With Aortic Insufficiency: A Clinical and Hemodynamic Study of 18 Proved Cases, Circulation 27: 203, 1963. Tatsuno, K., Konno, S., and Sakakibara, S.: Ventricular Septal Defect With Aortic Insufficiency, Am. Heart J. 85: 13, 1973. Treasure, R. L., Hopeman, A. R., Jahnke, and Czarnecki, S. W.: E. J., Green, D. Ventricular Septal Defect With Aortic Insufficiency, Ann. Thorac. Surg. 12: 411, 1971.
c.
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Ventricular septal defect with aortic insufficiency
Discussion DR. FRANK C. SPENCER New York, N. Y.
I will comment briefly on Dr. Trusler's paper, which I enjoyed very much. Last year we reported to this Association a collective experience with 20 patients from three different institutions, New York University, University of Pittsburgh, and St. Louis University. Some type of valvuloplasty was performed in all 20 patients, none of whom had a prosthetic replacement. Excellent results were obtained in several, and all were improved, though some continued to have insufficiency. The results presented today by Dr. Trusler are actually even better than those we reported, because he describes only mild insufficiency in most patients. I recently had the pleasure of hearing the experience of Professor Bourakovsky in Russia, who has applied a similar technique in several patients. Another significant report describing a large experience with leaflet reconstruction has recently appeared from Japan. Hence, reports from several' centers confirm the fact that reconstruction can be done in most cases. It is similarly clear that the pathology varies widely and that no one technique will yet work uniformly for all patients. All reports indicate some mild persisting insufficiency or some recurrence. Hence, repair must be individualized for each patient at operation, and the effectiveness of the repair must be carefully measured. Dr. Trusler mentioned an important aspect of technique, which I would like to emphasize. The
403
valve should be repaired first and the aorta closed. Then the repair should be inspected through the ventriculotomy and the ventricular septal defect. If the reverse approach is done, with the ventricular septal defect closed before the valve is repaired, the effectiveness of aortic valvuloplasty cannot be properly judged. I am particularly impressed with Dr. Trusler's method of cusp plication. From our experiences we have felt a plicated area should remain mobile. An earlier technique that failed in several groups involved attachment of the plicated segment to the aortic wall. The method reported today, however, seems to provide more secure fixation. In summary, data from several sources support Dr. Trusler's conclusion that in at least 90 per cent of patients some form of valvuloplasty can be done. Prosthetic replacement should seldom be necessary. DR. TRUSLER (Closing) I want to emphasize the point that Dr. Spencer made about the individuality of the pathology and, therefore, the method of treatment in these patients. Last year at this meeting, he described a technique of treatment that Dr. Weldon uses. It involves very rapid plication at the commissure. This technique should be kept in mind, because if there is still insufficiency when the right ventricle is opened, this technique can be used to adjust the position of the valve very quickly and achieve competence.
B. S. L. Kidd, M.D. (by invitation), Toronto, Ontario, Canada
Aortic insufficiency, secondary to ventricular septal defect, is usually caused by prolapse of an aortic valve leaflet with elongation of its free margin. Since the problem is essentially mechanical it is surprising that valvuloplasty has not been more successful in solving it. Both Garamella' and Starrand their colleagues shortened the free margin of the prolapsed cusp with some success. Similarly, Spencer and his associates" by taking a tuck in the elongated free margin of the prolapsed cusp, achieved almost complete aortic competence in 2 patients. Plauth and co-workers,' emphasizing the importance of accurate measurement, used sutures in the corpora Arantii as a guideline to making the length of the free margin of the prolapsed cusp equal to that of the adjacent normal cusps by plication. Frater? described a simple technique for comparing the length of the aortic leaflets by suspending the three corpora Arantii in a single suture. He showed by experiment that to maintain valve competence the free margin of each cusp should be equal to that of the opposing cusps. Recently Spencer and his colleagues" rekindled optimism in
valvuloplasty by presenting their largely successful experience with a combined group of 20 patients from three different centers. Valvuloplasty, accurately measured and carefully performed, should be effective. Perhaps some of the past failures were caused by breakdown of the repair. While accurately adjusting the size of the defective cusp to that of the other cusps, our technique emphasizes the security of the repair by reducing the possibility of later dehiscence. Our experience with 16 children treated over the past 4th years is the subject of this paper.
Clinical material Sixteen children, 10 girls and 6 boys ranging in age from 3 to 12 years, were operated upon for repair of ventricular septal defect and aortic insufficiency. The aortic insufficiency varied from mild to severe as graded by the intensity of the aortic diastolic murmur, the width of the pulse pressure, and the heart size (Table I). The severity of the aortic insufficiency was graded, by the appearance on the angiocardiogram, as mild in 2 children, moderate in 9, and severe in 5. The calculated pulmonaryIsystemic flow ratio varied from LOll to 2.0/1 in 15 children but was 2,8/1 in the sixteenth.
From the Departments of Surgery, Radiology. and Pediatrics, The Hospital for Sick Children, Toronto. and the University of Toronto. Toronto, Ontario, Canada. Read at the Fifty-third Annual Meeting of The American Association for Thoracic Surgery, Dallas, Texas, April 16, 17, and 18, 1973.
Operative findings
Address for reprints: Dr. G. A. Trusler, Department of Surgery, The Hospital for Sick Children, 555 University Ave., Toronto, Ontario, M5G lX8, Canada
The essential lesion causing aortic insufficiency in 13 of the 16 children was elonga-
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Fig. 1. Diagram of aortic valve repair showing the folIowing: A, Elongated free margin of prolapsed right leaflet. B, Sutures in corpora Arantii alIowing accurate comparison with opposing leaflets to determine extent of plication. C, Suture at commissure to maintain correct leaflet length. D, Fold of excess valve securely sandwiched against aortic wall by pledgetted mattress sutures. E, Commissure reinforced with hood of fine Dacron.
tion of the free margin of one aortic valve leaflet with prolapse of that leaflet into the left ventricle and adjacent ventricular septal defect. In 10 of the 13 children with this typical prolapsed aortic cusp, the ventricular septal defect was situated below the crista supraventricularis (subcristal) (Table I). Three had associated infundibular stenosis. The ventricular septal defect ranged from 8 to 15 mm. in diameter and, in 8 children, was situated directly below the right coronary leaflet which prolapsed, partly filling the defect. In 1 child the ventricular septal defect lay below the right commissure with some extension under the prolapsed right leaflet. In the tenth child the ventricular septal defect was situated below the right commissure of the aortic valve with prolapse of the adjacent posterior leaflet. In 3 of the 13 children with a prolapsed
aortic cusp the ventricular septal defect was situated above the crista supraventricularis (supracristal). These defects tended to be larger, ranging from 10 to 18 mm. in diameter. In 2 the defect lay immediately below a prolapsing right coronary leaflet. In the third child the defect was beneath the anterior commissure of the aortic valve. The adjacent part of the left coronary leaflet was prolapsed; its margin was thin, elongated, and attached slightly below the right coronary leaflet at the anterior commissure. In the other 3 children the aortic valve problem was atypical, with malformation of one or more commissures rather than a simple prolapse of one aortic leaflet. In 2 the ventricular septal defect was small, 2 and 5 mm. in diameter, and unrelated to the aortic insufficiency. From the right ventricular aspect, one was below and the other on the lower edge of the crista supraventric-
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Table I. Operative findings
Ventricular septal defect Case No.
1 2 3
4 5 6 7
8
9 10
Relation to aortic leaflet
Size (mm.)
5 8 4 9 6
10 9 7 3
12 8 8 12 8 12 9
5
15 8 8
7
14
Leaflet prolapsed
Subcristal ventricular septal defect Right Right Right Right Right Right Right Right Right Right Right and right commissure Right Right Right Right Right Right Right Posterior Right commissure
10
Supracristal ventricular septal defect Right Right Anterior commissure Left
10
18
Right
14
12
5
*
Right Commissure malformation Bicuspid leaflet
15
12
2
*
Bicuspid leaflet
16
12
10
Right commissure
Right and posterior
11
12
5
13
Other defects None None None None None None None Infundibular stenosis Infundibular stenosis Infundibular stenosis, slight fusion of right and posterior leaflet None Left coronary leaflet attachment low at anterior commissure None Bicuspid valve (right and posterior), infundibular stenosis Bicuspid valve (right and posterior) Abnormal formation of right commissure
*Not identified. tNd, Not done. ularis. The position relative to the aortic valve was not recorded. In both children the right and posterior leaflets were fused to form a single bicuspid leaflet which had a longer free margin than the third aortic leaflet and prolapsed into the ventricle, causing insufficiency. In the third child the subscristal ventricular septal defect, 10 mm. in diameter, was situated below the right commissure of the aortic valve. The adjacent right and posterior leaflets were shallow and poorly formed in the region of this commissure. Though the free margin was elongated the prolapse was not typical. The aortic valve ring seemed dilated but was not measured. Operation
Details of the operations included a median sternotomy incision, cardiopulmonary
bypass, left ventricular drainage, either normothermia or moderate hypothermia, and cardiac arrest without coronary perfusion. The aortic valve, repaired before the ventricular septal defect, was exposed by a curved transverse aortic incision which could be extended into the posterior sinus. The prolapsed leaflet, usually the right, was inspected and measured with particular regard to the length and appearance of the free margin and the formation and competence at each commissure. If the prolapse was severe and the free margin greatly elongated, the valve leaflet was plicated at both commissures (Fig. I). If the prolapse was less severe the valve was plicated at one commissure, usually the shallower and less well formed or where the valve leaflet was thin and weak. Plication at this site deepened the commissure and eliminated
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Results
allow-up (mo.)
54 38 30 25 18 17 10 39 30
Aortic diastolic murmur: Grade o to VI Before
25
II II III III II III III II II III
19 16
III III
12
II
30
III
14
III
6
II
I
After
Pulse pressure (mm. Hg)
Before
After
Before
75 90 80 85
40 35 30 35 30 35 30 30 35 40
Before
68 53 58 59 55 63 60 61 60 50
54 47 52 52 48 55 53 56 50 44
Moderate Moderate Severe Moderate Moderate Severe Severe Mild Moderate Moderate
110 88
40 40
54 58
51 53
Severe Mild
Nd Trace
70
40
56
51
Severe
Nd
70
50
50
46
Moderate
Mild
60
62
49
52
Moderate
Nd
50
52
53
54
Moderate
Nd
70 45 60 45 40
I I II
72
I
0 I
II
I
I
A ngiocardiographic estimate of insufficiency
After
0 0 0 0 0
0
I
Cardiothoracic ratio (per cent)
the weak portion of the leaflet. After the part of the valve to be taken up in the plication had been identified, small stay sutures were placed in the corpora Arantii of the two normal valve leaflets and at the future center point of the redundant right leaflet. The length of the free margin of the leaflet was adjusted to that of the other leaflets so that all three would be identical. When the amount of excess leaflet to be plicated had been determined, the appropriate point on the margin was tacked to the adjacent leaflet at the commissure with a fine silk suture. The excess leaflet tissue, folded at the commissure, was then secured to the aortic wall with two or three mattress sutures. These sutures were reinforced by Teflon felt pledgets, one within the aortic sinus and one on the outside of the aortic wall. This,
I
Aftert
0 Nd
0 0 0
Trace Nd Nd Nd Trace
in effect, sandwiched the folded valve tissue against the aortic wall. The pledget within the sinus extended over the free margin of the valve tissue to prevent blood dissecting the repair away from the aortic wall. Finally, the commissure was reinforced with a tiny patch of thin Dacron held with a mattress suture, the outer limb of which passed through the aortic wall into the external pledget and then back into the lumen of the aorta to secure the new commissure to the aortic wall. By forming a hood over the commissure and adjacent leaflets, the Dacron patch prevented blood from separating the two valve leaflets at this point. The aortotomy incision was then closed, the aortic clamp removed, and the right ventricle opened. Inspection of the aortic valve through the ventricular septal defect
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Fig. 2. A. Preoperative roentgenogram demonstrating cardiomegaly and moderate pulmonary plethora. B. At follow-up 4 112 years after the operation, the heart is much smaller and pulmonary vascularity is norm al.
revealed any remaining valve incompetence. Infundibular obstruction was relieved when present. The ventricular septal defect was closed with a patch of Dacron in all but 2 patients, whose defects were small enough to be closed directly. As an index of improvement, we compared the severity of the aortic diastolic murmur, the pulse pressure, the heart size (cardiothoracic ratio), and in 8 children the aortic root angiogram with the same parameters before the operation. Results No child died or had major complications such as heart block or recurrence of the ventricular septal defect. Results are summarized in Table 1. The status of all 10 children with subcristal ventricular septal defects and prolapsed leaflets is improved regardless of the presence or absence of associated infundibular stenosis. Four still have aortic diastolic murmurs, but the aortic pulse pressure is 40 mm. Hg or less in all, and heart size is significantly diminished except in 1 child (Fig. 2, A and B) . In this child (Case 2) , who had a subcristal ventricular septal defect and a severe infundibular stenosis similar to that found in tetralogy of Fallot, the redundant valve margin
had become thin and attenuated. The valvuloplasty in this patient did not include a Dacron hood to reinforce the commissures. The valve repair broke down soon after operation and a secondary repair was necessary 6 months later. Although clinically better than before operation and fully active, he still has a Grade 2 aortic diastolic murmur and a cardiothoracic ratio of 56 per cent. Operative results are good in the 3 children with supracristal ventricular septal defects. One has no aortic diastolic murmur and the other 2 have Grade 1 murmurs. In all 3 the pulse pressure is reduced to 40 mm. Hg and the heart size is decreased. One child (Case 12) was found by angiography to have poor left ventricular contraction before operation. This has not changed since repair although he has only a trivial degree of aortic incompetence. Seven children with a prolapsed leaflet have been restudied recently by cardiac catheterization including aortic root and left ventricular angiography. Four have completely competent aortic valves, while 3 have a barely visible degree of insufficiency (Fig. 3, A and B) and a Grade 1 diastolic murmur. In 3 children the angiographic appearance suggests some restric-
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Fig. 3. A, Preoperative aortic root angiogram showing moderate aortic valve regurgitation. B, Postoperatively, a barely visible degree of regurgitation is present.
tion of movement of the repaired right coronary cusp, and in 2 of these the cusp appears slightly thickened, but there is no pressure gradient across the aortic valve. The length of the follow-up period varies from 6 months to 4 112 years. In 1 child a diastolic murmur, present soon after the operation, disappeared over the next few months. No child has any evidence of late recurrence or increase in aortic insufficiency. Of the 3 children with commissure malformation, I is improved; the pulse pressure and cardiothoracic ratio are reduced, and postoperative angiography shows only mild residual aortic insufficiency. The other 2 children still have aortic insufficiency and are not improved. Discussion Nadas and colleagues' classified their cases of ventricular septal defect with aortic insufficiency into two groups according to the position of the defect, subcristal and supracristal. Van Praagh and MeNamara" further divided the subcristal defects into those with associated pulmonary infundibular stenosis and those without. They pointed out that major commissural malformations occur frequently in those patients with subcristal ventricular septal defect, thus rendering them inappropriate for valvuloplasty. Indeed, we encountered 3
children with major commissural malformations which were not really amenable to valvuloplasty, although 1 patient was improved by that procedure. All 3 had essentially subcristal defects. However, the presence of a subcristal defect is not as important as the exact mechanism of the aortic insufficiency. All 13 children with insufficiency from a redundant prolapsed aortic valve leaflet were improved by valvuloplasty, whether the defect was supracristal or subcristal. Six have no evidence of aortic insufficiency at this time and 6 are left with only trivial insufficiency, normal pulse pressure, and a Grade 1 diastolic murmur. One child has moderate aortic insufficiency due to an inadequate repair. The presence or absence of infundibular stenosis does not affect the result. A number of authors including Keck" and Nadas' and their co-workers mention some degree of dextrorotation of the aortic root. We noticed this on a number of occasions in both subcristal and supracristal ventricular septal defects. While this rotation suggests the malformation is complex and related to formation of the conus, further study is necessary to make clear the exact relationship of the conal abnormality and ventricular septal defect to the aortic insufficiency. The remarkable experience of Tatsuno
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Fig. 4. Lateral aortogram in diastole and systole. A, Diastole, showing moderate aortic valve regurgitation with downward protrusion of the inferior portion of the right coronary sinus (~). B, Systole, showing a "tear drop" protrusion of the right coronary sinus (~) .
Fig. 5. Aortic root angiogram showing a bicuspid aortic valve. The anterior sinus is large while the other is of normal size. An eccentric jet of contrast material is seen regurgitating into the left ventricle.
and his associates: " with angiographic identification of this malformation is valuable. Our retrospective study confirms their finding that the angiogram correlates well with the anatomic findings at operation. The position of the ventricular septal defect can usually be determined and the exact portion of aortic valve involved in the defect can be ascertained (Fig. 4). It is most important to identify those patients whose defect is not amenable to repair, such as the 3
children in our series whose malformations were primarily of the commissure. In retrospect, the 2 children whose bicuspid aortic valves represented a different entity could have been so identified. On angiography the valve appeared bicuspid (Fig. 5) and the usual cusp prolapse was not present. The ventricular septal defect in these 2 children was small. A small ventricular septal defect is an unreliable guide, because a prolapsing leaflet will often partially cover the defect. In the third child, three valve leaflets could be seen and there appeared to be slight prolapse of the posterior leaflet. We are still uncertain how to distinguish this child from the 13 who are good candidates for the repair. What mechanism produces the aortic insufficiency? In the typical case, the affected leaflet is situated directly over the ventricular septal defect. The usual explanation is that the valve leaflet lacks support; this causes prolapse and eventually leads to stretching and elongation of the free margin of the cusp, which slips below the support of other two leaflets and spills blood back into the ventricle . The prolapsed leaflet bulges down into and through the ventricular septal defect, sometimes extending into the right ventricular outflow tract. However, in some forms of transposition, tetralogy of Fallot, and double-outlet right
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Ventricular septal defect with aortic insufficiency
ventricle, relatively unsupported aortic valves may be seen but rarely do they prolapse, More that mere lack of support must be necessary to create the insufficiency. Perhaps a dynamic factor related to blood flow acts on the aortic cusp so intimately related to the ventricular septal defect. Starr and his colleagues" suggested the prolapse was due to the high-velocity jet of blood passing through the ventricular septal defect and pulling the leaflet downward. Blood flowing through the defect from the left to right ventricle could pull or drag on the belly of the leaflet in accordance with the Bernoulli principle, in much the same way that the negative pressure from the side arm of a laboratory water tap produces suction (Fig. 6). In the early stages the pull of this blood flowing across the ventricular septal defect may be just enough to stretch the valve leaflet, causing it to prolapse slightly to produce mild aortic insufficiency. Merely repairing the ventricular septal defect and stopping the flow before the valve leaflet has developed an elongated free margin would then stop the insufficiency, as has been advocated by Treasure and his co-workers. 11 In later stages, when the free margin of the ventricular septal defect is permanently elongated so that it can no longer maintain its position, a valvuloplasty is necessary. The essence of successful valvuloplasty is to measure the prolapsing leaflet precisely and then reduce the length of its free margin until it matches that of the adjacent normal leaflets. The excess free margin is taken up by some method of plication secure enough to prohibit recurrence. Weldon" plicates the abnormal leaflet with an ingenious running suture technique. Although it is simple and rapid, we feel that this technique may not be sufficiently secure to avoid recurrences. Spencer? advocates plication near, but not at, the commissure, and in a relatively mobile portion of the aortic valve, suggesting that a plicated segment anchored to a fixed point is more likely to dehisce. On the contrary we feel that, by placing pledgets
40 1
Fig. 6. Diagram illustrating hemodynamic forces on the aortic cusp adjacent to the ventricular septal defect. In accordance with the BernoulIi principle, blood flow through the defect produces forces that tend to pull the cusp down into the defect.
on both sides of the aortic wall, the plicated segment can be securely held and will be less likely to come apart than will a repair in a mobile segment of the valve leaflet. The mobile portion of the leaflet is then unencumbered by sutures or pledgets which might well form the nidus for degenerative change. In addition, by plicating the valve leaflet at one or both commissures, we are able to refashion and improve the shape of the valve at the commissure, deepening it where it is shallow or raising it where it is low. A small hood of Dacron binding the abnormal valve leaflet to the adjacent normal leaflet at the commissure ensures competence at this site and further reduces the possibility of recurrence. The early results in children to whom
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this technique was applied are good. The only child with more than minute aortic insufficiency was one in whom the original repair was incomplete. The follow-up period is now as long as 4yz years with no evidence of increasing insufficiency in any child. Although both mild and severe aortic insufficiency were relieved, the results of the operation appear to justify early rather than late repair of the ventricular septal defect and aortic insufficiency to avoid the deleterious effects of prolonged insufficiency on the aortic valve and left ventricle. Summary
Sixteen children with ventricular septal defect and aortic insufficiency have been treated by repair of the ventricular septal defect and valvuloplasty of the affected valve leaflet. The valvuloplasty involves precise measurement of the elongated free margin of the prolapsed leaflet, secure fixation of the excess to the aortic wall, and reconstruction of the adjacent commissure. Rather than the typical prolapsed leaflet abnormality, 3 of the 16 children had a malformation of one or more aortic valve commissures, 2 with bicuspid valves. These cases should be identified before operation because for them valvuloplasty is of little benefit. The other I 3 children had a typical prolapsed leaflet. The ventricular septal defect was subcristal in 10 children and supracristal in 3. One child operated upon early in the series, in whom repair was less complete, still has moderate aortic insufficiency. The other 12 are much improved with normal pulse pressures and decreasing heart size. In 7 the diastolic murmur disappeared and in 5 it was of Grade 1 intensity. Late postoperative aortic root angiography in 7 of these children indicated residual aortic insufficiency ranging from nil to a trace. The longest follow-up period was 4yz years with no evidence of increasing aortic insufficiency in any child. Aortic insufficiency secondary to the presence of ventricular
Thoracic and Cardiovascular Surgery
septal defect with a typical prolapsed aortic valve leaflet can be safely and effectively repaired by this technique. We are grateful to Dr. W. T. Mustard for assistance in the preparation of this paper and Dr. A. M. Albisser for advice about the hemodynamic forces acting on the aortic cusp. REFERENCES
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5 6
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10 11
Garamella, J. J., Cruz, A. B., Jr., Heupel, W. H., Dahl, 1. c., Jensen, N. K., and Berman, R.: Ventricular Septal Defect With Aortic Insufficiency: Successful Surgical Correction of Both Defects by the Transaortic Approach, Am. J. Cardio!. 5: 266, 1960. Starr, A., Menashe, V., and Dotter, C.: Surgical Correction of Aortic Insufficiency Associated With Ventricular Septal Defect, Surg. Gynecol, Obstet. 111: 71, 1960. Spencer, F. c., Bahnson, H. T., and Neil\, C. A.: The Treatment of Aortic Regurgitation Associated With a Ventricular Septal Defect, J. THoRAc. CARDIOVASC. SURG. 43: 222, 1962. Plauth, W. H., Braunwald, E., Rockoff, S. D., Mason, D. T., and Morrow, A. G.: Ventricular Septal Defect and Aortic Regurgitation: Clinical, Hemodynamic and Surgical Considerations, Am. J. Med. 39: 552, 1965. Frater, R. W. M.: The Prolapsing Aortic Cusp: Experimental and Clinical Observations, Ann. Thorac. Surg. 3: 63, 1967. Spencer, F. c., Doyle, E. F., Danilowicz, D. A., Bahnson, H. T., and Weldon, C. S.: Long-Term Evaluation of Aortic Valvuloplasty for Aortic Insufficiency and Ventricular Septal Defect, 1. THORAc. CARDIOVASC. SURG. 65: 15, 1973. Nadas, A. S., Thilenius, O. G., LaFarge, C. G., and Hauck, A. J.: Ventricular Septal Defect With Aortic Regurgitation: Medical and Pathologic Aspects, Circulation 29: 862, 1964. Van Praagh, R., and McNamara, J. J.: Anatomic Types of Ventricular Septal Defect With Aortic Insufficiency, Am. Heart J. 75: 604, 1968. Keck, E. W.O., Ongley, P. A., Kincaid, O. W., and Swan, H. J. C.: Ventricular Septal Defect With Aortic Insufficiency: A Clinical and Hemodynamic Study of 18 Proved Cases, Circulation 27: 203, 1963. Tatsuno, K., Konno, S., and Sakakibara, S.: Ventricular Septal Defect With Aortic Insufficiency, Am. Heart J. 85: 13, 1973. Treasure, R. L., Hopeman, A. R., Jahnke, and Czarnecki, S. W.: E. J., Green, D. Ventricular Septal Defect With Aortic Insufficiency, Ann. Thorac. Surg. 12: 411, 1971.
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Ventricular septal defect with aortic insufficiency
Discussion DR. FRANK C. SPENCER New York, N. Y.
I will comment briefly on Dr. Trusler's paper, which I enjoyed very much. Last year we reported to this Association a collective experience with 20 patients from three different institutions, New York University, University of Pittsburgh, and St. Louis University. Some type of valvuloplasty was performed in all 20 patients, none of whom had a prosthetic replacement. Excellent results were obtained in several, and all were improved, though some continued to have insufficiency. The results presented today by Dr. Trusler are actually even better than those we reported, because he describes only mild insufficiency in most patients. I recently had the pleasure of hearing the experience of Professor Bourakovsky in Russia, who has applied a similar technique in several patients. Another significant report describing a large experience with leaflet reconstruction has recently appeared from Japan. Hence, reports from several' centers confirm the fact that reconstruction can be done in most cases. It is similarly clear that the pathology varies widely and that no one technique will yet work uniformly for all patients. All reports indicate some mild persisting insufficiency or some recurrence. Hence, repair must be individualized for each patient at operation, and the effectiveness of the repair must be carefully measured. Dr. Trusler mentioned an important aspect of technique, which I would like to emphasize. The
403
valve should be repaired first and the aorta closed. Then the repair should be inspected through the ventriculotomy and the ventricular septal defect. If the reverse approach is done, with the ventricular septal defect closed before the valve is repaired, the effectiveness of aortic valvuloplasty cannot be properly judged. I am particularly impressed with Dr. Trusler's method of cusp plication. From our experiences we have felt a plicated area should remain mobile. An earlier technique that failed in several groups involved attachment of the plicated segment to the aortic wall. The method reported today, however, seems to provide more secure fixation. In summary, data from several sources support Dr. Trusler's conclusion that in at least 90 per cent of patients some form of valvuloplasty can be done. Prosthetic replacement should seldom be necessary. DR. TRUSLER (Closing) I want to emphasize the point that Dr. Spencer made about the individuality of the pathology and, therefore, the method of treatment in these patients. Last year at this meeting, he described a technique of treatment that Dr. Weldon uses. It involves very rapid plication at the commissure. This technique should be kept in mind, because if there is still insufficiency when the right ventricle is opened, this technique can be used to adjust the position of the valve very quickly and achieve competence.