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Right ventricle-to-aorta conduit in pulmonary atresia with intact ventricular septum and coronary sinusoids
CASE REPORT FREEMAN ET AL RIGHT VENTRICLE DECOMPRESSION
Ann Thorac Surg 1993;56:139>5
It is noted in this case, as has been reported by others [l],that the patient’s record often does not reveal whether these wires are removed or cut at the skin level and allowed to retract. Such a practice implies a belief that the retention of these wires is of little consequence. Although the incidence of complications from this practice is low, it is nonetheless not without hazard. We present this case to add to the list of potential complications caused by retained temporary epicardial pacing wires. This case also illustrates the need to record the disposition of these wires in the postoperative record and to consider these retained fragments as the source of unidentified complaints in the patient who has had a cardiac operation.
References 1. Del Nido P, Goldman BS. Temporary epicardial pacing after open heart surgery: complications and prevention. J Cardiac S;rg 1989;4:99-705. 2. Koromuai FL. Havward RH. Knight WL. Mieration of temuorary eGicardia1 p&er wire fragGent retain& after a cardiac operation. J Thorac Cardiovasc Surg 1987;94446. 3. Bolton JWR, Mayer JE. Unusual complication of temporary pacing wires in children. Ann Thorac Surg 1992;54:769-70.
Ri ht Ventricle-to-Aorta Conduit in Pu monary Atresia With Intact Ventricular Septum and Coronary Sinusoids
7
Jenny E. Freeman, MD, Serafin Y. DeLeon, MD, Stephen Lai, MD, Elizabeth A. Fisher, MD, E. Phillip Ow, MD, and Roque Pifarrk, MD
1393
D
espite some recent improvements, the surgical management of pulmonary atresia with intact septum, hypoplastic right ventricle, and major coronary sinusoids continues to be difficult and disappointing [l]. Leaving the hypertensive right ventricle without decompression can lead to progressive right ventricular hypertrophy and fatal dysrhythmias. Continued turbulent flows at the ventricular sinusoid-coronary artery junction can lead to progressive coronary artery stenosis and myocardial ischemia [2]. Decompression of the hypertensive right ventricle should minimize late dysrhythmias. However, in the presence of major ventriculocoronary connections, right ventricular decompression can lead to acute myocardial ischemia and infarction [3]. We report a patient with pulmonary atresia with intact ventricular septum and major right ventriculocoronary connections in whom we successfully interposed a conduit between the right ventricle and ascending aorta at the time of Fontan procedure. Our patient was diagnosed at birth as having pulmonary atresia with intact ventricular septum, hypoplastic right ventricle, and major ventricular-coronary connections. A left modified Blalock-Taussig shunt of 4-mm polytetrafluoroethylene graft was placed. At 8 months of age cardiac catheterization demonstrated adequate pulmonary artery growth, an arterial saturation of 80%, and a suprasystemic right ventricular pressure of 150 mm Hg. Prominent coronary sinusoids with a partially right ventricular-dependent circulation were present (Fig 1).A hemi-Fontan (bidirectional Glenn) was performed through a median sternotomy using cardiopulmonary bypass. Marking sutures were placed on the surface of the right ventricle on an area free from
Departments of Cardiovascular-Thoracic Surgery and Pediatrics, Loyola University Medical Center, Maywood, Illinois
A 20-month-old girl with pulmonary atresia, intact ventricular septum, and ventriculocoronary connections underwent successful interposition of a right ventricle-toaorta conduit and Fontan operation. The patient initially had a modified Blalock-Taussig shunt at birth and subsequently a bidirectional Glenn shunt at 8 months of age. After Fontan and right ventricle-to-aorta conduit placement, the suprasystemic right ventricular pressure dropped to systemic levels without causing myocardial injury. Additionally, the right ventricular cavity enlarged. We believe that the use of a right ventricle-toaorta conduit should provide a valuable alternative and improve the outlook of certain patients with pulmonary atresia, intact ventricular septum, and ventriculocoronary connections. (Ann Thorac Surg 1993;56:1393-5) Accepted for publication March 12, 1993. Address reprint requests to Dr DeLeon, Loyola University Medical Center, 2160 South First Ave, Maywood, 1L 60153.
Fig 1. Right ventricular angiogram demonstrating the hypoplastic right ventricle with major coronary sinusoids feeding the coronary arteries. (LCA = left coronary artery; PDA = posterior descending artery.)
1394
Ann Thorac Surg 1993:56:139>5
CASE REPORT FREEMAN ET AL RIGHT VENTRICLE DECOMPRESSION
/"
larger in size postoperatively, perhaps because of increased diastolic volume supplied by the conduit (Fig 3). The patient continues to do well 6 months postoperatively.
Comment
Fig 2. Six-millimeter polytetrafluoroethylene tube graft interposed between the right ventricle and the aorta. Note marking stitches previously placed to demonstrate a sinusoid-free area. (Ao = aorta; SVC = superior vena cava.)
sinusoids where a conduit could be anastomosed at a later operation. At 20 months cardiac catheterization demonstrated a functioning hemi-Fontan, a right ventricular pressure of 240 mm Hg, and a pulmonary resistance of 2.4 Wood units. The completion Fontan operation was performed by excising the piece of homograft separating the right atrium from the superior vena cava. A lateral tunnel using polytetrafluoroethylene graft was created to baffle the inferior vena cava to the right atrial-superior vena cava junction. An adjustable fenestration was created. During rewarming, a 6-mm polytetrafluoroethylene tube graft was interposed between the site previously marked on the right ventricle and the ascending aorta (Fig 2). Care was taken to excise some of the heavy musculature from the hypertrophic right ventricle at the site of anastomosis especially on the endocardia1 side to prevent systolic constriction. The marking sutures were very helpful for identifying the sinusoid-free area of the right ventricle as the surface was obscured by adhesions at reoperation. Because of excellent hemodynamics the atrial fenestration was closed intraoperatively. An obvious biphasic thrill was noted in the right ventricle-to-aorta conduit. The postoperative course was that of normal convalescence with no effusion or other complications. Doppler echocardiography demonstrated biphasic flow across the conduit with right ventricle-to-aorta flow during systole and aorta-to-right ventricle flow during diastole. The calculated right ventricular pressure had been reduced from 240 mm Hg to 115 mm Hg. The right ventricle was
Right ventricle-to-coronary connections in pulmonary atresia with intact ventricular septum are generally believed to be due to high right ventricular pressure causing a persistence of the ventricular sinusoids normally present embryologically [4]. Blood flows from the hypertensive right ventricle through sinusoids to the coronary arteries producing turbulence, tortuosity, and segmental obstruction of the coronary arteries. In certain patients, there is absence of antegrade coronary artery flow producing the so-called right ventricle-dependent coronary circulation. Histologic examination of the coronary arteries has shown thickening of the intima and varying degrees of obstruction [5]. Although recently the outlook of patients who have pulmonary atresia and intact ventricular septum without major sinusoids has improved, in patients with major ventriculocoronary connections, the outcome remains poor. It is probably safer not to completely decompress or exclude the right ventricle when major sinusoids are present as this can lead to myocardial ischemia and infarction [ 11. In general, a systemic to pulmonary artery shunt is performed in the newborn period. In the presence of major sinusoids but without a right ventricle-dependent coronary circulation tricuspid valve closure [6] or thromboembolism of the right ventricle [7] has on occasion been successfully performed. Patients who have had successful
Fig 3. Postoperative apical four-chamber v i m demonstrating the course of the right ventricle to aortic conduit. Note also the relatively larger size of the right ventricle. ( A 0 = aorta; LA = left atrium; LV = left ventricle; RA = right atrium.)
Ann Thorac Surg
1993;561395-7
initial palliation have subsequently undergone Fontantype procedures when biventricular repair was not possible. In the presence of right ventricle-dependent coronary artery circulation, biventricular repair is seldom possible. Atrial partitioning that directs oxygenated blood to the right ventricle has been successfully accomplished [B]. This, however, leaves the patient with serious right ventricular hypertension and the potential for later dysrhythmias. Interposition of a conduit between the right ventricle and ascending aorta can decompress the right ventricle from suprasystemic to systemic levels without compromising areas of right ventricle-dependent coronary artery circulation and producing myocardial injury. Such a drop in the right ventricular pressure should minimize progressive hypertrophy and fibroelastosis and thus late lifethreatening dysrhythmias. Equalization of systolic pressures between the right ventricle and the aorta also should reduce turbulent flow in the coronary arteries avoiding progressive dilatation and stenosis of coronary artery segments. Combination of such a conduit with a lateral tunnel Fontan provides oxygenated blood to the coronary arteries from both the right ventricle and the aorta at systemic pressure. Additionally, because the right ventricle can enlarge from the increase in diastolic volume resulting from diastolic flow through the conduit, there is a possibility of subsequent biventricular repair should the sinusoids regress. In this, our first patient, we chose to place the right ventricle to aorta conduit when the child's heart and mediastinal space were somewhat larger (ie, at the time of the Fontan). It may, however, be preferable to decompress the right ventricle earlier, either at the time of hemi-Fontan or even in the neonatal period. The theoretical advantages of minimizing progressive changes in the coronary arteries and the development of tricuspid insufficiency may be offset, however, by technical difficulties, mediastinal space considerations, and the safety of reoperation with a substernal conduit. As we progress with this technique these issues will be clarified.
References 1. Coles J, Williams WG, Trusler GA, Lightfoot N, Freedom RM. Surgical considerations and outcome. In: Freedom RM, ed. Pulmonary atresia with intact ventricular septum. New York: Futura, 1989:249-57. 2. Fyfe DA, Edwards WD, Driscoll DJ. Myocardial ischemia in patients with pulmonary atresia and intact ventricular septum. J Am Coll Cardiol 1986;8:402-6. 3. DeLeon SY, Duffy CE, Stout MJ. Myocardial infarction in children: causes and management. In: Pifarre R, ed. Cardiac surgery: state of the art reviews. Vol 6. Management of acute myocardial infarction and its complications. Philadelphia: Hanley and Belfus, 199217-35. 4. Yokose T, Doi M, Kimura Y, Ogata T. Ventriculo-coronary microcommunications in pulmonary atresia and sequential changes of coronary arteries. Acta Pathol Jpn 1987;371033-40. 5. Wilson GJ, Freedom RM, Koike K, Perrin D. The coronary arteries: anatomy and histopathology. In: Freedom RM, ed. Pulmonary atresia with intact ventricular septum. New York: Futura, 1989:75-88.
CASE REPORT IZZAT ET AL RETROGRADE CARDIOPLEGIA AND AGGLUTINATION
1395
Waldman JD, Lamberti JJ, Mathewson JW, George L. Surgical closure of the tricuspid valve for pulmonary atresia, intact ventricular septum, and right ventricle to coronary artery communications. Pediatr Cardiol 1984;5:2214. Williams WG, Burrows P, Freedom RM, et al. Thromboexclusion of the right ventricle in children with pulmonary atresia and intact ventricular septum. J Thorac Cardiovasc Surg 1991;101:222-9. Stein DG, Laks H, Drinkwater DC, et al. Results of total cavopulmonary connection in the treatment of patients with a functional single ventricle. J Thorac Cardiovasc Surg 1991;102: 280-7.
Use of Retrograde Cold Crystalloid Cardioplegia in a Patient With Unexpected Cold Agglutination Mohammad Bashar Izzat, FRCS, Pala B. Rajesh, FRCS, and Geoffrey H. Smith, FRCS Department of Cardiothoracic Surgery, Northern General Hospital, Sheffield, United Kingdom
Undetected cold agglutinins were encountered in a patient undergoing coronary artery bypass grafting using antegrade cold blood cardioplegia. Macroemboli were infused into the coronary arterial tree. These were flushed out by the use of retrograde cold crystalloid cardioplegia. Activated cold agglutinins may be hazardous in cold blood cardioplegia. (Ann T ~ O Y StlYg U C 2993;56:1395-7)
C
old agglutinins cause aggregation of red blood cells when activated by low temperatures. Because of the use of mild or deep hypothermia in cardiopulmonary bypass procedures, many cardiac surgical units routinely test for cold agglutinins and determine the temperatures at which they become activated. We report a case in which agglutination of red blood cells occurred during antegrade cold blood cardioplegia infusion and led to embolization in the coronary microcirculation. Infusion of cold crystalloid cardioplegia by the retrograde coronary sinus route seemed to be effective in preventing any damage to the myocardium. Laboratory procedures were reviewed and a policy of routine testing for cold agglutinins was introduced. A 58-year-old woman was admitted for coronary artery bypass grafting. Cardiac catheterization had shown good left ventricular function and triple-vessel disease. Her routine preoperative investigations did not include testing for cold antibodies below room temperature as this was the blood bank practice. At operation, she was placed on cardiopulmonary bypass with aortic and bicaval cannulaAccepted for publication March 18, 1993 Address reprint requests to Mr Izzat, Department of Cardiac Surgery, Bristol Royal Infirmary, Bristol 852 8HW, United Kingdom.
Ann Thorac Surg 1993;56:139>5
It is noted in this case, as has been reported by others [l],that the patient’s record often does not reveal whether these wires are removed or cut at the skin level and allowed to retract. Such a practice implies a belief that the retention of these wires is of little consequence. Although the incidence of complications from this practice is low, it is nonetheless not without hazard. We present this case to add to the list of potential complications caused by retained temporary epicardial pacing wires. This case also illustrates the need to record the disposition of these wires in the postoperative record and to consider these retained fragments as the source of unidentified complaints in the patient who has had a cardiac operation.
References 1. Del Nido P, Goldman BS. Temporary epicardial pacing after open heart surgery: complications and prevention. J Cardiac S;rg 1989;4:99-705. 2. Koromuai FL. Havward RH. Knight WL. Mieration of temuorary eGicardia1 p&er wire fragGent retain& after a cardiac operation. J Thorac Cardiovasc Surg 1987;94446. 3. Bolton JWR, Mayer JE. Unusual complication of temporary pacing wires in children. Ann Thorac Surg 1992;54:769-70.
Ri ht Ventricle-to-Aorta Conduit in Pu monary Atresia With Intact Ventricular Septum and Coronary Sinusoids
7
Jenny E. Freeman, MD, Serafin Y. DeLeon, MD, Stephen Lai, MD, Elizabeth A. Fisher, MD, E. Phillip Ow, MD, and Roque Pifarrk, MD
1393
D
espite some recent improvements, the surgical management of pulmonary atresia with intact septum, hypoplastic right ventricle, and major coronary sinusoids continues to be difficult and disappointing [l]. Leaving the hypertensive right ventricle without decompression can lead to progressive right ventricular hypertrophy and fatal dysrhythmias. Continued turbulent flows at the ventricular sinusoid-coronary artery junction can lead to progressive coronary artery stenosis and myocardial ischemia [2]. Decompression of the hypertensive right ventricle should minimize late dysrhythmias. However, in the presence of major ventriculocoronary connections, right ventricular decompression can lead to acute myocardial ischemia and infarction [3]. We report a patient with pulmonary atresia with intact ventricular septum and major right ventriculocoronary connections in whom we successfully interposed a conduit between the right ventricle and ascending aorta at the time of Fontan procedure. Our patient was diagnosed at birth as having pulmonary atresia with intact ventricular septum, hypoplastic right ventricle, and major ventricular-coronary connections. A left modified Blalock-Taussig shunt of 4-mm polytetrafluoroethylene graft was placed. At 8 months of age cardiac catheterization demonstrated adequate pulmonary artery growth, an arterial saturation of 80%, and a suprasystemic right ventricular pressure of 150 mm Hg. Prominent coronary sinusoids with a partially right ventricular-dependent circulation were present (Fig 1).A hemi-Fontan (bidirectional Glenn) was performed through a median sternotomy using cardiopulmonary bypass. Marking sutures were placed on the surface of the right ventricle on an area free from
Departments of Cardiovascular-Thoracic Surgery and Pediatrics, Loyola University Medical Center, Maywood, Illinois
A 20-month-old girl with pulmonary atresia, intact ventricular septum, and ventriculocoronary connections underwent successful interposition of a right ventricle-toaorta conduit and Fontan operation. The patient initially had a modified Blalock-Taussig shunt at birth and subsequently a bidirectional Glenn shunt at 8 months of age. After Fontan and right ventricle-to-aorta conduit placement, the suprasystemic right ventricular pressure dropped to systemic levels without causing myocardial injury. Additionally, the right ventricular cavity enlarged. We believe that the use of a right ventricle-toaorta conduit should provide a valuable alternative and improve the outlook of certain patients with pulmonary atresia, intact ventricular septum, and ventriculocoronary connections. (Ann Thorac Surg 1993;56:1393-5) Accepted for publication March 12, 1993. Address reprint requests to Dr DeLeon, Loyola University Medical Center, 2160 South First Ave, Maywood, 1L 60153.
Fig 1. Right ventricular angiogram demonstrating the hypoplastic right ventricle with major coronary sinusoids feeding the coronary arteries. (LCA = left coronary artery; PDA = posterior descending artery.)
1394
Ann Thorac Surg 1993:56:139>5
CASE REPORT FREEMAN ET AL RIGHT VENTRICLE DECOMPRESSION
/"
larger in size postoperatively, perhaps because of increased diastolic volume supplied by the conduit (Fig 3). The patient continues to do well 6 months postoperatively.
Comment
Fig 2. Six-millimeter polytetrafluoroethylene tube graft interposed between the right ventricle and the aorta. Note marking stitches previously placed to demonstrate a sinusoid-free area. (Ao = aorta; SVC = superior vena cava.)
sinusoids where a conduit could be anastomosed at a later operation. At 20 months cardiac catheterization demonstrated a functioning hemi-Fontan, a right ventricular pressure of 240 mm Hg, and a pulmonary resistance of 2.4 Wood units. The completion Fontan operation was performed by excising the piece of homograft separating the right atrium from the superior vena cava. A lateral tunnel using polytetrafluoroethylene graft was created to baffle the inferior vena cava to the right atrial-superior vena cava junction. An adjustable fenestration was created. During rewarming, a 6-mm polytetrafluoroethylene tube graft was interposed between the site previously marked on the right ventricle and the ascending aorta (Fig 2). Care was taken to excise some of the heavy musculature from the hypertrophic right ventricle at the site of anastomosis especially on the endocardia1 side to prevent systolic constriction. The marking sutures were very helpful for identifying the sinusoid-free area of the right ventricle as the surface was obscured by adhesions at reoperation. Because of excellent hemodynamics the atrial fenestration was closed intraoperatively. An obvious biphasic thrill was noted in the right ventricle-to-aorta conduit. The postoperative course was that of normal convalescence with no effusion or other complications. Doppler echocardiography demonstrated biphasic flow across the conduit with right ventricle-to-aorta flow during systole and aorta-to-right ventricle flow during diastole. The calculated right ventricular pressure had been reduced from 240 mm Hg to 115 mm Hg. The right ventricle was
Right ventricle-to-coronary connections in pulmonary atresia with intact ventricular septum are generally believed to be due to high right ventricular pressure causing a persistence of the ventricular sinusoids normally present embryologically [4]. Blood flows from the hypertensive right ventricle through sinusoids to the coronary arteries producing turbulence, tortuosity, and segmental obstruction of the coronary arteries. In certain patients, there is absence of antegrade coronary artery flow producing the so-called right ventricle-dependent coronary circulation. Histologic examination of the coronary arteries has shown thickening of the intima and varying degrees of obstruction [5]. Although recently the outlook of patients who have pulmonary atresia and intact ventricular septum without major sinusoids has improved, in patients with major ventriculocoronary connections, the outcome remains poor. It is probably safer not to completely decompress or exclude the right ventricle when major sinusoids are present as this can lead to myocardial ischemia and infarction [ 11. In general, a systemic to pulmonary artery shunt is performed in the newborn period. In the presence of major sinusoids but without a right ventricle-dependent coronary circulation tricuspid valve closure [6] or thromboembolism of the right ventricle [7] has on occasion been successfully performed. Patients who have had successful
Fig 3. Postoperative apical four-chamber v i m demonstrating the course of the right ventricle to aortic conduit. Note also the relatively larger size of the right ventricle. ( A 0 = aorta; LA = left atrium; LV = left ventricle; RA = right atrium.)
Ann Thorac Surg
1993;561395-7
initial palliation have subsequently undergone Fontantype procedures when biventricular repair was not possible. In the presence of right ventricle-dependent coronary artery circulation, biventricular repair is seldom possible. Atrial partitioning that directs oxygenated blood to the right ventricle has been successfully accomplished [B]. This, however, leaves the patient with serious right ventricular hypertension and the potential for later dysrhythmias. Interposition of a conduit between the right ventricle and ascending aorta can decompress the right ventricle from suprasystemic to systemic levels without compromising areas of right ventricle-dependent coronary artery circulation and producing myocardial injury. Such a drop in the right ventricular pressure should minimize progressive hypertrophy and fibroelastosis and thus late lifethreatening dysrhythmias. Equalization of systolic pressures between the right ventricle and the aorta also should reduce turbulent flow in the coronary arteries avoiding progressive dilatation and stenosis of coronary artery segments. Combination of such a conduit with a lateral tunnel Fontan provides oxygenated blood to the coronary arteries from both the right ventricle and the aorta at systemic pressure. Additionally, because the right ventricle can enlarge from the increase in diastolic volume resulting from diastolic flow through the conduit, there is a possibility of subsequent biventricular repair should the sinusoids regress. In this, our first patient, we chose to place the right ventricle to aorta conduit when the child's heart and mediastinal space were somewhat larger (ie, at the time of the Fontan). It may, however, be preferable to decompress the right ventricle earlier, either at the time of hemi-Fontan or even in the neonatal period. The theoretical advantages of minimizing progressive changes in the coronary arteries and the development of tricuspid insufficiency may be offset, however, by technical difficulties, mediastinal space considerations, and the safety of reoperation with a substernal conduit. As we progress with this technique these issues will be clarified.
References 1. Coles J, Williams WG, Trusler GA, Lightfoot N, Freedom RM. Surgical considerations and outcome. In: Freedom RM, ed. Pulmonary atresia with intact ventricular septum. New York: Futura, 1989:249-57. 2. Fyfe DA, Edwards WD, Driscoll DJ. Myocardial ischemia in patients with pulmonary atresia and intact ventricular septum. J Am Coll Cardiol 1986;8:402-6. 3. DeLeon SY, Duffy CE, Stout MJ. Myocardial infarction in children: causes and management. In: Pifarre R, ed. Cardiac surgery: state of the art reviews. Vol 6. Management of acute myocardial infarction and its complications. Philadelphia: Hanley and Belfus, 199217-35. 4. Yokose T, Doi M, Kimura Y, Ogata T. Ventriculo-coronary microcommunications in pulmonary atresia and sequential changes of coronary arteries. Acta Pathol Jpn 1987;371033-40. 5. Wilson GJ, Freedom RM, Koike K, Perrin D. The coronary arteries: anatomy and histopathology. In: Freedom RM, ed. Pulmonary atresia with intact ventricular septum. New York: Futura, 1989:75-88.
CASE REPORT IZZAT ET AL RETROGRADE CARDIOPLEGIA AND AGGLUTINATION
1395
Waldman JD, Lamberti JJ, Mathewson JW, George L. Surgical closure of the tricuspid valve for pulmonary atresia, intact ventricular septum, and right ventricle to coronary artery communications. Pediatr Cardiol 1984;5:2214. Williams WG, Burrows P, Freedom RM, et al. Thromboexclusion of the right ventricle in children with pulmonary atresia and intact ventricular septum. J Thorac Cardiovasc Surg 1991;101:222-9. Stein DG, Laks H, Drinkwater DC, et al. Results of total cavopulmonary connection in the treatment of patients with a functional single ventricle. J Thorac Cardiovasc Surg 1991;102: 280-7.
Use of Retrograde Cold Crystalloid Cardioplegia in a Patient With Unexpected Cold Agglutination Mohammad Bashar Izzat, FRCS, Pala B. Rajesh, FRCS, and Geoffrey H. Smith, FRCS Department of Cardiothoracic Surgery, Northern General Hospital, Sheffield, United Kingdom
Undetected cold agglutinins were encountered in a patient undergoing coronary artery bypass grafting using antegrade cold blood cardioplegia. Macroemboli were infused into the coronary arterial tree. These were flushed out by the use of retrograde cold crystalloid cardioplegia. Activated cold agglutinins may be hazardous in cold blood cardioplegia. (Ann T ~ O Y StlYg U C 2993;56:1395-7)
C
old agglutinins cause aggregation of red blood cells when activated by low temperatures. Because of the use of mild or deep hypothermia in cardiopulmonary bypass procedures, many cardiac surgical units routinely test for cold agglutinins and determine the temperatures at which they become activated. We report a case in which agglutination of red blood cells occurred during antegrade cold blood cardioplegia infusion and led to embolization in the coronary microcirculation. Infusion of cold crystalloid cardioplegia by the retrograde coronary sinus route seemed to be effective in preventing any damage to the myocardium. Laboratory procedures were reviewed and a policy of routine testing for cold agglutinins was introduced. A 58-year-old woman was admitted for coronary artery bypass grafting. Cardiac catheterization had shown good left ventricular function and triple-vessel disease. Her routine preoperative investigations did not include testing for cold antibodies below room temperature as this was the blood bank practice. At operation, she was placed on cardiopulmonary bypass with aortic and bicaval cannulaAccepted for publication March 18, 1993 Address reprint requests to Mr Izzat, Department of Cardiac Surgery, Bristol Royal Infirmary, Bristol 852 8HW, United Kingdom.