Late results after Starr-Edwards valve replacement in children

J

THoRAc CARDIOVASC SURG

88:583-589, 1984

Late results after Starr-Edwards valve replacement in children Selection of types of prosthetic heart valves for children remains controversial. The case histories of 50 children surviving valve replacement with Starr-Edwards prostheses between 1963 and 1978 were reviewed to evaluate the long-term performance of mechanical valves. The 31 boys and 19 girls ranged from 6 months to 18 years in age (mean 10.4 years); 19 patients bad bad aortic valve replacement, 24 patients bad bad mitral valve replacement,and one patient bad bad both. Among the six patients who bad bad tricuspid valve replacement, four bad corrected trampositioo, so that the tricuspid valve was the systemic atrioventricular valve. Mean (± standard deviation) follow-up interval was 7.9 ± 4.9 years (maximum 17 years). For all patients, the 5 year survival rate was 86% ± 6%. At 10 years postoperatively, the survival rate (± standard error) was 90% ± 7% after aortic valve replacement and 76 % ± 8 % after systemic atrioventricular valve replacement. At follow-up, 39 patients were alive, and 38 were in New York Heart Association Class I or II. Of the 11 deaths, four were valve-related. Seven patients bad major (requiring hospitalization) thromboembolic events, and five patients bad minor transient neurological symptOIm suggesting thromboembolism; 50 % of these patients were not taking warfarin (Coumadin) at the time of the thromboembolic event. The incidence of late (>30 days) thromboembolism was 5.3 per 100 patient-years after aortic and 2.0 per 100 patient-years after systemic atrioventricular valve replacement. At 10 years postoperatively, 66% ± 15% of patients who bad bad aortic valve replacement and 91 % ± 6% of those who bad bad systemic atrioventricular valve replacement were free of thromboembolism. The excellent long-term survival, absence of mechanical failure, and relatively low rate of thromboembolism with this prosthesiscontrast with our experience with biological valves, in which41 % of childrenrequired reoperation in 5 years. Currently, mechanical valves, such as the Starr-Edwards prostheses, are our preferred valves for pediatric patients.

Hartzell V. Schaff, M.D., Gordon K. Danielson, M.D., Roberto M. DiDonato, M.D., Francisco J. Puga, M.D., Douglas D. Mair, M.D., and Dwight C. McGoon, M.D., Rochester. Minn.

Recognition of accelerated calcification and degeneration of porcine bioprostheses in children has prompted reevaluation of mechanical cardiac valves.':' Assessment of long-term performance of mechanical valves in the younger age group is difficult because most reports combine data from various prostheses.v" In the present study, we analyzed the late results after valve replacement with the Starr-Edwards silicone rubber ball and bare strut valve in children. Particular attention was From the Section of Thoracic, Cardiovascular, Vascular, and General Surgery and the Division of Pediatric Cardiology, Mayo Clinic and Mayo Foundation, Rochester, Minn. Received for publication Oct. 19, 1983. Accepted for publication Dec. 5, 1983. Address for reprints: Dr. Hartzell V. Schaff, Mayo Clinic, Rochester, Minn. 55905.

given to thromboembolic complications, anticoagulantrelated complications, and the need for reoperation because of somatic growth.

Patients and methods From May 13, 1963, through Aug. 16, 1978, 50 patients 18 years of age or younger had undergone cardiac valve replacement with a Starr-Edwards prosthesis and had been dismissed from the hospital alive. The 19 girls and 31 boys had a mean (± standard deviation) age of 10.4 ± 4.9 years (range 6 months to 18 years) (Fig. 1). Nineteen patients had had just aortic valve replacement, 24 patients had had just mitral valve replacement, and one patient had had both. Among the six patients who had had tricuspid valve replacement, four patients had corrected transposition of the great arteries so that the tricuspid valve was the systemic 583

584

The Journal of Thoracic and Cardiovascular Surgery

Schaff et al.

18

r---------------------,

16

Table n. Concomitant procedures in children undergoing Starr-Edwards valve replacement

14

ci l::

12

til

10

C

.~

iii

n,

Patients (No.)

Procedure

8 6 4

2 0.5-4

5-9

10-14

15-18

Age (yr)

Fig. 1. Age distribution of children undergoing StarrEdwards valve replacement.

Table I. Prior operations in children undergoing Starr-Edwards valve replacement Operation Isolated valvotomy or valvuloplasty Repair of coarctation of aorta Repair of TOF Repair of TGA Pulmonary artery banding for truncus arteriosus Repair of VSD and aortic insufficiency Previous valve replacement

Patients (No.) *

6 6 5 4

4 2

2

Legend: TOF, Tetralogy of Fallot. TGA, Transposition of the great arteries. VSD, Ventricular septal defect. 'Some patients had two or more prior operations.

atrioventricular valve. Twenty-four patients had undergone 29 operations prior to valve replacement (Table I). Six patients had had previous valvotomy or valvuloplasty, and two patients had had previous valve replacement (one aortic homograft and one cloth-covered StarrEdwards valve). During the operation for Starr-Edwards valve replacement, concomitant procedures were necessary in 22 patients (Table 11). Two patients required graft replacement of the ascending aorta because of annuloaortic ectasia, and two patients had pericardial patch enlargement of the aortotomy. The predominant valve lesion was insufficiency in the aortic, mitral, and tricuspid positions (Table III). Sizes of the valves are presented in Table IV. It is notable that 41 of the 51 valves (82%) would be considered of adequate size for adults: 18 of 20 aortic prostheses were size 9A or larger, 18 of 25 mitral prostheses were size 2M or larger, and five of six tricuspid prostheses were size 2M or larger. Anticoagulation with warfarin (Coumadin) to achieve a prothrom-

Repair of truncus arteriosus Graft replacement of ascending aorta Patch enlargement of ascending aorta Excision of subvalvular aortic stenosis VSD closure VSD closure, conduit repair of pulmonary atresia Tricuspid valve annuloplasty Repair of ostium primum ASD Repair of complete atrioventricular canal VSD closure, relief of pulmonary stenosis Replacement of pulmonary artery homograft Mitral valve annuloplasty ASD closure

4 2 2 2 2 2 • 2 I I I I I I

Legend: VSD, Ventricular septal defect. ASD, Atrial septal defect.

Table m. Type of valve dysfunction in children receiving Starr-Edwards prostheses Dysfunction Aortic valve Stenosis Insufficiency Mitral valve Stenosis Insufficiency Mixed Tricuspid valve Insufficiency

Patients (No.) I 19

4

20 I

6

bin time 2 to 2.5 times control was recommended for all but two patients. For these two children, special circumstances prevented regular monitoring of anticoagulation, and warfarin was not used initially. Forty-seven of the 50 patients were in sinus rhythm at the time of dismissal from the hospital. Late postoperative status was assessed by correspondence with parents or referring physicians, by direct patient contact, or by a combination of these. Follow-up encompassed 396 patient-years with a mean interval of 7.9 ± 4.9 years (longest, 17 years). Patients and families were questioned specifically about the occurrence of neurological symptoms including dizziness, transient weakness, and stroke. Any neurological event requiring hospitalization was considered major. Transient neurological episodes for which the patient did not seek medical attention were classified as minor thromboembolic events. Similarly, hemorrhagic complications were termed major when hospitalization and blood transfu-

Volume 88 Number 4 October, 1984

585

Valve replacement in children

Table IV. Sizes ofprostheses in children undergoing Starr-Edwards valve replacement

Size Aortic prosthesis 7A 8A 9A lOA IIA 12A 13A Atrioventricular prosthesis OOM OM 1M 2M 3M 4M

Anulus diameter (mm)

Patients

20 21 23 24 26 27 29

I I 6 4 3 2 3

20 22 26 28 30 32

4 2 2 II

(No.)

100

(ij

>

's ...

:::J

III

8 4

""'J.,

80

Cf.

I

I

T

I

I

I

T

I

I

'r-

60 40

..... All patients

20

0-0 Atrioventricular valve replacement

........ Aortic valve replacement

o

2

3

4

5

6

7

8

9

10

Follow-up (yr)

Fig. 2. Late survival of children after Starr-Edwards valve replacement. Vertical lines indicate one standard error.

(ij

>

's ...

80

:::J

III

sion were required. Gingival bleeding and menometrorrhagia were considered minor bleeding complications.

Ql Ql

60

III

40

.:;: :::J

(5

-

E 20

0-<>

.t:J

Results At the time of last contact, 39 patients were living, and 38 of them were in New York Heart Association (NYHA) Class I or II. Late death in three patients was the result of progressive myocardial failure; all had the preoperative diagnosis of cardiomyopathy in addition to systemic atrioventricular valve insufficiency. Normal function of adequate-sized prostheses was confirmed by postoperative catheterization and autopsy. Postmortem examination did not establish the cause of late, sudden death in two other patients, and their cardiac prostheses were normal at autopsy. Complications of complex congenital heart disease caused late death in two patients. The deaths of four patients were definitely or possibly related to their prosthetic heart valves. One patient who underwent mitral valve replacement in 1965 died 1 month postoperatively because of dehiscence of the prosthesis. Two patients died of neurologic complications. One of these two, a 14-year-old boy who had had adequate anticoagulation but was in atrial fibrillation, died of cerebral embolus and hemorrhagic infarction 16 days postoperatively. The other, a 16-year-old girl, died 10 years after operation as a result of intracerebral hemorrhage. These events were counted both as embolism and as hemorrhagic complications of anticoagulation. In a fourth patient, who had had aortic valve replacement because of infective endocarditis, recurrent or persistent infection necessitated reoperation early

Aortic valve replacement Atrioventricular valve replacement

Ql

?t.

0 0

2

3

4

5

6

7

8

9

10

Follow-up (yr)

Fig. 3. Embolus-free survival after Starr-Edwards valve replacement in children. In the atrioventricular valve group, only patients with systemic atrioventricular valves were analyzed. Vertical lines represent one standard error.

postoperatively. He died of progressive cardiac failure 4 months later, and postmortem examination revealed periprosthetic leak. Survival of the entire cohort was 86% ± 6% at 5 years and 81% ± 6% at 10 years (Fig. 2). The 10 year survival rate was 90% ± 7% after aortic valve replacement and 76% ± 8% after systemic atrioventricular valve replacement. Twelve patients were found to have had thromboembolic episodes, and these were classified as major in seven patients (Table V). As mentioned earlier, fatal stroke occurred in two patients. There were two patients who were dismissed from the hospital without warfarin therapy, and both experienced embolism. Although the number of patients who had thromboembolic complications is too small for statistical analysis, several trends are apparent. First, major thromboembolism occurred most frequently in patients who had had mitral valve replacement, and in four of six patients these major complications occurred early after operation «30 days postoperatively). Three of the six patients were not in

The Journal of Thoracic and Cardiovascular Surgery

5 8 6 Schaff et al.

Table V. Thromboembolism after Starr-Edwards valve replacement in children Valve(s) replaced

Case No. 1* 2* 3 4 5* 6* 7

8t 9t 10 lit 12t

Cardiac rhythm

Therapeutic anticoagulation

Outcome

12 14 14 16

F F F F M M F

Mitral Mitral Mitral Mitral Mitral Mitral Aortic

30 days 10 days 2'/2 yr 6'/2 yr 6 days 16 days 10 yr

Major emboli Sinus Sinus Sinus Ventricular pacemaker Nodal Atrial fibrillation Sinus

No No Yes No No Yes Yes

Residual hemiparesis Recovered Recovered Recovered Residual hemiparesis Death Death

2 13 13 l7 l7

M F M M F

Mitral Aortic Aortic Aortic Aortic and mitral

II yr 6 yr 5Y2 yr 6'/2 yr 6 mo

Minor emboli Sinus Sinus Sinus Sinus Sinus

Yes Yes Unknown Yes No

Recovered Recovered Recovered Recovered Recovered

1

8 8

*Thromboemboli occurring :0:30 days postoperatively were not included in the calculation of linearized rates of thromboembolism or events per 100 patient-years; this follows the guidelines for reporting valve-related complications suggested by Edmunds. is tThese patients had multiple thromboembolic episodes.

sinus rhythm at the time of thromboembolism, and in only two patients was anticoagulation adequate at the time of thromboembolism. There has been only one major late thromboembolic event after isolated mitral valve replacement in children with sinus rhythm and therapeutic anticoagulation. Minor thromboembolic events were noted in five patients. Three of the five had isolated aortic valve replacement, and one had both aortic and mitral valve replacement. None of the minor emboli occurred less than 30 days postoperatively. Interestingly, four of the five patients had recurrent episodes of minor embolism. The overall incidence of late thromboembolism is 5.3 per 100 patient-years after aortic valve replacement and 2.0 per 100 patient-years after systemic atrioventricular valve replacement. (Incidence of late fatal thromboembolism is 0.6 per 100 patient-years after aortic valve replacement; there were no late fatal thromboembolic episodes after mitral valve replacement.) Actuarially determined embolus-free survival (± standard error) after aortic valve replacement is 91% ± 5% at 5 years and 66% ± 15% at 10 years. After systemic atrioventricular valve replacement, embolus-free survival is 95% ± 5% at 5 years and 91% ± 6% at 10 years (Fig 3). Hemorrhagic complications of anticoagulation occurred in seven patients and were classified as major in three. The two patients with fatal intracerebral hemorrhagic infarctions have been described; a third patient had intra-abdominal hemorrhage of unknown origin which necessitated blood transfusion.

Endocarditis developed in two patients. One had undergone aortic valve replacement because of endocarditis of the native valve and had recurrent infection of the prosthetic valve within 1 month postoperatively. He required reoperation with translocation of the aortic valve anulus and coronary artery bypass but died 4 months later of persistent congestive heart failure. One patient had prosthetic valve endocarditis 11 years after mitral valve replacement and was treated successfully with antibiotics. Of the 10 patients with "small" prostheses, four had required reoperation, * One, a 7-year-old boy, had received a size OM Starr-Edwards prosthesis for replacement of a congenitally stenotic mitral valve with a parachute deformity. Ten years postoperatively he had outgrown the prosthesis (body surface area increased from 0.8 to 1.48 m') and underwent successful reoperation for placement of a size 3M Starr-Edwards prosthesis. A second patient was 5 years old (body surface area 0.68 m-) and underwent repair of partial atrioventricular canal defect and mitral valve replacement with a size 1M Starr-Edwards prosthesis. Thirteen years later she noted mild fatigability, and catheterization demonstrated "mitral stenosis" with an end-diastolic gradient of 2 to 5 mm Hg across the prosthesis at rest. With isoproterenol stimulation the gradient increased to 21 mm Hg. At reoperation, a size 4M Starr-Edwards valve was implanted without difficulty. A third patient had repair of partial atrioventricular canal in infancy. Four *The anulus diameters of the Starr-Edwards prostheses are presented in Table IV.

Volume 88 Number 4 October. 1984

months postoperatively (1 year of age), the mitral valve was replaced with a size OOM Starr-Edwards prosthesis. Twelve years later the child was asymptomatic but had growth retardation (body surface area 1.05 m'). Cardiac catheterization documented pulmonary hypertension (60/40 rnm Hg) and a 26 rnm Hg diastolic gradient across the prosthetic valve. She had elective replacement of the size OOM valve with a 25 rnm aortic Bjork-Shiley prosthesis. The fourth patient was 2 years old when he had repair of partial atrioventricular canal and mitral valve replacement with a size 1M Starr-Edwards valve. Seventeen years later the patient (body surface area 1.76 m') had mild fatigability (NYHA Class II) and a transvalvular diastolic gradient of 16 to 20 rnm Hg. The prosthesis was replaced with a 27 rnm Bjork-Shiley mitral valve. Thus all four patients had successful reoperation with insertion of adult-sized prostheses. Sufficient time (6 to 16 years) has elapsed since operation in four of the six remaining children so that outgrowth of the "small" prosthetic valve would be anticipated. Three of these patients are asymptomatic and one has mild exercise limitation (NYHA Class

11).

Discussion Selection of prosthetic heart valves for infants and children requires consideration of several variables that are unique to this age group. First, because young patients are expected to have a long survival, durability of the prosthesis is particularly important. Long-term anticoagulation is a potentially serious liability in pediatric patients. Therapeutic anticoagulation with warfarin can be difficult to maintain in growing children and requires regular medical supervision. In addition, a child's physical activity is difficult to limit, and unavoidable minor trauma may have serious sequelae. Although successful pregnancy is possible in women on long-term anticoagulant therapy, the hazards of fetal loss and malformation are increased, and this may be an important issue for young girls facing prosthetic valve replacement." Finally, somatic growth should be considered. With certain conditions such as chronic mitral insufficiency and aortic insufficiency resulting from annuloaortic ectasia, adult-sized valves can be inserted in children with ease. For infants and children with stenotic lesions, the hemodynamic characteristics of the prosthesis in the small annular sizes become an important issue. The current generation of bioprostheses had great appeal for use in children, primarily because anticoagulation could be avoided for most patients. These valves were used in children in many institutions, and the late results have been uniformly poor. Since 1977 there have

Valve replacement in children

587

been numerous reports of accelerated calcification and degeneration of bioprosthetic valves in children; most of the valves were of the Hancock variety. The mechanism of these failures is unclear but probably is related to calcium metabolism in children.'? Williams and coworkers" found that only 58.5% of children with bioprosthetic valves were free of valve failure 5 years postoperatively. Until techniques for retarding calcification in tissue valves are perfected, bioprostheses probably should not be used in children. This experience with the Starr-Edwards silicone ball prosthesis (mitral model 6120, aortic model 1200/60) spans 15 years, with follow-up as long as 17 years. There have been no mechanical failures, and overall patient survival equals or exceeds that reported with other valves. Direct comparison of these results is difficult, because reviews of other major series of cardiac valve replacements in childhood grouped the various types of prostheses as mechanical or tissue. Careful analysis of available data does suggest that the type of mechanical valve may influence late morbidity and mortality. Shore, de Leval, and Stark" reviewed late results of valve replacement in children and reported a 5 year survival rate of 53% with mechanical valves and 84% with biological valves. Only 59% of children with mechanical valves were free of thromboembolism 5 years postoperatively. The Bjork-Shiley valve was the only mechanical prosthesis used in their patients, and three of six late deaths were the result of valve thrombosis. In one series of adult patients, the actuarial risk of thrombosis of a Bjork-Shiley mitral prosthesis was 13% at 4 years postoperatively. IS There were no episodes of valve thrombosis in this series. Attie and associates" followed 74 children with Starr-Edwards mitral valves for a mean of 6.4 years and encountered only one instance of valve thrombosis. Embolism and other late complications of cardiac valve replacement remain problematic. We have used the definitions suggested by Edmunds 's and have expressed late thromboembolism aetuarially as a function of time and cumulatively as events per 100 patientyears. The overall risk of late thromboembolism after aortic valve replacement seems to be the same for children as for adults. Interestingly, the risk of thromboembolism after mitral valve replacement appears to be substantially less in children than in adults. In our series the incidence was 2.6 per 100 patient-years, and Attie and associates" found an incidence of 1.7 per 100 patient-years. We have no evidence to suggest that therapeutic anticoagulation is better in children than in adults, and, indeed, the opposite is probably true. Perhaps the relatively low incidence of atrial fibrillation

The Journal of Thoracic and Cardiovascular Surgery

5 8 8 Schaff et a1.

in children accounts for some of the difference. The focus of this review is on the follow-up of hospital survivors-i.e., those children who survive the initial 30 days after Starr-Edwards valve replacement. Nevertheless, we have presented the early thromboembolic complications because they have produced significant morbidity in the mitral valve group. Differences in time of occurrence and manifestation of thromboembolism were noted in the mitral and aortic valve groups, and this may be the result of somewhat different mechanisms of thrombosis. Pumphrey, Fuster, and Chesbro" have speculated that fibrin thrombi develop in association with the lower velocity of flow across the mitral valve, whereas thrombi consisting mostly of platelets are the result of high-velocity flow across the aortic prosthesis. In a prospective study in adults by Chesebro and associates," addition of dipyridamole to the warfarin regimen reduced thromboembolic complications of mechanical heart valves significantly. Routine use of dipyridamole (with warfarin) in children has not been established, but antiplatelet therapy seems reasonable, especially for patients who have had suspected thromboembolism, particularly in the aortic valve group. Mechanical valves with the tilting-disc design are generally conceded to have better hemodynamic properties than do prostheses with a ball-and-eage structure," The relative importance of small differences in transvalvular gradients in valves with equivalent anulus size is debatable. For 82% of our patients the size of the Starr-Edwards valve utilized was large enough for adults, and replacement is not anticipated. Children receiving smaller prostheses had stenotic lesions or were less than 6 years old. Initial implantation of a valve with more favorable hemodynamic properties might delay but probably would not eliminate the need for later replacement because of somatic growth. In our experience the smaller sizes of Starr-Edwards valve (OOM and OM) in the atrioventricular position are adequate to permit most patients to reach adolescence, at which time elective replacement with a larger valve can be accomplished. No patient has required multiple subsequent replacements. Friedman, Edmunds, and Cuaso" reported on their experience with mitral valve re-replacement in three children who had undergone initial valve replacement with small (OOM and OM) Starr-Edwards valves. They found functional mitral stenosis with pulmonary hypertension at the time of cardiac catheterization prior to reoperation. Replacement of the small mitral prosthesis did not reduce pulmonary vascular resistance, and the authors cautioned against use of the small Starr-

Edwards valve in the mitral position. However, in two of these patients a different type of prosthesis was inserted at reoperation. One 7-year-old boy received a Hancock valve, and a 13~-year-old boy received a Bjork-Shiley valve. As noted previously, currently available information suggests that the chance of bioprosthesis failure is extremely high, and the Bjork-Shiley valve subsequently had to be replaced because fibrous tissue interfered with the tilting disc mechanism. It seems likely that any prosthetic valve inserted in an infant with congenital mitral stenosis will require replacement as a result of somatic growth. The normal orifice area of the mitral valve in a child 6 to 8 months of age is 1.37 cm 2•24 Thus a prosthetic valve with "ideal" hemodynamic properties might be expected to produce relative mitral stenosis in an adult; the best one might hope to achieve is a single re-replacement as the child develops. Our experience suggests that this strategy is possiblewith the Starr-Edwards valve. For children with stenotic lesions of the aortic valve not amenable to repair, aortic anulus enlargement may allow insertion of an adequate-sized prosthesis.P" If the aortic anulus is 19 mm in diameter or less, use of a tilting disc valve should be considered.27 We gratefully acknowledge the assistance of Peter C. O'Brien, Ph.D., in the statistical analysis and Donna M. Stucky for secretarial assistance.

2

3

4 5

6

7

REFERENCES Brown JW, Dunn JM, Spooner E, Kirsh MM: Late spontaneous disruption of a porcine xenograft mitral valve. Clinical, hemodynamic, echocardiographic, and pathological fmdings. J THORAC CARDIOVASC SURG 75:606-611, 1978 Geha AS, Laks H, Stansel HC Jr, Cornhill JF, Kilman JW, Buckley MJ, Roberts WC: Late failure of porcine valve heterografts in children. J THORAC CARDIOVASC SURG 78:351-361, 1979 Silver MM, Pollock J, Silver MD, Williams WG, Trusler GA: Calcification in porcine xenograft valves in children. Am J Cardiol 45:685-689, 1980 Dunn JM: Porcine valve durability in children. Ann Thorac Surg 32:357-366, 1981 Miller DC, Stinson EB, Oyer PE, Billingham ME, Pitlick PT, Reitz BA, Jamieson SW, Baumgartner WA, Shumway NE: The durability of porcine xenograft valves and conduits in children. Circulation 66:Suppl I:172-185, 1982 Williams DB, Danielson GK, McGoon DC, Puga FJ, Mair DD, Edwards WD: Porcine heterograft valve replacement in children. J THORAC CARDIOVASC SURG 84:446-450, 1982 Odell JA: Calcification of porcine bioprostheses in chil-

Volume 88 Number 4 October, 1984

dren, Cardiac Bioprostheses, Proceedings of the Second International Symposium, LH Cohn, V Gallucci, eds., New York, 1982, Yorke Medical Books, pp 231-237 8 Chen S, Laks H, Fagan L, Terschluse D, Kaiser G, Barner H, Willman VL: Valve replacement in children. Circulation 56:SuppI2:117-121, 1977 9 Gardner TJ, Roland J-M, Neill CA, Donahoo JS: Valve replacement in children. A fifteen-year perspective. J THORAC CARDIOVASC SURG 83: 178-184, 1982 10 Mathews RA, Park SC, Neches WH, Lenox CC, Zuberbuhler JR, Fricker FJ, Siewers RD, Hardesty RL, Lerberg DB, Bahnson HT: Valve replacement in children and adolescents. J THORAC CARDIOVASC SURG 73:872-876, 1977 11 Sade RM, Ballenger JF, Hohn AR, Arrants JE, Riopel DA, Taylor AB: Cardiac valve replacement in children. Comparison of tissue with mechanical prostheses. J THORAC CARDIOVASC SURG 78:123-127, 1979 12 Smith JM III, Cooley DA, Ott DA, Ferreira W, Reul GJ Jr: Aortic valve replacement in preteenage children. Ann Thorac Surg 29:512-518, 1980 13 Wada J, Yokoyama M, Hashimoto A, Imai Y, Kitamura N, Takao A, Momma K: Long-term follow-up of artillcial valves in patients under 15 years old. Ann Thorac Surg 29:519-521,1980 14 Williams WG, Pollock JC, Geiss DM, Trussler GA, Fowler RS: Experience with aortic and mitral valve replacement in children. J THORAC CARDIOVASC SURG 81:326-333, 1981 15 Edmunds LH Jr: Thromboembolic complications of current cardiac valvular prostheses. Ann Thorac Surg 34:96106, 1982 16 Murphy ES, Kloster FE: Late results of valve replacement surgery. II. Complications of prosthetic heart valves. Mod Concepts Cardiovasc Dis 48:59-66, 1979 17 Shore DF, de Leval MR, Stark J: Valve replacement in children. Biologic versus mechanical valves, Cardiac Bioprostheses, Proceedings of the Second International Symposium, LH Cohn, V Gallucci, eds., New York, 1982, Yorke Medical Books, pp 238-247

Valve replacement in children 589

18 Karp RB, Cyrus RJ, Blackstone EH, Kirklin JW, Kouchoukos NT, Pacifico AD: The Bjork-Shiley valve. Intermediate-term follow-up. J THORAC CARDIOVASC SURG 81:602-614, 1981 19 Attie F, Kuri J, Zanoniani C, Renteria V, Buendia A, Ovseyevitz J, Lopez-Soriano F, Garcia-Cornejo M, Martinez-Rios MA: Mitral valve replacement in children with rheumatic heart disease. Circulation 64:812-817, 1981 20 Pumphrey CW, Fuster V, Chesebro JH: Systemic thromboembolism in valvular heart disease and prosthetic heart valves. Mod Concepts Cardiovasc Dis 51:131-136, 1982 21 Chesebro JH, Fuster V, Pumphrey CW, McGoon DC, Pluth JR, Puga FJ, Orszulak TA, Piehler JM, Schaff HV, Danielson GK: Combined warfarin-platelet inhibitor antithrombotic therapy in prosthetic heart valve replacement (abstr). Circulation 64:Suppl 4:76, 1981 22 Olin C: Pulsatile flow studies of prosthetic aortic valves. Scand J Thorac Cardiovasc Surg 5: 1-12, 1971 23 Friedman S, Edmunds LH Jr, Cuaso CC: Long-term mitral valve replacement in young children. Influence of somatic growth on prosthetic valve adequacy. Circulation 57:981-986, 1978 24 Schulz DM, Giordano DA: Hearts of infants and children. Weights and measurements. Arch Pathol 74:464-471, 1962 25 Piehler JM, Danielson GK, Pluth JR, Orszulak TA, Puga FJ, Schaff HV, Edwards WD, Shub C: Enlargement of the aortic root or anulus with autogenous pericardial patch during aortic valve replacement. Long-term follow-up. J THORAC CARDIOVASC SURG 86:350-358, 1983 26 Konno S, Imai Y, Iida Y, Nakajima M, Tatsuno K: A new method for prosthetic valve replacement in congenital aortic stenosis associated with hypoplasia of the aortic valve ring. J THORAC CARDIOVASC SURG 70:909-917, 1975 27 Schaff HV, Borkon AM, Hughes C, Achuff S, Donahoo JS, Gardner TJ, Watkins L Jr, Gott VL, Morrow AG, Brawley RK: Clinical and hemodynamic evaluation of the 19 mm Bjork-Shiley aortic valve prosthesis. Ann Thorac Surg 32:50-57, 1981