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Pulmonary valve replacement
Pulmonary valve replacement Report of an operation performed for calcific pulmonic stenosis associated with total anomalous pulmonary venous drainage and atrial septal defect Calcification of the pulmonic valve is an uncommon lesion that is usually associated with other congenital cardiac defects. Prior attempts at valvotomy or partial excision of the pulmonic valve have carried a high mortality rate. Pulmonary valve replacement itself is an equally uncommon surgical procedure and, in the past, has been performed only during reconstruction of the right ventricular outflow tract, when the pulmonic valve itself had to be utilized as an aortic prosthesis, and in one patient in whom pulmonary regurgitation following valvotomy was not well tolerated. A case of calcific pulmonic stenosis in association with an atrial septal defect and total anomalous pulmonary venous drainage is reported. The patient was treated successfully by pulmonary valve replacement with a Hancock stented porcine xenograft aortic prosthesis in association with correction of the other congenital cardiac lesions. Cary W. Akins, M . D . , * Mortimer J. Buckley, M.D.,** J. Gordon Scannell, M.D.,*** and W. Gerald Austen, M.D.,**** Boston, Mass.
O ince Sosman 23 described the first case of a calcified pulmonary valve in 1943, thirty-one cases of this lesion have been reported. In 1963, Northway and Abrams, 16 in their summary of the number of cases of pulmonary valve calcification to that date, described the first patient who was operated upon for this entity. Since then, nine more patients have been reported to have undergone either valvotomy or partial excision of the pulmonic valve for treatment for calcific pulmonic stenosis. The purpose of this paper is to report the first case of From Massachusetts General Hospital and Harvard Medical School, Boston, Mass. Received for publication Sept. 29, 1975. Accepted for publication Nov. 4, 1975. Address for reprints: Mortimer J. Buckley, M.D., Department of Surgery, Massachusetts General Hospital, Boston, Mass. 02114. *Chief Resident, Department of Cardiovascular Surgery, Massachusetts General Hospital. **Chief, Clinical Section, Cardiac Surgical Unit, Massachusetts General Hospital; Associate Professor of Surgery, Harvard Medical School. ***Clinical Professor of Surgery, Harvard Medical School; Visiting Surgeon, Massachusetts General Hospital. ****Edward D. Churchill Professor of Surgery, Harvard Medical School; Chief of the Surgical Services, Massachusetts General Hospital.
calcific pulmonic stenosis managed by pulmonary valve replacement with a Hancock stented porcine xenograft aortic valve. Case report E. H., a 52-year-old white man, was first admitted to the Massachusetts General Hospital in March, 1975, for cardiac catheterization. The patient had been the product of a normal pregnancy, and a heart murmur had first been noted at the age of 2 years. Because of the heart murmur, his activity was restricted during his school years. The time of onset of cyanosis is unclear, but the patient was first aware of being cyanotic while swimming at the age of 22 years. He did, however, lead a normal life except for refraining from sports and heavy work. Three months prior to his admission to the Massachusetts General Hospital he noted the sudden onset of aphasia and transient right-sided weakness. The motor deficit resolved entirely over the course of several days, but he was left with residual moderate expressive aphasia. Because of his obvious cyanosis, abnormal chest x-ray findings and decreasing exercise tolerance, cardiac catheterization was suggested. Upon admission to the Massachusetts General Hospital, physical examination revealed a plethoric, middle-aged gentleman with cyanosis and clubbing of the fingers and toes. Blood pressure was 110/70 mm. Hg, pulse rate was 72 beats per minute, and respirations were 16 breaths per minute. There was an increased A wave in the jugular venous pulse and carotid pulsations were normal. The lungs were clear, and cardiac examination revealed a faint left ventricular
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The Journal of Thoracic and Cardiovascular Surgery
Fig. 1A. Preoperative posteroanterior and lateral chest x-ray films showing mild cardiomegaly, diffusely enlarged pulmonary arteries, calcified pulmonic valve and enlarged superior vena cava and ascending left-sided vein. impulse with a mildly sustained right ventricular heave at the left sternal border. The first heart sound was normal and the second heart sound was single. A right ventricular S3 gallop and loud right ventricular S4 gallop were audible. There was a Grade 3/6 harsh holosystolic murmur heard best in the left second intercostal space at the sternal margin and radiating into the left infraclavicular area. The electrocardiogram revealed normal sinus rhythm with an axis of +135 degrees. There was right atrial enlargement and right ventricular hypertrophy. Chest roentgenography revealed left ventricular enlargement with diffusely enlarged pulmonary arteries and a heavily calcified pulmonic valve (Fig. 1). The aortic arch was left sided, and there was a large vascular structure arising at the level of the left pulmonary hilum and coursing cephalad and lateral to the aorta on the left. The superior vena cava was dilated. Cardiac catheterization demonstrated a mean right atrial pressure of 3 mm. Hg and also a mean left atrial pressure of 3 mm. Hg, which was measured across a large atrial septal defect. The pressure in the right ventricular body and infundibulum was 125/15 mm. Hg, while the pulmonary artery pressure was 20/5 mm. Hg. The left ventricular pressure was 125/12 mm. Hg. Right ventricular angiogram demonstrated severe calcific pulmonic stenosis and a supracardiac type of total anomalous pulmonary venous drainage. There was a common pulmonary vein behind the left atrium which drained into the vertical ascending vein on the left side and then into the innominate vein and superior vena cava. At operation on April 25, 1975, a markedly enlarged left innominate vein was observed to drain into an extremely large superior vena cava. The right ventricle and right atrium were also considerably enlarged. There were scattered areas
of myocardial fibrosis throughout the wall of the right ventricle, indicative of probable previous myocardial ischemia. An extremely calcified pulmonic valve with a prominent thrill of pulmonic stenosis was palpable through the pulmonary artery. The pulmonary veins drained into a common channel behind the pericardium. This channel then emptied into an anterior left-sided ascending vein which drained into the left innominate vein. The patient was placed on cardiopulmonary bypass and cooled to 28° C. with local cardiac cooling with 4° C. Ringer's lactate solution. The right atrium was opened to reveal a 3 by 6 cm. atrial septal defect through which a normal mitral valve could be seen. The common pulmonary venous trunk behind the pericardium was then isolated between tourniquets, and an anastomosis was performed in a side-to-side fashion with the posterior wall of the left atrium. The atrial septal defect was then closed with a Dacron patch. The pulmonary artery was opened vertically to reveal a severely scarred pulmonic valve with the leaflets totally replaced by calcification, so that the central orifice was very small. The valve was excised leaving a pliable annulus, and a No. 23 Hancock stented porcine xenograft valve prosthesis was sewn into position. In order for this size prosthesis to be properly seated, the annulus was divided and expanded with a diamond-shaped gusset of pericardium backed with Teflon felt. The ascending venous channel on the left was then ligated. The patient was weaned from cardiopulmonary bypass without difficulty. One notable fact is that although the pulmonary annulus had been enlarged with the gusset of pericardium and Teflon felt to accommodate the Hancock prosthesis, there was a persistent 20 mm. Hg gradient across the pulmonary valve after the procedure, with a pulmonary
Volume 71 Number 5 May, 1976
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Fig. IB. Postoperative posteroanterior and lateral chest x-rayfilmsshowing Hancock valve in place, with some decrease in the size of the left-sided ascending vein. artery pressure of 20/5 mm. Hg and a right ventricular pressure of 40/7 mm. Hg. The patient's entire postoperative course was benign, and he is doing well 5 months postoperatively. Discussion Though Gabriele and Scatliff9 implied in their paper in 1970 that calcification of the congenitally stenotic pulmonary valve was more common than had previously been thought, only 32 cases, including the one reported in this paper, have been reported to date. The first reported case was by Sosman23 in 1943. He mentioned a case of calcification of the pulmonary valve which was recognized at autopsy. By 1953, when Rawson17 reported calcification of the pulmonary valve recognized by roentgenography, there had been 4 cases of this lesion reported in the literature. North way and Abrams16 in 1963 described the first case of a patient with calcific pulmonic stenosis undergoing operative correction with valvotomy. In the following years Mirowski,15 Dinsmore,5' 6 Roberts,18 Hardy,12 and Rodriguez19 described 9 more cases of calcific pulmonic stenosis with attempted operative correction. Of the 19 patients in whom sufficient evidence is available, 15 had associated congenital defects, including atrial septal defect, ventricular septal defect, tetralogy of Fallot, corrected transposition of the great vessels, and, in the patient reported in this paper, atrial septal defect in association with total anomalous pulmonary venous drainage.
The etiology of calcification of the pulmonic valve is uncertain, although several possible explanations have been offered: injury-related changes in the pH of the soft tissues sufficient to precipitate calcium out of plasma,16 inflammation and subsequent deformity, past endocarditis,5' 6 and age. However, Mirowski and associates15 reported calcification in the pulmonary valve of an 11-year-old girl. Partial calcification was confirmed at operation, and the valve was completely calcified 11 years later at reoperation. The high incidence of associated congenital cardiac lesions with calcific pulmonary stenosis is unclear. The high mortality rate associated with attempts at surgical correction of calcific pulmonic stenosis is notable. Of the 5 patients who survived surgical correction of calcific pulmonic stenosis, 4 underwent valvotomy and one underwent partial excision of the pulmonary valve. Of the 5 patients who have died either intraoperatively or very soon postoperatively, 3 underwent valvotomy; in 2 the nature of the exact operative procedure was not described. One factor may be the development of right ventricular failure after the creation of pulmonic regurgitation. Though Talbert and co-workers24 reported that pulmonary regurgitation may be well tolerated, Austen and associates1 experimentally showed by partial or total excision of the pulmonary valve in dogs that "severe regurgitation, caused by excision or immobilization of one or more valve leaflets, is apt to result in
724
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more significant impairment of effective function of the ventricle." Indeed, the first pulmonary valve replacement reported by Fuller and co-workers 8 in 1966 was performed because their patient's clinical condition deteriorated in association with right ventricular failure after pulmonary valvotomy. Ross and Somerville 22 in 1971 also demonstrated that pulmonary regurgitation is not well tolerated in patients in whom the fascia lata reconstruction of the right ventricular outflow tract gradually degenerates. Pulmonary valve replacement itself is a very uncommon surgical procedure, with only 22 cases reported in the literature to date. In 1966 Fuller 8 first described the replacement of a pulmonic valve with a homograft pulmonic valve in a patient who did not tolerate pulmonary valvotomy. In the same year Ross and Somerville 21 described the use of a homograft aortic valve for replacement of the pulmonary valve in a case of pulmonary atresia. The largest series of pulmonary valve replacement is included in an article by Trusler and associates, 25 who reported eleven pulmonic valve replacements, eight with homograft aortic valves, two with stented pericardial valves, and one with a stented fascia lata valve. These were all performed in children with various types of congenital heart disease. In 1971 Ross and Somerville 22 reported on 9 more patients who had undergone pulmonary valve replacement; 2 had pulmonary atresia, and in the remaining 7 patients the pulmonary valve was utilized to replace the aortic valve. The replacement of the pulmonary valve for pulmonic stenosis, particularly of the calcific type, has never been previously reported. In the case reported in this paper it was obvious at the time of surgery that debridement or valvotomy of this totally calcified pulmonic valve was technically impossible. We decided to replace the pulmonic valve because, preoperatively, the patient had manifested signs of right ventricular failure and also because of the evidence of probable prior right ventricular myocardial ischemia as manifested by the fibrosis scattered throughout the wall of the right ventricle. Total replacement with an aortic homograft or valve-bearing conduit was thought unnecessary because of the normal pulmonary artery and infundibulum. The small residual pressure gradient across the prosthesis after bypass was thought to be acceptable, and the patient's subsequent clinical course has been gratifying. REFERENCES 1 Austen, W. G., Greenfield, L. J., Ebert, P. A., and Morrow, A. G.: Experimental Study of Right Ventricular Function After Surgical Procedures Involving the Right
The Journal of Thoracic and Cardiovascular Surgery
Ventricle and Pulmonic Valve, Ann. Surg. 155: 606, 1962. 2 Barrett, D. W.: Simple Pulmonary Stenosis, Br. Heart J. 16: 381, 1954. 3 Brock, R. C : Congenital Pulmonary Stenosis, Am. J. Med. 12: 706, 1952. 4 Bouvrain, Y., and Bescol-Liversac, J.: Etude anatomique, radiologique et histologique des calcifications cardiaques orificielles, Arch. Mai. Coeur 43: 289, 1950. 5 Dinsmore, R. E., Sanders, C. A., Harthorne, J. W., and Austen, W. G.: Calcification of the Congenitally Stenotic Pulmonary Valve, N. Engl. J. Med. 275: 99, 1966. 6 Dinsmore, R. E., Sanders, C. A., Harthorne, J. W., and Austen, W. G.: Congenital Pulmonary Stenosis With Calcification, Radiology 87: 429, 1966. 7 Duke, M.: Severe Pulmonic Stenosis in Late Adult Life: Report of Two Cases, Chest 51: 320, 1967. 8 Fuller, D. M., Marchand, P., Zion, M. M., andZwi, S.: Homograft Replacement of the Pulmonary Valve, Thorax 21: 337, 1966. 9 Gabriele, O. F., and Scatliff, J. M.: Pulmonary Valve Calcification, Am. Heart J. 80: 299, 1970. 10 Genovese, P. D., and Rosenbaum, D.: Pulmonary Stenosis With Survival to the Age of 78 Years, Am. Heart J. 41: 755, 1951. 11 Gerachi, J. L., Burchell, M. B., and Edwards, J. E.: Congenital Pulmonary Stenosis With Intact Ventricular Septum in Persons More than 50 Years Old, Mayo Clin. Proc. 28: 346, 1953. 12 Hardy, W. E., Gnoj, J., and Ayres, S. M.: Pulmonic Stenosis in Associated Atrial Septal Defects in Older Patients, Am. J. Cardiol. 24: 130, 1969. 13 Holmes, R. B.: Calcifications of the Heart, J. Can. Assoc. Radiol. 15: 163, 1964. 14 McGinnis, K. D., Byler, W. R., and Alverez, H.: Cardiac Laminagraphy, Radiology 77: 553, 1961. 15 Mirowski, M., Mehrizi, A., and Shah, K. D.: Right Ventricular Aneurysm. A Complication of Transventricular Pulmonary Valvulotomy: Report of Two Cases, One Associated with Gonadal Agenesis, Am. Heart J. 68: 799, 1964. 16 Northway, W. H., and Abrams, H. L.: Calcific Pulmonic Stenosis, Am. J. Roentgenol. Radium Ther. Nucl. Med. 89: 323, 1963. 17 Rawson, F. L., Jr., and Doerner, A. A.: Functional Cor Triloculare, Am. Heart J. 46: 779, 1953. 18 Roberts, W. C , Mason, D. T., Morrow, A. G., and Braunwald, E.: Calcific Pulmonic Stenosis, Circulation 37: 973, 1968. 19 Rodriguez, G. R., Bennett, K. R., and Lehan, P. H.: Calcification of the Pulmonary Valve, Chest 59: 160, 1971. 20 Rogers, J. V., Chandler, M. W., and Branch, R. H.: Calcification of the Tricuspid Annulus, Am. J. Roentgenol. Radium Ther. Nucl. Med. 106: 550, 1969.
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21 Ross, D. N., and Somerville, J.: Correction of Pulmonary Atresia With a Homograft Aortic Valve, Lancet 2: 1446, 1966. 22 Ross, D. N., and Somerville, J.: Fascia-lata Reconstruction of the Right Ventricular Outflow Tract, Lancet 1: 941, 1971. 23 Sosman, M. C : Technique for Locating and Identifying Pericardial and Intracardiac Calcifications, Am. J.
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Roentgenol. Radium Ther. Nucl. Med. 50: 641, 1943. 24 Talbert, J. L., Morrow, A. G., Collins, N. P., and Gilbert, J.: The Incidence and Significance of Pulmonic Regurgitation After Pulmonary Valvulotomy, Am. Heart J. 65: 590, 1963. 25 Trusler, G. A., Iyengar, S. R., and Mustard, W. T.: Reconstruction of the Pulmonary Valve and Outflow Tract, J. THORAC. CARDIOVASC. SURG. 65: 245,
1973.
O ince Sosman 23 described the first case of a calcified pulmonary valve in 1943, thirty-one cases of this lesion have been reported. In 1963, Northway and Abrams, 16 in their summary of the number of cases of pulmonary valve calcification to that date, described the first patient who was operated upon for this entity. Since then, nine more patients have been reported to have undergone either valvotomy or partial excision of the pulmonic valve for treatment for calcific pulmonic stenosis. The purpose of this paper is to report the first case of From Massachusetts General Hospital and Harvard Medical School, Boston, Mass. Received for publication Sept. 29, 1975. Accepted for publication Nov. 4, 1975. Address for reprints: Mortimer J. Buckley, M.D., Department of Surgery, Massachusetts General Hospital, Boston, Mass. 02114. *Chief Resident, Department of Cardiovascular Surgery, Massachusetts General Hospital. **Chief, Clinical Section, Cardiac Surgical Unit, Massachusetts General Hospital; Associate Professor of Surgery, Harvard Medical School. ***Clinical Professor of Surgery, Harvard Medical School; Visiting Surgeon, Massachusetts General Hospital. ****Edward D. Churchill Professor of Surgery, Harvard Medical School; Chief of the Surgical Services, Massachusetts General Hospital.
calcific pulmonic stenosis managed by pulmonary valve replacement with a Hancock stented porcine xenograft aortic valve. Case report E. H., a 52-year-old white man, was first admitted to the Massachusetts General Hospital in March, 1975, for cardiac catheterization. The patient had been the product of a normal pregnancy, and a heart murmur had first been noted at the age of 2 years. Because of the heart murmur, his activity was restricted during his school years. The time of onset of cyanosis is unclear, but the patient was first aware of being cyanotic while swimming at the age of 22 years. He did, however, lead a normal life except for refraining from sports and heavy work. Three months prior to his admission to the Massachusetts General Hospital he noted the sudden onset of aphasia and transient right-sided weakness. The motor deficit resolved entirely over the course of several days, but he was left with residual moderate expressive aphasia. Because of his obvious cyanosis, abnormal chest x-ray findings and decreasing exercise tolerance, cardiac catheterization was suggested. Upon admission to the Massachusetts General Hospital, physical examination revealed a plethoric, middle-aged gentleman with cyanosis and clubbing of the fingers and toes. Blood pressure was 110/70 mm. Hg, pulse rate was 72 beats per minute, and respirations were 16 breaths per minute. There was an increased A wave in the jugular venous pulse and carotid pulsations were normal. The lungs were clear, and cardiac examination revealed a faint left ventricular
721
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Akins et al.
The Journal of Thoracic and Cardiovascular Surgery
Fig. 1A. Preoperative posteroanterior and lateral chest x-ray films showing mild cardiomegaly, diffusely enlarged pulmonary arteries, calcified pulmonic valve and enlarged superior vena cava and ascending left-sided vein. impulse with a mildly sustained right ventricular heave at the left sternal border. The first heart sound was normal and the second heart sound was single. A right ventricular S3 gallop and loud right ventricular S4 gallop were audible. There was a Grade 3/6 harsh holosystolic murmur heard best in the left second intercostal space at the sternal margin and radiating into the left infraclavicular area. The electrocardiogram revealed normal sinus rhythm with an axis of +135 degrees. There was right atrial enlargement and right ventricular hypertrophy. Chest roentgenography revealed left ventricular enlargement with diffusely enlarged pulmonary arteries and a heavily calcified pulmonic valve (Fig. 1). The aortic arch was left sided, and there was a large vascular structure arising at the level of the left pulmonary hilum and coursing cephalad and lateral to the aorta on the left. The superior vena cava was dilated. Cardiac catheterization demonstrated a mean right atrial pressure of 3 mm. Hg and also a mean left atrial pressure of 3 mm. Hg, which was measured across a large atrial septal defect. The pressure in the right ventricular body and infundibulum was 125/15 mm. Hg, while the pulmonary artery pressure was 20/5 mm. Hg. The left ventricular pressure was 125/12 mm. Hg. Right ventricular angiogram demonstrated severe calcific pulmonic stenosis and a supracardiac type of total anomalous pulmonary venous drainage. There was a common pulmonary vein behind the left atrium which drained into the vertical ascending vein on the left side and then into the innominate vein and superior vena cava. At operation on April 25, 1975, a markedly enlarged left innominate vein was observed to drain into an extremely large superior vena cava. The right ventricle and right atrium were also considerably enlarged. There were scattered areas
of myocardial fibrosis throughout the wall of the right ventricle, indicative of probable previous myocardial ischemia. An extremely calcified pulmonic valve with a prominent thrill of pulmonic stenosis was palpable through the pulmonary artery. The pulmonary veins drained into a common channel behind the pericardium. This channel then emptied into an anterior left-sided ascending vein which drained into the left innominate vein. The patient was placed on cardiopulmonary bypass and cooled to 28° C. with local cardiac cooling with 4° C. Ringer's lactate solution. The right atrium was opened to reveal a 3 by 6 cm. atrial septal defect through which a normal mitral valve could be seen. The common pulmonary venous trunk behind the pericardium was then isolated between tourniquets, and an anastomosis was performed in a side-to-side fashion with the posterior wall of the left atrium. The atrial septal defect was then closed with a Dacron patch. The pulmonary artery was opened vertically to reveal a severely scarred pulmonic valve with the leaflets totally replaced by calcification, so that the central orifice was very small. The valve was excised leaving a pliable annulus, and a No. 23 Hancock stented porcine xenograft valve prosthesis was sewn into position. In order for this size prosthesis to be properly seated, the annulus was divided and expanded with a diamond-shaped gusset of pericardium backed with Teflon felt. The ascending venous channel on the left was then ligated. The patient was weaned from cardiopulmonary bypass without difficulty. One notable fact is that although the pulmonary annulus had been enlarged with the gusset of pericardium and Teflon felt to accommodate the Hancock prosthesis, there was a persistent 20 mm. Hg gradient across the pulmonary valve after the procedure, with a pulmonary
Volume 71 Number 5 May, 1976
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723
Fig. IB. Postoperative posteroanterior and lateral chest x-rayfilmsshowing Hancock valve in place, with some decrease in the size of the left-sided ascending vein. artery pressure of 20/5 mm. Hg and a right ventricular pressure of 40/7 mm. Hg. The patient's entire postoperative course was benign, and he is doing well 5 months postoperatively. Discussion Though Gabriele and Scatliff9 implied in their paper in 1970 that calcification of the congenitally stenotic pulmonary valve was more common than had previously been thought, only 32 cases, including the one reported in this paper, have been reported to date. The first reported case was by Sosman23 in 1943. He mentioned a case of calcification of the pulmonary valve which was recognized at autopsy. By 1953, when Rawson17 reported calcification of the pulmonary valve recognized by roentgenography, there had been 4 cases of this lesion reported in the literature. North way and Abrams16 in 1963 described the first case of a patient with calcific pulmonic stenosis undergoing operative correction with valvotomy. In the following years Mirowski,15 Dinsmore,5' 6 Roberts,18 Hardy,12 and Rodriguez19 described 9 more cases of calcific pulmonic stenosis with attempted operative correction. Of the 19 patients in whom sufficient evidence is available, 15 had associated congenital defects, including atrial septal defect, ventricular septal defect, tetralogy of Fallot, corrected transposition of the great vessels, and, in the patient reported in this paper, atrial septal defect in association with total anomalous pulmonary venous drainage.
The etiology of calcification of the pulmonic valve is uncertain, although several possible explanations have been offered: injury-related changes in the pH of the soft tissues sufficient to precipitate calcium out of plasma,16 inflammation and subsequent deformity, past endocarditis,5' 6 and age. However, Mirowski and associates15 reported calcification in the pulmonary valve of an 11-year-old girl. Partial calcification was confirmed at operation, and the valve was completely calcified 11 years later at reoperation. The high incidence of associated congenital cardiac lesions with calcific pulmonary stenosis is unclear. The high mortality rate associated with attempts at surgical correction of calcific pulmonic stenosis is notable. Of the 5 patients who survived surgical correction of calcific pulmonic stenosis, 4 underwent valvotomy and one underwent partial excision of the pulmonary valve. Of the 5 patients who have died either intraoperatively or very soon postoperatively, 3 underwent valvotomy; in 2 the nature of the exact operative procedure was not described. One factor may be the development of right ventricular failure after the creation of pulmonic regurgitation. Though Talbert and co-workers24 reported that pulmonary regurgitation may be well tolerated, Austen and associates1 experimentally showed by partial or total excision of the pulmonary valve in dogs that "severe regurgitation, caused by excision or immobilization of one or more valve leaflets, is apt to result in
724
Akins et al.
more significant impairment of effective function of the ventricle." Indeed, the first pulmonary valve replacement reported by Fuller and co-workers 8 in 1966 was performed because their patient's clinical condition deteriorated in association with right ventricular failure after pulmonary valvotomy. Ross and Somerville 22 in 1971 also demonstrated that pulmonary regurgitation is not well tolerated in patients in whom the fascia lata reconstruction of the right ventricular outflow tract gradually degenerates. Pulmonary valve replacement itself is a very uncommon surgical procedure, with only 22 cases reported in the literature to date. In 1966 Fuller 8 first described the replacement of a pulmonic valve with a homograft pulmonic valve in a patient who did not tolerate pulmonary valvotomy. In the same year Ross and Somerville 21 described the use of a homograft aortic valve for replacement of the pulmonary valve in a case of pulmonary atresia. The largest series of pulmonary valve replacement is included in an article by Trusler and associates, 25 who reported eleven pulmonic valve replacements, eight with homograft aortic valves, two with stented pericardial valves, and one with a stented fascia lata valve. These were all performed in children with various types of congenital heart disease. In 1971 Ross and Somerville 22 reported on 9 more patients who had undergone pulmonary valve replacement; 2 had pulmonary atresia, and in the remaining 7 patients the pulmonary valve was utilized to replace the aortic valve. The replacement of the pulmonary valve for pulmonic stenosis, particularly of the calcific type, has never been previously reported. In the case reported in this paper it was obvious at the time of surgery that debridement or valvotomy of this totally calcified pulmonic valve was technically impossible. We decided to replace the pulmonic valve because, preoperatively, the patient had manifested signs of right ventricular failure and also because of the evidence of probable prior right ventricular myocardial ischemia as manifested by the fibrosis scattered throughout the wall of the right ventricle. Total replacement with an aortic homograft or valve-bearing conduit was thought unnecessary because of the normal pulmonary artery and infundibulum. The small residual pressure gradient across the prosthesis after bypass was thought to be acceptable, and the patient's subsequent clinical course has been gratifying. REFERENCES 1 Austen, W. G., Greenfield, L. J., Ebert, P. A., and Morrow, A. G.: Experimental Study of Right Ventricular Function After Surgical Procedures Involving the Right
The Journal of Thoracic and Cardiovascular Surgery
Ventricle and Pulmonic Valve, Ann. Surg. 155: 606, 1962. 2 Barrett, D. W.: Simple Pulmonary Stenosis, Br. Heart J. 16: 381, 1954. 3 Brock, R. C : Congenital Pulmonary Stenosis, Am. J. Med. 12: 706, 1952. 4 Bouvrain, Y., and Bescol-Liversac, J.: Etude anatomique, radiologique et histologique des calcifications cardiaques orificielles, Arch. Mai. Coeur 43: 289, 1950. 5 Dinsmore, R. E., Sanders, C. A., Harthorne, J. W., and Austen, W. G.: Calcification of the Congenitally Stenotic Pulmonary Valve, N. Engl. J. Med. 275: 99, 1966. 6 Dinsmore, R. E., Sanders, C. A., Harthorne, J. W., and Austen, W. G.: Congenital Pulmonary Stenosis With Calcification, Radiology 87: 429, 1966. 7 Duke, M.: Severe Pulmonic Stenosis in Late Adult Life: Report of Two Cases, Chest 51: 320, 1967. 8 Fuller, D. M., Marchand, P., Zion, M. M., andZwi, S.: Homograft Replacement of the Pulmonary Valve, Thorax 21: 337, 1966. 9 Gabriele, O. F., and Scatliff, J. M.: Pulmonary Valve Calcification, Am. Heart J. 80: 299, 1970. 10 Genovese, P. D., and Rosenbaum, D.: Pulmonary Stenosis With Survival to the Age of 78 Years, Am. Heart J. 41: 755, 1951. 11 Gerachi, J. L., Burchell, M. B., and Edwards, J. E.: Congenital Pulmonary Stenosis With Intact Ventricular Septum in Persons More than 50 Years Old, Mayo Clin. Proc. 28: 346, 1953. 12 Hardy, W. E., Gnoj, J., and Ayres, S. M.: Pulmonic Stenosis in Associated Atrial Septal Defects in Older Patients, Am. J. Cardiol. 24: 130, 1969. 13 Holmes, R. B.: Calcifications of the Heart, J. Can. Assoc. Radiol. 15: 163, 1964. 14 McGinnis, K. D., Byler, W. R., and Alverez, H.: Cardiac Laminagraphy, Radiology 77: 553, 1961. 15 Mirowski, M., Mehrizi, A., and Shah, K. D.: Right Ventricular Aneurysm. A Complication of Transventricular Pulmonary Valvulotomy: Report of Two Cases, One Associated with Gonadal Agenesis, Am. Heart J. 68: 799, 1964. 16 Northway, W. H., and Abrams, H. L.: Calcific Pulmonic Stenosis, Am. J. Roentgenol. Radium Ther. Nucl. Med. 89: 323, 1963. 17 Rawson, F. L., Jr., and Doerner, A. A.: Functional Cor Triloculare, Am. Heart J. 46: 779, 1953. 18 Roberts, W. C , Mason, D. T., Morrow, A. G., and Braunwald, E.: Calcific Pulmonic Stenosis, Circulation 37: 973, 1968. 19 Rodriguez, G. R., Bennett, K. R., and Lehan, P. H.: Calcification of the Pulmonary Valve, Chest 59: 160, 1971. 20 Rogers, J. V., Chandler, M. W., and Branch, R. H.: Calcification of the Tricuspid Annulus, Am. J. Roentgenol. Radium Ther. Nucl. Med. 106: 550, 1969.
Volume 71 Number 5 May, 1976
21 Ross, D. N., and Somerville, J.: Correction of Pulmonary Atresia With a Homograft Aortic Valve, Lancet 2: 1446, 1966. 22 Ross, D. N., and Somerville, J.: Fascia-lata Reconstruction of the Right Ventricular Outflow Tract, Lancet 1: 941, 1971. 23 Sosman, M. C : Technique for Locating and Identifying Pericardial and Intracardiac Calcifications, Am. J.
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Roentgenol. Radium Ther. Nucl. Med. 50: 641, 1943. 24 Talbert, J. L., Morrow, A. G., Collins, N. P., and Gilbert, J.: The Incidence and Significance of Pulmonic Regurgitation After Pulmonary Valvulotomy, Am. Heart J. 65: 590, 1963. 25 Trusler, G. A., Iyengar, S. R., and Mustard, W. T.: Reconstruction of the Pulmonary Valve and Outflow Tract, J. THORAC. CARDIOVASC. SURG. 65: 245,
1973.