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Coronary artery compression with fatal myocardial ischemia
J THORAC CARDIOVASC SURG 85:546-551, 1983
Coronary artery compression with fatal myocardial ischemia A rare complication of valved extracardiac conduits in children with congenital heart disease Three children with congenital heart disease died after surgical procedures involving the placement of valved extracardiac conduits; their deaths were caused by myocardial ischemia following coronary artery compression by the metallic stent of the conduit valve. The first and second patients died of acute myocardial ischemia or infarction during the immediate postoperative period. whereas the third patient died of chronic myocardial ischemia and progressive heart failure several months after the operation. In a fourth patient the problem of possible coronary artery compression was suspected on completion of the surgical procedure. and the valve stent was then repositioned away from the coronary artery; this resulted in marked hemodynamic improvement. Fatal myocardial ischemia from coronary artery compression is a rare but potential complication of valved extracardiac conduit placement in children with congenital heart disease. Preoperative assessment of coronary artery distribution is indicated in those patients with prior intrapericardial operations and subsequent pericardial adhesions. Such assessment in previously unoperated patients may be undertaken at the time of conduit operation. Proper conduit placement and intraoperative recognition of possible coronary artery compression by the conduit are important in preventing significant ischemic complications.
Dimitris A. Daskalopoulos, M.D.,* William D. Edwards, M.D.,** David 1. Driscoll, M.D.,*** Gordon K. Danielson, M.D.,**** and Francisco J. Puga, M.D.,**** Rochester, Minn.
Myocardial injury or infarction may complicate cardiac surgical procedures using cardiopulmonary bypass. It may occur in patients with preexisting coronary artery disease who are undergoing coronary artery bypass graft operations, 1. 2 or it may occur after repair or replacement of heart valves and after repair of con-
From the Mayo Clinic and Mayo Foundation. Rochester. Minn. Presented in part at the Fifty-first Annual Meeting of the American Academy of Pediatrics, Section on Cardiology. New York, N. Y. Oct. 22-24, 1982. Received for publication April 20, 1982. Accepted for publication May 25, 1982. Address for reprints: William D. Edwards, M.D., Department of Pathology, Mayo Clinic, Rochester, Minn. 55905. *Division of Pediatric Cardiology and Mayo Graduate School of Medicine. **Department of Pathology. ***Division of Pediatric Cardiology. ****Section of Thoracic and Cardiovascular Surgery.
546
genital heart disease." Myocardial infarction also may result from intraoperative injury to the coronary arteries .4-9 We describe three children with congenital heart disease, who, after repair of their defects with extracardiac conduits, developed fatal myocardial ischemia as a result of coronary artery compression by the metallic stent of the conduit valves. In addition, we describe a fourth patient who demonstrates, by his favorable outcome, the importance of intraoperative recognition of this rare but catastrophic problem.
Case reports CASE I. A 7-year-old boy had complete transposition of the great arteries, valvular pulmonary stenosis, and a ventricular septal defect of the paramernbranous malalignment type that had a hypertrophied infundibular septum and was divided into two portions by the anomalous insertion of a straddling tricuspid papillary muscle. At operation the septal defect was enlarged and closed by patch deviation so that the left ventricle was in continuity with the aorta. The pulmonary trunk was ligated, and a 25 mm Hancock conduit was inserted
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Coronary compression by conduit
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April, 1983
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Fig. 1. Schematic diagram of heart from Patient I (complete transposition with ventricular septal defect and pulmonary stenosis), showing operative repair (left) and coronary arterial anatomy (right). Metallic valve stent of Hancock conduit compressed the left anterior descending coronary artery (LAD). Ao, Aorta. LCX, Left circumflex artery. RCA, Right coronary artery.
Compression site
LAD Expected LCX
RCA ...-
-j-
Expected
LAD
Fig. 2. Schematic diagram of heart from Patient 2 (corrected transposition with ventricular septal defect and pulmonary stenosis), showing anomalous coronary arterial anatomy. Metallic valve stent of Carpentier-Edwards conduit (not shown in the diagram) had compressed the left anterior descending coronary artery. For abbreviations see Fig. I legend.
between the right ventricle and the distal pulmonary trunk, to the left of the aorta. At the end of the procedure there was a 55 mm Hg pressure gradient between the left ventricle and the aorta. Five hours after operation the patient developed hypotension and had a cardiac arrest. He was resuscitated, and reoperation revealed compression of the left anterior descending coronary artery by the metallic ring of the conduit valve (Fig. I). Despite replacement of the conduit to the right of the aorta and insertion of a conduit from the left ventricle to the aorta in order to relieve the residual left ventricular outflow tract obstruction, the patient died. At necropsy, acute myocardial ischemia (4 to 8 hours old) involved the anterolateral left ventricular subendocardium.
CASE 2. An 8-year-old boy had corrected transposition of the great arteries, severe valvular and subvavular pulmonary stenosis, a large ventricular septal defect, and a large atrial septal defect. Surgical repair was performed with patch closure of the ventricular septal defect and suture closure of the atrial septal defect. The pulmonary trunk was divided and oversewn, and a 25 mm Carpentier-Edwards conduit was inserted between the morphologically left ventricle and the distal pulmonary trunk, to the right of the aorta. At the end of the procedure the cardiac output was initially unsatisfactory but improved with inotropic support. Postoperatively, the cardiac output gradually fell despite pharmacologic support, and the patient died 24 hours after operation. At necropsy, the left circumflex coronary artery was absent
548
The Journal of Thoracic and Cardiovascular Surgery
Daskalopoulos et al.
Compression site
RCA
LCX
Fig. 3. Schematic diagram of heart from Patient 3 (pulmonary atresia with ventricular septal defect), showing operative repair (left) and coronary arterial anatomy (right). Metallic valve stent of Ionescu-Shiley conduit compressed the right coronary artery. For abbreviations see Fig. I legend. and the left anterior descending artery followed an aberrant course midway between the anterior interventricular and the right atrioventricular sulci (Fig. 2). The conduit was moderately compressed by the sternum, and as a result the aberrant left anterior descending artery was compressed extrinsically by the metallic stent of the conduit valve. Acute subendocardial myocardial infarction involved the morphologically left ventricle and the inferior morphologically right ventricle. CASE 3. A 2-year-old boy had pulmonary atresia, a large ventricular septal defect, a small atrial septal defect, an overriding aorta mostly committed to the right ventricle, and mild hypoplasia of confluent pulmonary arteries, which were supplied by a severely stenotic ductus arteriosus. At operation, the ventricular septal defect was closed with a patch so that left ventricular blood was directed to the aorta. A 22 mm Ionescu-Shiley conduit was inserted between the right ventricle and the pulmonary confluence, to the left of the aorta. The ductus arteriosus was ligated, and the atrial septal defect was closed with sutures. Although the patient's condition was good at the end of the procedure, his postoperative course was difficult and long because of low cardiac output, acute renal failure, pneumonia, sepsis, disseminated intravascular coagulopathy, ventilator dependence requiring tracheostomy, seizures, and congestive heart failure. Four months after operation he was transferred to a local hospital in stable and fair condition and was discharged home a month later. The electrocardiogram at that time showed ST-T changes in Leads I, a V L, and V3- V5' He remained tired, emaciated, and in congestive heart failure. Eight months after operation he died suddenly; cardiopulmonary resuscitation was unsuccessful, and he was pronounced dead on arrival at a local hospital. The necropsy specimen of heart and lungs was sent to the Mayo Clinic for examination. The dominant right coronary artery was compressed by the metallic stent of the overlying conduit valve (Figs. 3 and 4 a and b), and the right ventricle and inferior left ventricle were the site of chronic myocardial ischemia with calcification (Fig. 4, c and d).
CASE 4. A 19-month-old boy had complete transposition of the great arteries, severe valvular and subvalvular pulmonary stenosis, a ventricular septal defect, and an atrial septal defect. At operation the ventricular defect was enlarged and closed with a patch so that the left ventricle was in continuity with the aorta. The pulmonary trunk was ligated, and an 18 mm Hancock conduit was inserted between the right ventricle and the distal pulmonary trunk, to the left of the aorta. When cardiopulmonary bypass was discontinued, poor left ventricular contractions and bradycardia appeared and prompted reinstitution of bypass. The cardiac output remained low despite the use of an intravenous isoproterenol infusion and an intra-aortic injection of calcium chloride. The conduit was inspected and the valve stent was shifted distally to avoid possible compression of the left anterior descending coronary artery. After this, and a second injection of calcium chloride, the cardiac output improved markedly and cardiopulmonary bypass was discontinued. The patient's postoperative course was uneventful, and 10 days after operation he was discharged from the hospital in good condition.
Discussion
Certain forms of congenital heart disease are frequently associated with anomalies of coronary arterial origin or distributionv " and, accordingly, may be at risk for injury during ventriculotomy. Such operative injury may result in myocardial ischemia or infarction and may be fatal. In tetralogy of Fallot, in particular, the risk of transecting an anomalous coronary artery and the need for preoperative coronary angiography have been well documented.v " The risk of intraoperative injury to aberrant coronary arteries has also been reported in truncus arteriosus," complete and corrected transposition of the great arteries," and univentricular heart." Such anomalous epicardial coronary arteries are
Volume 85 Number 4 April, 1983
Coronary compression by conduit
5 49
Fig. 4. Necrospy specimen from Patient 3. a, Cross-sectional two-chamber view of right atrium (RA) and right ventricle (RV). showing patch closure of ventricular septal defect (D) and right ventricular anastomosis of conduit (dashed line). b. Close-up of aorta (AD), showing proximity of conduit valve (Valve) to aortic valve (AD V) and to right coronary artery (RCA, dashed lines). Thick metallic valve stent (arrows) had compressed the proximal RCA. L, Left coronary artery ostium. R, Right coronary artery ostium. SVC, Superior vena cava. TV, Tricuspid valve. c, and d. Photomicrographs from right ventricular inflow tract, showing chronic myocardial ischemia manifested by patchy subendocardial fibrosis (c. arrows) with focal calcification (d). (Hematoxylin and eosin: orig. mag.; c. x 35; d. x 175.)
at risk not only for operative transection but also for extrinsic compression by the metallic valvular stent of a prosthetic extracardiac conduit, particularly if the sternum is also pressing the conduit onto the underlying epicardium. Harris and colleagues'" have described a 4-monthold infant who died in the operating room immediately after the repair of truncus arteriosus as a result of compression of the left main coronary artery by the metallic stent of the valved conduit. We agree with their emphasis on the importance of proper positioning of the conduit to avoid pressure on a coronary artery. In the case reported by these authors and in all four patients in the present study, the compressed coronary artery coursed over the anterosuperior aspect of the heart; as a result it was "exposed" and susceptible to extrinsic compres-
sion by the conduit connecting the pulmonary ventricle to the pulmonary artery. In two patients (Cases 2 and 3) the coronary artery distribution was atypical for the underlying cardiac anomaly. In our four patients the clinical manifestation of coronary compression was low cardiac output. The sudden deterioration of the first patient's condition a few hours after operation prompted reoperation. The problem was recognized, but despite elevation of the conduit valve ring and revision of the distal conduit anastomosis, the contractility of the left ventricle remained very poor and the patient died in the operating room. In the second patient the problem was not recognized before death. The third patient had a difficult and complicated postoperative course requiring a long hospitalization.
The Journal of
550 Daskalopoulos et al.
He too developed signs of low cardiac output immediately after operation; but unlike the first two cases, extensive acute myocardial ischemia apparently did not occur because the right coronary compression was probably incomplete. It appears, however, that coronary compression by the overlying conduit resulted in significant chronic myocardial ischemia and probably played a major role in the pathogenesis of this child's chronic congestive heart failure and eventual sudden death. In the fourth patient, hypocontractility of the left ventricle and low cardiac output appeared when cardiopulmonary bypass was temporarily discontinued at the end of the operation. The cardiac output increased markedly after distal shifting of the conduit valve. A cause-and-effect relationship between this maneuver and the improvement of hemodynamic status cannot be proved. Nevertheless, this case at least illustrates the importance of recognizing this potential complication during operation so as to prevent irreversible myocardial injury. The complication of fatal myocardial ischemia from iatrogenic coronary artery compression is rare. Over 860 operations involving valved prosthetic extracardiac conduits have been performed in our institution to date; therefore, the three deaths represent only 0.35% of our total experience. Prevention of this catastrophic complication depends on three factors: (l) accurate assessment of the epicardial coronary arterial distribution, (2) conduit insertion ensuring that the valve ring does not contact an underlying coronary artery, and (3) recognition of coronary compression when it occurs. Intraoperative examination of the coronary arterial anatomy before ventriculotomy and placement of the conduit is obviously very important. However, in patients who have had previous intrapericardial operation the epicardial coronary distribution may be obscured by fibrous adhesions. In this latter group of patients, for whom surgical procedures are planned using valved prosthetic extracardiac conduits, we recommend a careful preoperative angiographic study of the coronary artery anatomy. Proper conduit placement is determined by several factors. The conduit must not be too short, or it will be held tightly against the epicardium during each ventricular diastole. We often have found it advantageous to incise the pericardium on the left (anterior to the phrenic nerve) and to open into the left pleural space so as to provide more lateral room for the conduit, particularly in small patients with relatively large conduits. The conduit should be placed so as to avoid or minimize compression by the sternum, which may cause
Thoracic and Cardiovascular Surgery
conduit obstruction. 14 For this reason, placement of the conduit to the left of the aorta is currently preferred in patients with complete transposition of the great arteries. Accordingly, sternal compression of the valvebearing segment should be particularly avoided, since the compressed valve may in tum compress an underlying coronary artery, as occurred in Case 2. To avoid this complication, the valve should be near the distal pulmonary arterial anastomosis. Although care should be taken to prevent coronary artery compression by a valved extracardiac conduit, suspecting and recognizing this problem when it occurs are also importnat. If poor ventricular contractions and low cardiac output occur when cardiopulmonary bypass is discontinued at the end of the procedure, the surgeon should inspect the conduit and try to reposition the valve stent away from the coronary arteries, as illustrated by Case 4, or revise the conduit if necessary. Severe deterioration of hemodynamic status can occur postoperatively from coronary artery compression; when the latter exists as a possibility, the patient should be considered for reoperation to relieve the compression, as illustrated in Case 1. Chronic progressive deterioration may occur in the setting of incomplete coronary obstruction, as observed in Case 3. Appreciation is expressed to Dr. H. J. Kuehn. Omaha. Neb., for follow-up information (Case 3). REFERENCES
2
3
4
5
6
Assad-Morell JL, Frye RL, Connolly DC, Gau GT, Pluth JR, Bamhorst DA, Wallace RB, Davis GD. Elveback LR, Danielson GK: Relation of intraoperative or early postoperative transmural myocardial infarction to patency of aortocoronary bypass grafts and to diseased ungrafted coronary arteries. Am J Cardiol 35:767-773, 1975 Righetti A, Crawford MH, O'Rourke RA, Hardarson T, Schelbert H, Daily PO, DeLuca M, Ashburn W, Ross J Jr: Detection of perioperative myocardial damage after coronary artery bypass graft surgery. Circulation 55: 173-178, 1977 Young DJ, Utley JR, Damron JR, Todd EP, Kuo C-S. Deland F, Atwood A, Mobley S: Results and patterns of perioperative myocardial infarction. J THoRAc CARD10VASC SURG 76:528-532, 1978 Berry BE, McGoon DC: Total correction for tetralogy of Fallot with anomalous coronary artery. Surgery 74:894898, 1973 Fellows KE, Freed MD, Keane JF, Van Praagh R, Bernhard WF, Castaneda AC: Results of routine preoperative coronary angiography in tetralogy of Fallot. Circulation 51:561-566, 1975 Dabizzi RP, Caprioli G, Aiazzi L, Castelli C, Baldrighi G, Parenzan L, Baldrighi V: Distribution and anomalies
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8
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of coronary arteries in tetralogy of Fallot. Circulation 61:95-102, 1980 Anderson KR, McGoon DC, Lie IT: Surgical significance of the coronary arterial anatomy in truncus arteriosus communis. Am J CardioI41:76-81, 1978 Anderson KR, McGoon DC, Lie IT: Vulnerability of coronary arteries in surgery for transposition of the great arteries. J THORAC CARDIOVASC SURG 76:135-139,1978 Keeton BR, Lie JT, McGoon DC, Danielson GK, Ritter DG, Wallace RB: Anatomy of coronary arteries in univentricular hearts and its surgical implications. Am J Cardiol 43:569-580, 1979 Shaher RM, Puddu GC: Coronary arterial anatomy in
II
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14
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complete transposition of the great vessels. Am J Cardiol 17:355-361,1966 Elliot LP, Amplatz K, Edwards JE: Coronary arterial patterns in transposition complexes. Anatomic and angiocardiographic studies. Am J CardioI17:362-378, 1966 Cardell BS: Corrected transposition of the great vessels. Br Heart J 18: 186-192, 1956 Harris JP, Stewart S, Anderson V, Mitchell ML, Manning JA: Coronary artery injury by a valved external conduit. Ann Thorac Surg 31:271-273, 1980 Ciaravella JM Jr, McGoon DC, Danielson GK, Wallace RB, Mair DD: Experience with the extracardiac conduit. J THORAC CARDIOVASC SURG 78:920-930, 1979
Bound volumes available to subscribers Bound volumes of THE JOURNAL OF THORACIC AND CARDIOVASCULAR SURGERY are available to subscribers (only) for the 1983 issues from the Publisher, at a cost of $58.50 ($73.00 international) for Vol. 85 (January-June) and Vol. 86 (July-December). Shipping charges are included. Each bound volume contains a subject and author index and all advertising is removed. Copies are shipped within 30 days after publication of the last issue of the volume. The binding is durable buckram with the JOURNAL name, volume number, and year stamped in gold on the spine. Payment must accompany all orders. Contact Mr. Deans Lynch at The C. V. Mosby Company, 11830 Westline Industrial Drive, SI. Louis, Missouri 63141, USA. Subscriptions must be in force to qualify. Bound volumes are not available in place of a regular JOURNAL subscription.
Coronary artery compression with fatal myocardial ischemia A rare complication of valved extracardiac conduits in children with congenital heart disease Three children with congenital heart disease died after surgical procedures involving the placement of valved extracardiac conduits; their deaths were caused by myocardial ischemia following coronary artery compression by the metallic stent of the conduit valve. The first and second patients died of acute myocardial ischemia or infarction during the immediate postoperative period. whereas the third patient died of chronic myocardial ischemia and progressive heart failure several months after the operation. In a fourth patient the problem of possible coronary artery compression was suspected on completion of the surgical procedure. and the valve stent was then repositioned away from the coronary artery; this resulted in marked hemodynamic improvement. Fatal myocardial ischemia from coronary artery compression is a rare but potential complication of valved extracardiac conduit placement in children with congenital heart disease. Preoperative assessment of coronary artery distribution is indicated in those patients with prior intrapericardial operations and subsequent pericardial adhesions. Such assessment in previously unoperated patients may be undertaken at the time of conduit operation. Proper conduit placement and intraoperative recognition of possible coronary artery compression by the conduit are important in preventing significant ischemic complications.
Dimitris A. Daskalopoulos, M.D.,* William D. Edwards, M.D.,** David 1. Driscoll, M.D.,*** Gordon K. Danielson, M.D.,**** and Francisco J. Puga, M.D.,**** Rochester, Minn.
Myocardial injury or infarction may complicate cardiac surgical procedures using cardiopulmonary bypass. It may occur in patients with preexisting coronary artery disease who are undergoing coronary artery bypass graft operations, 1. 2 or it may occur after repair or replacement of heart valves and after repair of con-
From the Mayo Clinic and Mayo Foundation. Rochester. Minn. Presented in part at the Fifty-first Annual Meeting of the American Academy of Pediatrics, Section on Cardiology. New York, N. Y. Oct. 22-24, 1982. Received for publication April 20, 1982. Accepted for publication May 25, 1982. Address for reprints: William D. Edwards, M.D., Department of Pathology, Mayo Clinic, Rochester, Minn. 55905. *Division of Pediatric Cardiology and Mayo Graduate School of Medicine. **Department of Pathology. ***Division of Pediatric Cardiology. ****Section of Thoracic and Cardiovascular Surgery.
546
genital heart disease." Myocardial infarction also may result from intraoperative injury to the coronary arteries .4-9 We describe three children with congenital heart disease, who, after repair of their defects with extracardiac conduits, developed fatal myocardial ischemia as a result of coronary artery compression by the metallic stent of the conduit valves. In addition, we describe a fourth patient who demonstrates, by his favorable outcome, the importance of intraoperative recognition of this rare but catastrophic problem.
Case reports CASE I. A 7-year-old boy had complete transposition of the great arteries, valvular pulmonary stenosis, and a ventricular septal defect of the paramernbranous malalignment type that had a hypertrophied infundibular septum and was divided into two portions by the anomalous insertion of a straddling tricuspid papillary muscle. At operation the septal defect was enlarged and closed by patch deviation so that the left ventricle was in continuity with the aorta. The pulmonary trunk was ligated, and a 25 mm Hancock conduit was inserted
Volume 85
Coronary compression by conduit
Number 4
April, 1983
5 47
Fig. 1. Schematic diagram of heart from Patient I (complete transposition with ventricular septal defect and pulmonary stenosis), showing operative repair (left) and coronary arterial anatomy (right). Metallic valve stent of Hancock conduit compressed the left anterior descending coronary artery (LAD). Ao, Aorta. LCX, Left circumflex artery. RCA, Right coronary artery.
Compression site
LAD Expected LCX
RCA ...-
-j-
Expected
LAD
Fig. 2. Schematic diagram of heart from Patient 2 (corrected transposition with ventricular septal defect and pulmonary stenosis), showing anomalous coronary arterial anatomy. Metallic valve stent of Carpentier-Edwards conduit (not shown in the diagram) had compressed the left anterior descending coronary artery. For abbreviations see Fig. I legend.
between the right ventricle and the distal pulmonary trunk, to the left of the aorta. At the end of the procedure there was a 55 mm Hg pressure gradient between the left ventricle and the aorta. Five hours after operation the patient developed hypotension and had a cardiac arrest. He was resuscitated, and reoperation revealed compression of the left anterior descending coronary artery by the metallic ring of the conduit valve (Fig. I). Despite replacement of the conduit to the right of the aorta and insertion of a conduit from the left ventricle to the aorta in order to relieve the residual left ventricular outflow tract obstruction, the patient died. At necropsy, acute myocardial ischemia (4 to 8 hours old) involved the anterolateral left ventricular subendocardium.
CASE 2. An 8-year-old boy had corrected transposition of the great arteries, severe valvular and subvavular pulmonary stenosis, a large ventricular septal defect, and a large atrial septal defect. Surgical repair was performed with patch closure of the ventricular septal defect and suture closure of the atrial septal defect. The pulmonary trunk was divided and oversewn, and a 25 mm Carpentier-Edwards conduit was inserted between the morphologically left ventricle and the distal pulmonary trunk, to the right of the aorta. At the end of the procedure the cardiac output was initially unsatisfactory but improved with inotropic support. Postoperatively, the cardiac output gradually fell despite pharmacologic support, and the patient died 24 hours after operation. At necropsy, the left circumflex coronary artery was absent
548
The Journal of Thoracic and Cardiovascular Surgery
Daskalopoulos et al.
Compression site
RCA
LCX
Fig. 3. Schematic diagram of heart from Patient 3 (pulmonary atresia with ventricular septal defect), showing operative repair (left) and coronary arterial anatomy (right). Metallic valve stent of Ionescu-Shiley conduit compressed the right coronary artery. For abbreviations see Fig. I legend. and the left anterior descending artery followed an aberrant course midway between the anterior interventricular and the right atrioventricular sulci (Fig. 2). The conduit was moderately compressed by the sternum, and as a result the aberrant left anterior descending artery was compressed extrinsically by the metallic stent of the conduit valve. Acute subendocardial myocardial infarction involved the morphologically left ventricle and the inferior morphologically right ventricle. CASE 3. A 2-year-old boy had pulmonary atresia, a large ventricular septal defect, a small atrial septal defect, an overriding aorta mostly committed to the right ventricle, and mild hypoplasia of confluent pulmonary arteries, which were supplied by a severely stenotic ductus arteriosus. At operation, the ventricular septal defect was closed with a patch so that left ventricular blood was directed to the aorta. A 22 mm Ionescu-Shiley conduit was inserted between the right ventricle and the pulmonary confluence, to the left of the aorta. The ductus arteriosus was ligated, and the atrial septal defect was closed with sutures. Although the patient's condition was good at the end of the procedure, his postoperative course was difficult and long because of low cardiac output, acute renal failure, pneumonia, sepsis, disseminated intravascular coagulopathy, ventilator dependence requiring tracheostomy, seizures, and congestive heart failure. Four months after operation he was transferred to a local hospital in stable and fair condition and was discharged home a month later. The electrocardiogram at that time showed ST-T changes in Leads I, a V L, and V3- V5' He remained tired, emaciated, and in congestive heart failure. Eight months after operation he died suddenly; cardiopulmonary resuscitation was unsuccessful, and he was pronounced dead on arrival at a local hospital. The necropsy specimen of heart and lungs was sent to the Mayo Clinic for examination. The dominant right coronary artery was compressed by the metallic stent of the overlying conduit valve (Figs. 3 and 4 a and b), and the right ventricle and inferior left ventricle were the site of chronic myocardial ischemia with calcification (Fig. 4, c and d).
CASE 4. A 19-month-old boy had complete transposition of the great arteries, severe valvular and subvalvular pulmonary stenosis, a ventricular septal defect, and an atrial septal defect. At operation the ventricular defect was enlarged and closed with a patch so that the left ventricle was in continuity with the aorta. The pulmonary trunk was ligated, and an 18 mm Hancock conduit was inserted between the right ventricle and the distal pulmonary trunk, to the left of the aorta. When cardiopulmonary bypass was discontinued, poor left ventricular contractions and bradycardia appeared and prompted reinstitution of bypass. The cardiac output remained low despite the use of an intravenous isoproterenol infusion and an intra-aortic injection of calcium chloride. The conduit was inspected and the valve stent was shifted distally to avoid possible compression of the left anterior descending coronary artery. After this, and a second injection of calcium chloride, the cardiac output improved markedly and cardiopulmonary bypass was discontinued. The patient's postoperative course was uneventful, and 10 days after operation he was discharged from the hospital in good condition.
Discussion
Certain forms of congenital heart disease are frequently associated with anomalies of coronary arterial origin or distributionv " and, accordingly, may be at risk for injury during ventriculotomy. Such operative injury may result in myocardial ischemia or infarction and may be fatal. In tetralogy of Fallot, in particular, the risk of transecting an anomalous coronary artery and the need for preoperative coronary angiography have been well documented.v " The risk of intraoperative injury to aberrant coronary arteries has also been reported in truncus arteriosus," complete and corrected transposition of the great arteries," and univentricular heart." Such anomalous epicardial coronary arteries are
Volume 85 Number 4 April, 1983
Coronary compression by conduit
5 49
Fig. 4. Necrospy specimen from Patient 3. a, Cross-sectional two-chamber view of right atrium (RA) and right ventricle (RV). showing patch closure of ventricular septal defect (D) and right ventricular anastomosis of conduit (dashed line). b. Close-up of aorta (AD), showing proximity of conduit valve (Valve) to aortic valve (AD V) and to right coronary artery (RCA, dashed lines). Thick metallic valve stent (arrows) had compressed the proximal RCA. L, Left coronary artery ostium. R, Right coronary artery ostium. SVC, Superior vena cava. TV, Tricuspid valve. c, and d. Photomicrographs from right ventricular inflow tract, showing chronic myocardial ischemia manifested by patchy subendocardial fibrosis (c. arrows) with focal calcification (d). (Hematoxylin and eosin: orig. mag.; c. x 35; d. x 175.)
at risk not only for operative transection but also for extrinsic compression by the metallic valvular stent of a prosthetic extracardiac conduit, particularly if the sternum is also pressing the conduit onto the underlying epicardium. Harris and colleagues'" have described a 4-monthold infant who died in the operating room immediately after the repair of truncus arteriosus as a result of compression of the left main coronary artery by the metallic stent of the valved conduit. We agree with their emphasis on the importance of proper positioning of the conduit to avoid pressure on a coronary artery. In the case reported by these authors and in all four patients in the present study, the compressed coronary artery coursed over the anterosuperior aspect of the heart; as a result it was "exposed" and susceptible to extrinsic compres-
sion by the conduit connecting the pulmonary ventricle to the pulmonary artery. In two patients (Cases 2 and 3) the coronary artery distribution was atypical for the underlying cardiac anomaly. In our four patients the clinical manifestation of coronary compression was low cardiac output. The sudden deterioration of the first patient's condition a few hours after operation prompted reoperation. The problem was recognized, but despite elevation of the conduit valve ring and revision of the distal conduit anastomosis, the contractility of the left ventricle remained very poor and the patient died in the operating room. In the second patient the problem was not recognized before death. The third patient had a difficult and complicated postoperative course requiring a long hospitalization.
The Journal of
550 Daskalopoulos et al.
He too developed signs of low cardiac output immediately after operation; but unlike the first two cases, extensive acute myocardial ischemia apparently did not occur because the right coronary compression was probably incomplete. It appears, however, that coronary compression by the overlying conduit resulted in significant chronic myocardial ischemia and probably played a major role in the pathogenesis of this child's chronic congestive heart failure and eventual sudden death. In the fourth patient, hypocontractility of the left ventricle and low cardiac output appeared when cardiopulmonary bypass was temporarily discontinued at the end of the operation. The cardiac output increased markedly after distal shifting of the conduit valve. A cause-and-effect relationship between this maneuver and the improvement of hemodynamic status cannot be proved. Nevertheless, this case at least illustrates the importance of recognizing this potential complication during operation so as to prevent irreversible myocardial injury. The complication of fatal myocardial ischemia from iatrogenic coronary artery compression is rare. Over 860 operations involving valved prosthetic extracardiac conduits have been performed in our institution to date; therefore, the three deaths represent only 0.35% of our total experience. Prevention of this catastrophic complication depends on three factors: (l) accurate assessment of the epicardial coronary arterial distribution, (2) conduit insertion ensuring that the valve ring does not contact an underlying coronary artery, and (3) recognition of coronary compression when it occurs. Intraoperative examination of the coronary arterial anatomy before ventriculotomy and placement of the conduit is obviously very important. However, in patients who have had previous intrapericardial operation the epicardial coronary distribution may be obscured by fibrous adhesions. In this latter group of patients, for whom surgical procedures are planned using valved prosthetic extracardiac conduits, we recommend a careful preoperative angiographic study of the coronary artery anatomy. Proper conduit placement is determined by several factors. The conduit must not be too short, or it will be held tightly against the epicardium during each ventricular diastole. We often have found it advantageous to incise the pericardium on the left (anterior to the phrenic nerve) and to open into the left pleural space so as to provide more lateral room for the conduit, particularly in small patients with relatively large conduits. The conduit should be placed so as to avoid or minimize compression by the sternum, which may cause
Thoracic and Cardiovascular Surgery
conduit obstruction. 14 For this reason, placement of the conduit to the left of the aorta is currently preferred in patients with complete transposition of the great arteries. Accordingly, sternal compression of the valvebearing segment should be particularly avoided, since the compressed valve may in tum compress an underlying coronary artery, as occurred in Case 2. To avoid this complication, the valve should be near the distal pulmonary arterial anastomosis. Although care should be taken to prevent coronary artery compression by a valved extracardiac conduit, suspecting and recognizing this problem when it occurs are also importnat. If poor ventricular contractions and low cardiac output occur when cardiopulmonary bypass is discontinued at the end of the procedure, the surgeon should inspect the conduit and try to reposition the valve stent away from the coronary arteries, as illustrated by Case 4, or revise the conduit if necessary. Severe deterioration of hemodynamic status can occur postoperatively from coronary artery compression; when the latter exists as a possibility, the patient should be considered for reoperation to relieve the compression, as illustrated in Case 1. Chronic progressive deterioration may occur in the setting of incomplete coronary obstruction, as observed in Case 3. Appreciation is expressed to Dr. H. J. Kuehn. Omaha. Neb., for follow-up information (Case 3). REFERENCES
2
3
4
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Assad-Morell JL, Frye RL, Connolly DC, Gau GT, Pluth JR, Bamhorst DA, Wallace RB, Davis GD. Elveback LR, Danielson GK: Relation of intraoperative or early postoperative transmural myocardial infarction to patency of aortocoronary bypass grafts and to diseased ungrafted coronary arteries. Am J Cardiol 35:767-773, 1975 Righetti A, Crawford MH, O'Rourke RA, Hardarson T, Schelbert H, Daily PO, DeLuca M, Ashburn W, Ross J Jr: Detection of perioperative myocardial damage after coronary artery bypass graft surgery. Circulation 55: 173-178, 1977 Young DJ, Utley JR, Damron JR, Todd EP, Kuo C-S. Deland F, Atwood A, Mobley S: Results and patterns of perioperative myocardial infarction. J THoRAc CARD10VASC SURG 76:528-532, 1978 Berry BE, McGoon DC: Total correction for tetralogy of Fallot with anomalous coronary artery. Surgery 74:894898, 1973 Fellows KE, Freed MD, Keane JF, Van Praagh R, Bernhard WF, Castaneda AC: Results of routine preoperative coronary angiography in tetralogy of Fallot. Circulation 51:561-566, 1975 Dabizzi RP, Caprioli G, Aiazzi L, Castelli C, Baldrighi G, Parenzan L, Baldrighi V: Distribution and anomalies
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Coronary compression by conduit
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of coronary arteries in tetralogy of Fallot. Circulation 61:95-102, 1980 Anderson KR, McGoon DC, Lie IT: Surgical significance of the coronary arterial anatomy in truncus arteriosus communis. Am J CardioI41:76-81, 1978 Anderson KR, McGoon DC, Lie IT: Vulnerability of coronary arteries in surgery for transposition of the great arteries. J THORAC CARDIOVASC SURG 76:135-139,1978 Keeton BR, Lie JT, McGoon DC, Danielson GK, Ritter DG, Wallace RB: Anatomy of coronary arteries in univentricular hearts and its surgical implications. Am J Cardiol 43:569-580, 1979 Shaher RM, Puddu GC: Coronary arterial anatomy in
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complete transposition of the great vessels. Am J Cardiol 17:355-361,1966 Elliot LP, Amplatz K, Edwards JE: Coronary arterial patterns in transposition complexes. Anatomic and angiocardiographic studies. Am J CardioI17:362-378, 1966 Cardell BS: Corrected transposition of the great vessels. Br Heart J 18: 186-192, 1956 Harris JP, Stewart S, Anderson V, Mitchell ML, Manning JA: Coronary artery injury by a valved external conduit. Ann Thorac Surg 31:271-273, 1980 Ciaravella JM Jr, McGoon DC, Danielson GK, Wallace RB, Mair DD: Experience with the extracardiac conduit. J THORAC CARDIOVASC SURG 78:920-930, 1979
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