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Massive calcification and obstruction in a homograft after the rastelli procedure for transposition of great arteries
Massive Calcification and Obstruction in a Homograft After the Rastelli Procedure for Transposition of Great Arteries
SANG C. PARK, MD WILLIAM H. NECHES, MD CORA C. LENOX, MD, FACC JAMES R. ZUBERBUHLER, MD, FACC HENRY T. BAHNSON, MD, FACC
Pittsburgh, Pennsylvania
In a 9 1 / 2 year old boy with transposition of the great arteries, ventricular septal defect and pulmonic stenosis, massive calcification and obstruction of the homograft developed within 17 months after a Rastelli procedure. The calcified homograft was resected and replaced with a prosthetic graft. The morphologic changes in the resected homograft and the possible mechanism of the calcification are reviewed. An aortic h o m o g r a f t was first used by Gross et al. 1 in 1948 to replace a c o a r c t a t e d s e g m e n t of thoracic aorta. Arterial grafts were widely used in v a s c u l a r surgery in the early 1950's. However, because of difficulty in o b t a i n i n g a sufficient n u m b e r of s u i t a b l e h o m o g r a f t s a n d because of p o t e n t i a l l o n g - t e r m morphologic alterations, t h e y were generally r e p l a c e d by woven s y n t h e t i c m a t e r i a l s when the l a t t e r bec a m e available in 1956. In the last few years aortic h o m o g r a f t s h a v e been r e i n t r o d u c e d for correction of t r u n c u s arteriosus, certain c o m p l i c a t e d forms of transposition of the great arteries a n d p u l m o n a r y a t r e s i a or severe forms of t e t r a l o g y of Fallot. 2-5 In these conditions the aortic h o m o g r a f t functions b o t h as a c o n d u i t a n d as a p u l m o n i c valve. U n f o r t u n a t e l y , the l o n g - t e r m surgical experience with these aortic h o m o g r a f t s seems to be si~nilar to t h a t of h o m o g r a f t s used for v a s c u l a r surgery: T h e wall of the h o m o g r a f t often b e c o m e s calcified within a year. 6-s This report describes a p a t i e n t who h a d m a s s i v e calcification a n d a l m o s t c o m p l e t e o b s t r u c t i o n in a h o m o g r a f t within 17 m o n t h s after operation for t r a n s p o s i t i o n of the great arteries with v e n t r i c u l a r septal defect a n d p u l m o n i c stenosis.
Case Report
From the Departments of Pediatrics and Surgery of the University of Pittsburgh School of Medicine and the Section of Pediatric Cardiology of the Children's Hospital of Pittsburgh, Pittsburgh, Pa. Manuscript accepted February 28, 1973. Address for reprints: Sang C. Park, MD, Section of Pediatric Cardiology, Children's Hospital of Pittsburgh, 125 De Soto St., Pittsburgh, Pa. 15213.
860
November 1973
The patient was born after an uncomplicated full-term pregnancy and weighed 6 lb, 1/2 oz. at birth. Cyanosis and a cardiac murmur were first noted at age 7 months. Cardiac catheterization was performed at age 9 months, and a diagnosis of transposition of the great arteries with ventricular septal defect and pulmonic stenosis was made. The hemodynamic data are summarized in Table I. Although the patient remained moderately cyanotic and had limited exercise tolerance, he did relatively well and had no episodes of congestive heart failure or hypoxic spells. His hemoglobin and hematocrit remained stable at about 18 g/100 ml and 58 percent, respectively. At a second cardiac catheterization performed at age 7 1/2 years (Table I), a large ventricular septal defect was still present. Both infundibular and valvular pulmonic stenosis were found, and a small patent ductus arteriosus and juxtaposition of the atrial appendages were noted. Surgical procedure: Subsequently, at age 8 years, the patient underwent cardiac surgery. The pulmonary annulus was hypoplastic, and there was severe infundibular and valvular stenosis. A Rastelli procedure was performed with use of an aortic homograft.5 The donor of the aortic homograft was a 15 year old Caucasian girl who died of Ewing's sarcoma with pulmonary metastases. Before death she had
The American Journal of CARDIOLOGY
Volume 32
HOMOGRAFT CALCIFICATION AFTER RASTELLI PROCEDURE--PARK ET AL.
TABLE I Cardiac Catheterization Data
November18, 1963 (age 9 mo) Site
Pressure (ram Hg)
Superior vena cava Right atrium Right ventricle Aorta
5/2 60/4 60/30
30 ... 46
Pulmonary vein Left atrium Left ventricle Pulmonary artery
... 5/2 65/5 NE
94 ... ... ...
.
.
02 Saturation (%)
.
.
.
.
July 19, 1972 (postoperative) (age 9 yr, 8 mo)
October8, 1970 (age 7 yr, 8 too)
.
Pressure (mm Hg)
.
02 Saturation (%)
. (m 5) 97/5 97/62 (m 80) . . (m 5) 97/5 20/10 (m 15)
52 53 63 77 .
.
.
. ... 91 82
.
.
Pressure (ram H8)
02 Saturation (%)
...
43 46 48 70
(m 10) 105/5 80/50 (m 63) . . . (m 10) 85/5 105/5"
. 88 74 54*
* In the homograft beyond the homograft valve but proximal to obstruction. m = mean; NE = not entered.
received radiation therapy, corticosteroids and various chemotherapeutic agents including vincris~ine sulfate (Oncovin®), cyclophosphamide (Cytoxan®) and actinomycin D (Dactinomycin-cosmegan®). The graft was obtained at autopsy about 6 hours after death, was deep-frozen at -70 ° C and sterilized by radiation. The interval between harvest of the graft and operation was 78 days. Several difficulties were encountered during operation. After ligation of the patent ductus arteriosus, complete atresia of the left pulmonary artery between the main pulmonary artery and the point where the ductus joined the left pulmonary artery was found. The left pulmonary artery could not be reconstructed and was eventually ligated. The surgical procedure was prolonged, and there was considerable bleeding which was eventually controlled by transfusion of fresh frozen plasma and platelets. The chest wall could not be closed in the usual fashion because of protrusion of the homograft. Transection of the first costochondral junction bilaterally provided enough room to permit chest closure. After a stormy postoperative course, the patient was discharged.
P o s t o p e r a t i v e course: The patient was initially completely asymptomatic and able to participate in all normal activities without difficulty. Eight months after operation he began to reduce his activity and by 13 months his effort tolerance was as limited as before operation. Cyanosis reappeared and increased progressively. By 15 months after operation the hemoglobin and hematocrit had increased to 19.6 g/100 ml and 60 percent, respectively. Seventeen months after operation the patient was hospitalized for reevaluation. A grade 3/6 harsh ejection systolic murmur was heard at the upper left sternal border. The second heart sound was single, and no diastolic murmur was heard. Chest roentogenogram showed a moderately enlarged heart with diffuse calcification in the area of the homograft (Fig. 1); this calcification had first been noticed 9 months postoperatively. The.electrocardiogram disclosed complete right bundle branch block and right ventricular hypertrophy. A third cardiac catheterization was performed (Table I). Right ventricular pressure exceeded left ventricular pressure. Aortic oxygen saturation was 70 percent. Indica-
FIGURE 1. Postoperative chest roentogenograms (posteroanterior and lateral views) showing moderate cardiomegaly. Arrows outline the diffusely calcified homograft.
November 1973
The American Journal of CARDIOLOGY
Volume 32
861
HOMOGRAFT CALCIFICATION AFTER RASTELLI PROCEDURE--PARK ET AL.
FIGURE 2. Selective cineangiogram. A single frame after injection into the homograft (steep right anterior oblique view) showing large irregular filling defects.
tor-dilution curves showed bidirectional shunting at the ventricular level. The pulmonary to systemic flow ratio was 0.83:1. Selective left and right ventricular cineangiograms demonstrated a residual ventricular septal defect with bidirectional shunting. A catheter was advanced into the homograft area beyond the homograft valve but could not be manipulated into the distal pulmonary artery. Multiple cineangiograms in the area of the homograft showed a large irregular area of obstruction beyond the valve extending the entire length of the homograft (Fig. 2). This filling defect occupied more than 80 percent of the entire diameter of the vessel. The wall of the homograft was heavily calcified. Reoperation: Eighteen months after the initial Rastelli procedure the patient was again operated upon. The calcified homograft was totally resected and an 18 mm woven Dacron® prosthesis without a valve was inserted in a similar position. The residual ventricular septal defect was
FIGURE 3. Resected homograft (gross specimen after longitudinal dissection to display intraluminal changes). The left side of specimen was the proximal portion of the graft which had been anastomosed to the right ventricle (see text).
FIGURE 4. Resected homograft (microscopic cross section). There is massive calcium deposition in entire intima and most of media, resulting in severe luminal obliteration.
862
November 1973
The American Journal of CARDIOLOGY
Volume 32
HOMOGRAFT CALCIFICATION AFTER RASTELLI PROCEDURE--PARK ET AL.
closed. The patient did well and was discharged from the hospital 17 days after the operation. Six months postoperatively the patient is completely asymptomatic and free of cyanosis. A grade 3/6 harsh systolic ejection murmur is heard at the high left sternal border, and a grade 2-3/6 diastolic murmur at the mid left sternal border. Chest roentgenograms have shown no significant change in cardiac size. Pathologic findings: The resected homograft specimen measured 2 cm in maximal diameter and 7 1/2 cm in length (Fig. 3). It had a bony consistency except for the most distal portion. The inside of the graft was massively covered with glistening calcific granules to different depths over the entire lumen with a maximal thickness of 13 ram. Only some rudimentary homograft valve tissue was seen; most of the valvular tissue was almost totally distorted by the surrounding massive calcium deposits. Microscopic study (Fig. 4) showed that the entire intima and a large portion of the media were replaced by irregular calcific nodules. Focal mural fibrin thrombi were noted over the inner surface of the nodules. The adventi~ia was thickened with fibrosis and contained areas of vascular proliferation and round cell infiltration.
Discussion The occurrence of calcification in homografts is well known in man 6-1~ and in experimental animals. ~7,1s However, there have been no reports of either severe calcification or obstruction of the homo~ a f t in man, although each has been found in experimental studies in pigs. is At most, calcification in patients consisted of mild degrees of calcific changes either on roentogenographic study or on microscopic examination of the homograft. This is the first reported case of massive calcification and obstruction in the homograft occurring after a Rastelli procedure. The mechanism of calcification of the homograft is not known. Urist and Adams ~9 suggested that calci-
fication is caused by many factors. They emphasized the importance of biochemical derangement and tissue damage in the graft as well as humoral factors in the host. Brock 16 found a greater incidence of calcification in freeze-dried or frozen and irradiated grafts than in fresh grafts. Similarly, the rate of failure and incidence of calcification in aortic valve homografts are significantly higher when the valve graft is prepared by the freeze-irradiation technique than when fresh graft is used. 2°-22 It is possible that the method of preparation of the homograft may be related at least in part to the incidence of subsequent calcification. However, the mechanism for this is not well explained since valve tissue itself is probably not altered by the freeze-irradiation process. 23 Several unusual host and donor factors may explain the rapid and massive calcification of the homograft in our patient. The donor of the graft had been treated with various chemotherapeutic agents, corticosteroids and irradiation before death. The homograft itself was subjected to freezing, further irradiation and more than 2 months of storage. In addition, the patient received massive blood transfusions during and after operation (40 pints of blood). Lastly, large volumes of buffer solutions such as sodium bicarbonate and 1/6 molar T H A M ® were used to correct severe acidosis during the early postoperative period. It is a reasonable assumption that the multiple derangements of the physiologic status in the host in conjunction with the preexisting changes in the graft at the time of operation accelerated the process of calcification and increased the degree of calcium deposition in the homograft in our patient. In retrospect the donor was not ideal. In the future we will use either a fresh homograft from a more suitable donor or a woven Dacron conduit.
References 1. Gross RE, Hurwitt ES, Bill AH Jr, et ah Preliminary observations on the use of human arterial grafts in the treatment of certain cardiovascular defects. N Engl J Med 239:578-579, 1948 2. Ross DN, Somerville J: Correction of pulmonary atresia with a homograft aortic valve. Lancet 2:1446-1447, 1986 3. McGoon DC, Rastelli GC, Ongley PA: An operation for the correction of truncus arteriosus. JAMA 205:69-73, 1968 4. Rastelli GC, McGoon DC, Wallace RB: Anatomic correction of the great arteries with ventricular septal defect and subpulmonary stenosis. J Thorac Cardiovasc Surg 58:545552, 1969 5. Rastelli GC, Wallace RB, Ongley PA: Complete repair of transposition of the great arteries with pulmonic stenosis: a review and report of a case corrected by using a new surgical technique. Circulation 39:83-95, 1969 6. McGoon DC, Rastelli GC, Wallace RB: DiscontinfJity between right ventricle and pulmonary artery: surgical treatment. Ann Surg 172:680-689, 1970 7. Brawley RK, Gardner TJ, Donahoo JS, et ah Late results after right ventricular outflow tract reconstruction with aortic root homografts. J Thorac Cardiovasc Surg 64:314-321, 1972 8. McGoon DC, Wallace RB, Danielson GK: Homografts in reconstruction of congenital cardiac anomalies: expanded
9. 10.
11. 12. 13. 14. 15. 16.
November 1973
operability in .complex congenital heart disease. Mayo Clin Proc 47:101-104, 1972 Gross RE: Discussion of Creech O, DeBakey ME, Self M, et ah The fate of heterologous arterial grafts: an experimental study. Surgery 36:431-444, 1954 Creech D, DeBakey ME, Cooley DA, et ah Structural alterations in human aortic grafts one to two and one half years after transplantation, Surg Gynecol Obstet 103:147154, 1956 Shucksmith HS, Mitchell WM, Zinnemann K: Two and a half years' survival of a grafted aortic aneurysm with histologic studies. Br J Surg 46:141-146, 1958 Pollock AM, Pratt D, Smiddy FG: Aortic homograft replacement: a sequel. Ann Surg 153:472-476, 1961 Shuster SR, Gross RE: Surgery for coarctation of the aorta. A review of 500 cases. J Thorac Cardiovasc Surg 43:54-70, 1962 Foster JH, Collins HA, Jacobs JK, et al: Long term followup of homografts used in the treatment of coarctation of the aorta. J Cardiovasc Surg 6:111-120, 1965 Meade JW, Linton RR, Darling RC, et ah Arterial homografts: a long term clinical follow-up. Arch Surg 93:392399, 1966 Brock L: Long term degenerative changes in aortic segment homografts with particular reference to calcification. Thorax
The American Journal of CARDIOLOGY
Volume 32
863
HOMOGRAFT CALCIFICATION AFTER RASTELLi PROCEDURE--PARK ET AL.
23:249-255, 1968 17. Coleman CC Jr, Deuterling RA Jr, Parshley MS: Some long term observations on aortic hom0gtafts. Surgery 37:64-79, 1955 18. Sauvage LR, Wesolowski SA: The healing and fate of arterial grafts. Surgery 38:1090-1131, 1955 19. Urist MR, Adams JM Jr: Localization mechanism of calcification in transplants of aorta. Ann Surg 166:1-18, 1967 20. Beach PM Jr, Bowman FO Jr, Kaiser GA, et ah Aortic valve replacement with frozen irradiated homografts, long term
864
November 1973
The American Journal of CARDIOLOGY
evaluation. Circulation 45-46: suppl h 29-35, 1972 21. Barratt-Boyes BG, Roche AHG, Brandt PWT, et ah Aortic homograft valve replacement: a long term follow-up of an initial series of 101 patients. Circulation 40:763-775, 1969 22. Barratt-Boyes BG, Roche AHG: A review of aortic valve homograft over a six and one-half year period. Ann Surg 170:483-492, 1969 23. Harris PD, Kovalik ATW, Marks JA, et ah Factors modifying aortic homograft structure and function. Surgery 63:45-51, 1968
Volume 32
SANG C. PARK, MD WILLIAM H. NECHES, MD CORA C. LENOX, MD, FACC JAMES R. ZUBERBUHLER, MD, FACC HENRY T. BAHNSON, MD, FACC
Pittsburgh, Pennsylvania
In a 9 1 / 2 year old boy with transposition of the great arteries, ventricular septal defect and pulmonic stenosis, massive calcification and obstruction of the homograft developed within 17 months after a Rastelli procedure. The calcified homograft was resected and replaced with a prosthetic graft. The morphologic changes in the resected homograft and the possible mechanism of the calcification are reviewed. An aortic h o m o g r a f t was first used by Gross et al. 1 in 1948 to replace a c o a r c t a t e d s e g m e n t of thoracic aorta. Arterial grafts were widely used in v a s c u l a r surgery in the early 1950's. However, because of difficulty in o b t a i n i n g a sufficient n u m b e r of s u i t a b l e h o m o g r a f t s a n d because of p o t e n t i a l l o n g - t e r m morphologic alterations, t h e y were generally r e p l a c e d by woven s y n t h e t i c m a t e r i a l s when the l a t t e r bec a m e available in 1956. In the last few years aortic h o m o g r a f t s h a v e been r e i n t r o d u c e d for correction of t r u n c u s arteriosus, certain c o m p l i c a t e d forms of transposition of the great arteries a n d p u l m o n a r y a t r e s i a or severe forms of t e t r a l o g y of Fallot. 2-5 In these conditions the aortic h o m o g r a f t functions b o t h as a c o n d u i t a n d as a p u l m o n i c valve. U n f o r t u n a t e l y , the l o n g - t e r m surgical experience with these aortic h o m o g r a f t s seems to be si~nilar to t h a t of h o m o g r a f t s used for v a s c u l a r surgery: T h e wall of the h o m o g r a f t often b e c o m e s calcified within a year. 6-s This report describes a p a t i e n t who h a d m a s s i v e calcification a n d a l m o s t c o m p l e t e o b s t r u c t i o n in a h o m o g r a f t within 17 m o n t h s after operation for t r a n s p o s i t i o n of the great arteries with v e n t r i c u l a r septal defect a n d p u l m o n i c stenosis.
Case Report
From the Departments of Pediatrics and Surgery of the University of Pittsburgh School of Medicine and the Section of Pediatric Cardiology of the Children's Hospital of Pittsburgh, Pittsburgh, Pa. Manuscript accepted February 28, 1973. Address for reprints: Sang C. Park, MD, Section of Pediatric Cardiology, Children's Hospital of Pittsburgh, 125 De Soto St., Pittsburgh, Pa. 15213.
860
November 1973
The patient was born after an uncomplicated full-term pregnancy and weighed 6 lb, 1/2 oz. at birth. Cyanosis and a cardiac murmur were first noted at age 7 months. Cardiac catheterization was performed at age 9 months, and a diagnosis of transposition of the great arteries with ventricular septal defect and pulmonic stenosis was made. The hemodynamic data are summarized in Table I. Although the patient remained moderately cyanotic and had limited exercise tolerance, he did relatively well and had no episodes of congestive heart failure or hypoxic spells. His hemoglobin and hematocrit remained stable at about 18 g/100 ml and 58 percent, respectively. At a second cardiac catheterization performed at age 7 1/2 years (Table I), a large ventricular septal defect was still present. Both infundibular and valvular pulmonic stenosis were found, and a small patent ductus arteriosus and juxtaposition of the atrial appendages were noted. Surgical procedure: Subsequently, at age 8 years, the patient underwent cardiac surgery. The pulmonary annulus was hypoplastic, and there was severe infundibular and valvular stenosis. A Rastelli procedure was performed with use of an aortic homograft.5 The donor of the aortic homograft was a 15 year old Caucasian girl who died of Ewing's sarcoma with pulmonary metastases. Before death she had
The American Journal of CARDIOLOGY
Volume 32
HOMOGRAFT CALCIFICATION AFTER RASTELLI PROCEDURE--PARK ET AL.
TABLE I Cardiac Catheterization Data
November18, 1963 (age 9 mo) Site
Pressure (ram Hg)
Superior vena cava Right atrium Right ventricle Aorta
5/2 60/4 60/30
30 ... 46
Pulmonary vein Left atrium Left ventricle Pulmonary artery
... 5/2 65/5 NE
94 ... ... ...
.
.
02 Saturation (%)
.
.
.
.
July 19, 1972 (postoperative) (age 9 yr, 8 mo)
October8, 1970 (age 7 yr, 8 too)
.
Pressure (mm Hg)
.
02 Saturation (%)
. (m 5) 97/5 97/62 (m 80) . . (m 5) 97/5 20/10 (m 15)
52 53 63 77 .
.
.
. ... 91 82
.
.
Pressure (ram H8)
02 Saturation (%)
...
43 46 48 70
(m 10) 105/5 80/50 (m 63) . . . (m 10) 85/5 105/5"
. 88 74 54*
* In the homograft beyond the homograft valve but proximal to obstruction. m = mean; NE = not entered.
received radiation therapy, corticosteroids and various chemotherapeutic agents including vincris~ine sulfate (Oncovin®), cyclophosphamide (Cytoxan®) and actinomycin D (Dactinomycin-cosmegan®). The graft was obtained at autopsy about 6 hours after death, was deep-frozen at -70 ° C and sterilized by radiation. The interval between harvest of the graft and operation was 78 days. Several difficulties were encountered during operation. After ligation of the patent ductus arteriosus, complete atresia of the left pulmonary artery between the main pulmonary artery and the point where the ductus joined the left pulmonary artery was found. The left pulmonary artery could not be reconstructed and was eventually ligated. The surgical procedure was prolonged, and there was considerable bleeding which was eventually controlled by transfusion of fresh frozen plasma and platelets. The chest wall could not be closed in the usual fashion because of protrusion of the homograft. Transection of the first costochondral junction bilaterally provided enough room to permit chest closure. After a stormy postoperative course, the patient was discharged.
P o s t o p e r a t i v e course: The patient was initially completely asymptomatic and able to participate in all normal activities without difficulty. Eight months after operation he began to reduce his activity and by 13 months his effort tolerance was as limited as before operation. Cyanosis reappeared and increased progressively. By 15 months after operation the hemoglobin and hematocrit had increased to 19.6 g/100 ml and 60 percent, respectively. Seventeen months after operation the patient was hospitalized for reevaluation. A grade 3/6 harsh ejection systolic murmur was heard at the upper left sternal border. The second heart sound was single, and no diastolic murmur was heard. Chest roentogenogram showed a moderately enlarged heart with diffuse calcification in the area of the homograft (Fig. 1); this calcification had first been noticed 9 months postoperatively. The.electrocardiogram disclosed complete right bundle branch block and right ventricular hypertrophy. A third cardiac catheterization was performed (Table I). Right ventricular pressure exceeded left ventricular pressure. Aortic oxygen saturation was 70 percent. Indica-
FIGURE 1. Postoperative chest roentogenograms (posteroanterior and lateral views) showing moderate cardiomegaly. Arrows outline the diffusely calcified homograft.
November 1973
The American Journal of CARDIOLOGY
Volume 32
861
HOMOGRAFT CALCIFICATION AFTER RASTELLI PROCEDURE--PARK ET AL.
FIGURE 2. Selective cineangiogram. A single frame after injection into the homograft (steep right anterior oblique view) showing large irregular filling defects.
tor-dilution curves showed bidirectional shunting at the ventricular level. The pulmonary to systemic flow ratio was 0.83:1. Selective left and right ventricular cineangiograms demonstrated a residual ventricular septal defect with bidirectional shunting. A catheter was advanced into the homograft area beyond the homograft valve but could not be manipulated into the distal pulmonary artery. Multiple cineangiograms in the area of the homograft showed a large irregular area of obstruction beyond the valve extending the entire length of the homograft (Fig. 2). This filling defect occupied more than 80 percent of the entire diameter of the vessel. The wall of the homograft was heavily calcified. Reoperation: Eighteen months after the initial Rastelli procedure the patient was again operated upon. The calcified homograft was totally resected and an 18 mm woven Dacron® prosthesis without a valve was inserted in a similar position. The residual ventricular septal defect was
FIGURE 3. Resected homograft (gross specimen after longitudinal dissection to display intraluminal changes). The left side of specimen was the proximal portion of the graft which had been anastomosed to the right ventricle (see text).
FIGURE 4. Resected homograft (microscopic cross section). There is massive calcium deposition in entire intima and most of media, resulting in severe luminal obliteration.
862
November 1973
The American Journal of CARDIOLOGY
Volume 32
HOMOGRAFT CALCIFICATION AFTER RASTELLI PROCEDURE--PARK ET AL.
closed. The patient did well and was discharged from the hospital 17 days after the operation. Six months postoperatively the patient is completely asymptomatic and free of cyanosis. A grade 3/6 harsh systolic ejection murmur is heard at the high left sternal border, and a grade 2-3/6 diastolic murmur at the mid left sternal border. Chest roentgenograms have shown no significant change in cardiac size. Pathologic findings: The resected homograft specimen measured 2 cm in maximal diameter and 7 1/2 cm in length (Fig. 3). It had a bony consistency except for the most distal portion. The inside of the graft was massively covered with glistening calcific granules to different depths over the entire lumen with a maximal thickness of 13 ram. Only some rudimentary homograft valve tissue was seen; most of the valvular tissue was almost totally distorted by the surrounding massive calcium deposits. Microscopic study (Fig. 4) showed that the entire intima and a large portion of the media were replaced by irregular calcific nodules. Focal mural fibrin thrombi were noted over the inner surface of the nodules. The adventi~ia was thickened with fibrosis and contained areas of vascular proliferation and round cell infiltration.
Discussion The occurrence of calcification in homografts is well known in man 6-1~ and in experimental animals. ~7,1s However, there have been no reports of either severe calcification or obstruction of the homo~ a f t in man, although each has been found in experimental studies in pigs. is At most, calcification in patients consisted of mild degrees of calcific changes either on roentogenographic study or on microscopic examination of the homograft. This is the first reported case of massive calcification and obstruction in the homograft occurring after a Rastelli procedure. The mechanism of calcification of the homograft is not known. Urist and Adams ~9 suggested that calci-
fication is caused by many factors. They emphasized the importance of biochemical derangement and tissue damage in the graft as well as humoral factors in the host. Brock 16 found a greater incidence of calcification in freeze-dried or frozen and irradiated grafts than in fresh grafts. Similarly, the rate of failure and incidence of calcification in aortic valve homografts are significantly higher when the valve graft is prepared by the freeze-irradiation technique than when fresh graft is used. 2°-22 It is possible that the method of preparation of the homograft may be related at least in part to the incidence of subsequent calcification. However, the mechanism for this is not well explained since valve tissue itself is probably not altered by the freeze-irradiation process. 23 Several unusual host and donor factors may explain the rapid and massive calcification of the homograft in our patient. The donor of the graft had been treated with various chemotherapeutic agents, corticosteroids and irradiation before death. The homograft itself was subjected to freezing, further irradiation and more than 2 months of storage. In addition, the patient received massive blood transfusions during and after operation (40 pints of blood). Lastly, large volumes of buffer solutions such as sodium bicarbonate and 1/6 molar T H A M ® were used to correct severe acidosis during the early postoperative period. It is a reasonable assumption that the multiple derangements of the physiologic status in the host in conjunction with the preexisting changes in the graft at the time of operation accelerated the process of calcification and increased the degree of calcium deposition in the homograft in our patient. In retrospect the donor was not ideal. In the future we will use either a fresh homograft from a more suitable donor or a woven Dacron conduit.
References 1. Gross RE, Hurwitt ES, Bill AH Jr, et ah Preliminary observations on the use of human arterial grafts in the treatment of certain cardiovascular defects. N Engl J Med 239:578-579, 1948 2. Ross DN, Somerville J: Correction of pulmonary atresia with a homograft aortic valve. Lancet 2:1446-1447, 1986 3. McGoon DC, Rastelli GC, Ongley PA: An operation for the correction of truncus arteriosus. JAMA 205:69-73, 1968 4. Rastelli GC, McGoon DC, Wallace RB: Anatomic correction of the great arteries with ventricular septal defect and subpulmonary stenosis. J Thorac Cardiovasc Surg 58:545552, 1969 5. Rastelli GC, Wallace RB, Ongley PA: Complete repair of transposition of the great arteries with pulmonic stenosis: a review and report of a case corrected by using a new surgical technique. Circulation 39:83-95, 1969 6. McGoon DC, Rastelli GC, Wallace RB: DiscontinfJity between right ventricle and pulmonary artery: surgical treatment. Ann Surg 172:680-689, 1970 7. Brawley RK, Gardner TJ, Donahoo JS, et ah Late results after right ventricular outflow tract reconstruction with aortic root homografts. J Thorac Cardiovasc Surg 64:314-321, 1972 8. McGoon DC, Wallace RB, Danielson GK: Homografts in reconstruction of congenital cardiac anomalies: expanded
9. 10.
11. 12. 13. 14. 15. 16.
November 1973
operability in .complex congenital heart disease. Mayo Clin Proc 47:101-104, 1972 Gross RE: Discussion of Creech O, DeBakey ME, Self M, et ah The fate of heterologous arterial grafts: an experimental study. Surgery 36:431-444, 1954 Creech D, DeBakey ME, Cooley DA, et ah Structural alterations in human aortic grafts one to two and one half years after transplantation, Surg Gynecol Obstet 103:147154, 1956 Shucksmith HS, Mitchell WM, Zinnemann K: Two and a half years' survival of a grafted aortic aneurysm with histologic studies. Br J Surg 46:141-146, 1958 Pollock AM, Pratt D, Smiddy FG: Aortic homograft replacement: a sequel. Ann Surg 153:472-476, 1961 Shuster SR, Gross RE: Surgery for coarctation of the aorta. A review of 500 cases. J Thorac Cardiovasc Surg 43:54-70, 1962 Foster JH, Collins HA, Jacobs JK, et al: Long term followup of homografts used in the treatment of coarctation of the aorta. J Cardiovasc Surg 6:111-120, 1965 Meade JW, Linton RR, Darling RC, et ah Arterial homografts: a long term clinical follow-up. Arch Surg 93:392399, 1966 Brock L: Long term degenerative changes in aortic segment homografts with particular reference to calcification. Thorax
The American Journal of CARDIOLOGY
Volume 32
863
HOMOGRAFT CALCIFICATION AFTER RASTELLi PROCEDURE--PARK ET AL.
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evaluation. Circulation 45-46: suppl h 29-35, 1972 21. Barratt-Boyes BG, Roche AHG, Brandt PWT, et ah Aortic homograft valve replacement: a long term follow-up of an initial series of 101 patients. Circulation 40:763-775, 1969 22. Barratt-Boyes BG, Roche AHG: A review of aortic valve homograft over a six and one-half year period. Ann Surg 170:483-492, 1969 23. Harris PD, Kovalik ATW, Marks JA, et ah Factors modifying aortic homograft structure and function. Surgery 63:45-51, 1968
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