- Email: [email protected]
Minimally invasive direct coronary artery bypass controversy: the truly minimally invasive coronary artery bypass versus the “H” graft
Ann Thorac Surg 2000;69:1295–1302
CORRESPONDENCE
1297
innominate vein, may have been responsible for aortic buckling and segmental narrowing. Microdeletions in chromosome 22q11 may result in insufficiency of the neural crest cells and developmental abnormalities in the conotruncus and the embryonic pharyngeal arches [2, 4]. The high aortic arch in our case is a frequent finding in cases with tetralogy associated with 22q11 deletions [4]. Coarctation repair followed immediately or later by tetralogy repair was successful in 4 of the 5 operative survivors.
References
Amir Elami, MD
Minimally Invasive Direct Coronary Artery Bypass Controversy: The Truly Minimally Invasive Coronary Artery Bypass Versus the “H” Graft To the Editor:
Department of Cardiothoracic Surgery Hadassah University Hospital PO Box 12000 Jerusalem 91120, Israel e-mail: [email protected].
References 1. Ad N, Vidne BA. Coarctation of the aorta with right aortic arch: surgical technique and new classification. Ann Thorac Surg 1999;67:1125–9. 2. McElhinney DB, Tworetzky W, Hanley FL, Rudolph AM. Congenital obstructive lesions of the right aortic arch. Ann Thorac Surg 1999;67:1194 –202. 3. Elami A, Rein AJJT, Preminger T, Milgalter E. Tetralogy of Fallot, absent pulmonary valve, partial anomalous pulmonary venous return and coarctation of the aorta. Int J Cardiol 1995; 52:203– 6. 4. Momma K. Tetralogy of Fallot, absent pulmonary valve and coarctation of the aorta [Letter]. Int J Cardiol 1996;54:287.
Reply To the Editor: We read with interest Dr Elami’s letter and agree that tetralogy of Fallot right aortic arch and coarctation of the aorta is a rare combination of congenital anomalies. Moreover, we feel that the pathophysiology and the surgical approach should be discussed in detail. However, in our article we specifically discussed the rare combination of right aortic arch and coarctation of the aorta without additional intracardiac congenital malformations. We also discussed a new classification for right aortic arch which we feel is simple and easy to use [1]. The group from the University of San Francisco discussed in more detail congenital obstructive lesions of the right aortic arch and the clinical implications of such anomalies. In their review they discussed in detail the hemodynamic theory for coarctation as well as the high prevalence of chromosomal and genetic abnormalities in patients with right aortic arch [2]. Regarding the theoretical explanation that Dr Elami suggested in his letter, although it is very attractive, we do not believe that it can be implicated to tetralogy of Fallot and right aortic arch in general as it is a relatively common association. One should expect to diagnose aortic coarctation more often under the same circumstances. Niv Ad, MD Bernardo A. Vidne, MD Department of Cardiothoracic Surgery Rabin Medical Center Beilinson Campus Petach Tikva 49100, Israel © 2000 by The Society of Thoracic Surgeons Published by Elsevier Science Inc
1. Ad N, Vidne BA. Coarctation of the aorta with right aortic arch: surgical technique and new classification. Ann Thorac Surg 1999;67:1125–9. 2. McElhinney DB, Tworetzky W, Hanley FL, Rudolph AM. Congenital obstructive lesions of the right aortic arch. Ann Thorac Surg 1999;67:1194 –202.
The recent case report by Miyaji and colleagues [1] brings to the forefront some controversial issues in minimally invasive direct coronary artery bypass (MIDCAB) surgical procedures. In their article [1], a saphenous vein graft was placed between the left internal mammary artery (LIMA) and the left anterior descending coronary artery (LAD) to avoid the stress of mobilizing the LIMA as the patient was elderly and had significant comorbidities. We are entirely in agreement with this approach [2], and in our original article we also described additional ways of reducing surgical stress. The platform stabilizer should be attached to the operating room table rather than to the patient’s rib cage to reduce chest wall trauma. Removal of appropriate intercostal nerves and implantation of a pain catheter for postoperative bupivacaine injections also contribute to a striking reduction in postoperative pain and morbidity. From this point on, however, we find ourselves in disagreement with Miyaji and colleagues’ technique. The “H” graft is essentially an extended side-to-side LIMA-to-LAD anastomosis that leaves the distal internal mammary artery (IMA) patent and in continuity with the LAD. As the authors state, this may “detract from the blood flow going to the coronary artery.” It would thus probably be better in these cases to use the truly minimally invasive coronary artery bypass (TRUCAB) technique [3], in which the IMA distal to the anastomosis, the draining limb of the “H” arrangement, is clipped to prevent steal. We have found that using a clip to occlude the distal IMA results in increased flow in the conduit. In addition, once the distal IMA is removed from the equation, it is easy to measure simultaneous pressures in the proximal IMA and in the conduit going to the LAD. In this way, it can be established that there is a satisfactory diastolic pressure gradient during the operation, and if necessary, appropriate corrections can be made [4]. Unfortunately, with the “H” arrangement, this critical measurement cannot be made. Another point of contention relates to the lie of the graft. In the “H” graft technique, as the name implies, the conduit necessarily enters the coronary artery at a right angle. This may cause turbulence in the lumen of the LAD and may contribute to the premature formation of neointimal hyperplasia. In the TRUCAB technique, the graft is positioned so that it enters the coronary artery at an acute angle, in the manner of a freeway on-ramp. Blood from the graft merges with the extant coronary blood flow in a hemodynamically superior manner. The direct LIMA-to-LAD anastomosis is the gold standard in MIDCAB surgical procedures. Because it is technically so easy to perform, it is tempting to use the TRUCAB instead of the MIDCAB. However, until it is proved that long-term patency of the TRUCAB is equivalent to that of conventional MIDCAB, the 0003-4975/00/$20.00
1298
CORRESPONDENCE
TRUCAB technique is best reserved for use as a palliative procedure in the high-risk patient population in whom there is no intention of ever reoperating. In this context, there may be a small subset of younger patients in whom the “H” arrangement could be used as a temporizing procedure when it is anticipated that the whole length of the IMA will be needed for more extensive revascularization procedures in the years ahead. Alan S. Coulson, MD, PhD Shahroukh A. Bakhshay, MD Timothy J. Sloan, MD Michael F. Borges, MD Dameron Hospital Heart Institute 420 W Acacia St Stockton, CA 95203 e-mail: [email protected].
References 1. Miyaji K, Wolf RK, Flege JB. Minimally invasive direct coronary artery bypass using “H” graft for pleural symphysis. Ann Thorac Surg 1999;68:234–5. 2. Coulson AS, Bakhshay SA, Borges M. Modification of minimally invasive coronary artery bypass surgery for high-risk patients. Surg Rounds 1998;21:126–38. 3. Coulson AS, Bakhshay SA, Spohn P, Borges M. Truly minimally invasive coronary artery bypass: the TRUCAB [Letter]. J Thorac Cardiovasc Surg 1998;116:181. 4. Coulson AS, Bakhshay SA. The “T-MIDCAB” procedure. Use of extension grafts from the undisturbed internal mammary artery in high-risk patients. Heart Surg Forum 1998;1:54 –9.
Anaphylactic Aprotinin Reaction To the Editor: We refer to the article by Cohen and colleagues [1] presenting the unusual case of a 3.5-year-old boy with a near-fatal reaction to a test dose of aprotinin administered intravenously before complete surgical repair of tetralogy of Fallot. The boy survived thanks to resuscitation using cardiopulmonary bypass support. An enzyme-linked immunosorbent assay (ELISA) revealed aprotinin-specific IgE. Former contacts or cross-sensitizations seemed to be disclosed. We congratulate the authors for managing this near-fatal situation and saving the boy’s life, but question some details of the case. The history as presented does not disclose previous aprotinin contacts. However, formation of aprotinin-specific IgE is very improbable without former antigen contacts. As intravenous contacts and cross-sensitizations are ruled out, hidden local contacts by fibrin tissue adhesives have to be considered. Most commercially available fibrin sealants contain small doses of aprotinin which can induce temporarily detectable levels of specific IgE as we have observed in a study of 49 children [2]. Even self-made fibrin glues may contain aprotinin [3]. Repeated local contacts can also cause generalized allergic reactions [4]. In the present case report we miss a statement on the possibility of former local aprotinin contacts although it had not been documented. The formation of allergen-specific antibodies is a timedependent dynamic process. Antibody screening tests must be interpreted with regard to the time lapse between the last allergen contact and the time of antibody screening. Concerning aprotinin, we have made some observations, which could con© 2000 by The Society of Thoracic Surgeons Published by Elsevier Science Inc
Ann Thorac Surg 2000;69:1295–1302
tribute to the discussion of the present case. Aprotinin-specific IgE may become detectable 1 week after primary aprotinin contact [2]. Consequently, only positive IgE tests dating from before or immediately after the reaction indicate preexistent sensitization. If the highly positive IgE test in this boy dates from later than a few days after the reaction, it can also be due to the primary immune response to the test dose. Then the adverse reaction would not have been IgE mediated and thus not anaphylactic. However, this consideration does not rule out aprotinin from being the causative agent, because there is still the possibility of an antibody-independent anaphylactoid reaction. For precise assessment of the actual mechanism of the case presented, the authors need to report the exact time lapse between the incriminated aprotinin administration and the time of IgE testing thereafter. According to our experience, it is extremely difficult to obtain reproducible ELISA results for aprotinin-specific IgE as the authors did. This is due to the extremely low amount of specific serum IgE. Therefore we rely on a fluorescence enzyme immunoassay, which is more sensitive for allergen-specific IgE. We do agree with Cohen and colleagues that the possibility of an allergic reaction should be considered whenever aprotinin is used. But we have doubts concerning the interpretation of the present case as an anaphylactic reaction due to a primary exposure. Wolfram Beierlein, MD Albertus M. Scheule, MD Gerhard Ziemer, MD, PhD Division of Thoracic, Cardiac and Vascular Surgery Eberhard-Karls-University Tu¨bingen Hoppe-Seyler-Str 3 D-72076 Tu¨bingen, Germany
References 1. Cohen DM, Norberto J, Cartabuke R, Ryu G. Severe anaphylactic reaction after primary exposure to aprotinin. Ann Thorac Surg 1999;67:837– 8. 2. Scheule AM, Beierlein W, Wendel HP, Eckstein FS, Heinemann MK, Ziemer G. Fibrin sealant, aprotinin, and immune response in children undergoing operations for congenital heart disease. J Thorac Cardiovasc Surg 1998;115:883–9. 3. Spotnitz WD. Fibrin sealant in the United States: clinical use at the University of Virginia. Thromb Haemost 1995;74:482–5. 4. Beierlein W, Scheule AM, Antoniadis G, Braun C, Schosser R. An immediate allergic skin reaction to aprotinin after reexposure to fibrin sealant. Transfusion (in press).
Collagen-Thrombin-Plasma Composite Hemostat To the Editor: In connection with the paper: “A sprayable hemostat containing fibrillar collagen, bovine thrombin, and autologous plasma,” I would like to sound a serious caveat. As the paper illustrates, microfibrillar collagen is a needle-shaped substance with a small diameter and a considerable length. We have also found it (mixed with plasma components) to be most effective in inducing hemostasis [1]. Our studies, however, also revealed that if shed blood, which contains microfibrillar collagen, is reintroduced into the circulation, such as it may occur through cellsaver devices, it has a high potential of causing severe organ, 0003-4975/00/$20.00
CORRESPONDENCE
1297
innominate vein, may have been responsible for aortic buckling and segmental narrowing. Microdeletions in chromosome 22q11 may result in insufficiency of the neural crest cells and developmental abnormalities in the conotruncus and the embryonic pharyngeal arches [2, 4]. The high aortic arch in our case is a frequent finding in cases with tetralogy associated with 22q11 deletions [4]. Coarctation repair followed immediately or later by tetralogy repair was successful in 4 of the 5 operative survivors.
References
Amir Elami, MD
Minimally Invasive Direct Coronary Artery Bypass Controversy: The Truly Minimally Invasive Coronary Artery Bypass Versus the “H” Graft To the Editor:
Department of Cardiothoracic Surgery Hadassah University Hospital PO Box 12000 Jerusalem 91120, Israel e-mail: [email protected].
References 1. Ad N, Vidne BA. Coarctation of the aorta with right aortic arch: surgical technique and new classification. Ann Thorac Surg 1999;67:1125–9. 2. McElhinney DB, Tworetzky W, Hanley FL, Rudolph AM. Congenital obstructive lesions of the right aortic arch. Ann Thorac Surg 1999;67:1194 –202. 3. Elami A, Rein AJJT, Preminger T, Milgalter E. Tetralogy of Fallot, absent pulmonary valve, partial anomalous pulmonary venous return and coarctation of the aorta. Int J Cardiol 1995; 52:203– 6. 4. Momma K. Tetralogy of Fallot, absent pulmonary valve and coarctation of the aorta [Letter]. Int J Cardiol 1996;54:287.
Reply To the Editor: We read with interest Dr Elami’s letter and agree that tetralogy of Fallot right aortic arch and coarctation of the aorta is a rare combination of congenital anomalies. Moreover, we feel that the pathophysiology and the surgical approach should be discussed in detail. However, in our article we specifically discussed the rare combination of right aortic arch and coarctation of the aorta without additional intracardiac congenital malformations. We also discussed a new classification for right aortic arch which we feel is simple and easy to use [1]. The group from the University of San Francisco discussed in more detail congenital obstructive lesions of the right aortic arch and the clinical implications of such anomalies. In their review they discussed in detail the hemodynamic theory for coarctation as well as the high prevalence of chromosomal and genetic abnormalities in patients with right aortic arch [2]. Regarding the theoretical explanation that Dr Elami suggested in his letter, although it is very attractive, we do not believe that it can be implicated to tetralogy of Fallot and right aortic arch in general as it is a relatively common association. One should expect to diagnose aortic coarctation more often under the same circumstances. Niv Ad, MD Bernardo A. Vidne, MD Department of Cardiothoracic Surgery Rabin Medical Center Beilinson Campus Petach Tikva 49100, Israel © 2000 by The Society of Thoracic Surgeons Published by Elsevier Science Inc
1. Ad N, Vidne BA. Coarctation of the aorta with right aortic arch: surgical technique and new classification. Ann Thorac Surg 1999;67:1125–9. 2. McElhinney DB, Tworetzky W, Hanley FL, Rudolph AM. Congenital obstructive lesions of the right aortic arch. Ann Thorac Surg 1999;67:1194 –202.
The recent case report by Miyaji and colleagues [1] brings to the forefront some controversial issues in minimally invasive direct coronary artery bypass (MIDCAB) surgical procedures. In their article [1], a saphenous vein graft was placed between the left internal mammary artery (LIMA) and the left anterior descending coronary artery (LAD) to avoid the stress of mobilizing the LIMA as the patient was elderly and had significant comorbidities. We are entirely in agreement with this approach [2], and in our original article we also described additional ways of reducing surgical stress. The platform stabilizer should be attached to the operating room table rather than to the patient’s rib cage to reduce chest wall trauma. Removal of appropriate intercostal nerves and implantation of a pain catheter for postoperative bupivacaine injections also contribute to a striking reduction in postoperative pain and morbidity. From this point on, however, we find ourselves in disagreement with Miyaji and colleagues’ technique. The “H” graft is essentially an extended side-to-side LIMA-to-LAD anastomosis that leaves the distal internal mammary artery (IMA) patent and in continuity with the LAD. As the authors state, this may “detract from the blood flow going to the coronary artery.” It would thus probably be better in these cases to use the truly minimally invasive coronary artery bypass (TRUCAB) technique [3], in which the IMA distal to the anastomosis, the draining limb of the “H” arrangement, is clipped to prevent steal. We have found that using a clip to occlude the distal IMA results in increased flow in the conduit. In addition, once the distal IMA is removed from the equation, it is easy to measure simultaneous pressures in the proximal IMA and in the conduit going to the LAD. In this way, it can be established that there is a satisfactory diastolic pressure gradient during the operation, and if necessary, appropriate corrections can be made [4]. Unfortunately, with the “H” arrangement, this critical measurement cannot be made. Another point of contention relates to the lie of the graft. In the “H” graft technique, as the name implies, the conduit necessarily enters the coronary artery at a right angle. This may cause turbulence in the lumen of the LAD and may contribute to the premature formation of neointimal hyperplasia. In the TRUCAB technique, the graft is positioned so that it enters the coronary artery at an acute angle, in the manner of a freeway on-ramp. Blood from the graft merges with the extant coronary blood flow in a hemodynamically superior manner. The direct LIMA-to-LAD anastomosis is the gold standard in MIDCAB surgical procedures. Because it is technically so easy to perform, it is tempting to use the TRUCAB instead of the MIDCAB. However, until it is proved that long-term patency of the TRUCAB is equivalent to that of conventional MIDCAB, the 0003-4975/00/$20.00
1298
CORRESPONDENCE
TRUCAB technique is best reserved for use as a palliative procedure in the high-risk patient population in whom there is no intention of ever reoperating. In this context, there may be a small subset of younger patients in whom the “H” arrangement could be used as a temporizing procedure when it is anticipated that the whole length of the IMA will be needed for more extensive revascularization procedures in the years ahead. Alan S. Coulson, MD, PhD Shahroukh A. Bakhshay, MD Timothy J. Sloan, MD Michael F. Borges, MD Dameron Hospital Heart Institute 420 W Acacia St Stockton, CA 95203 e-mail: [email protected].
References 1. Miyaji K, Wolf RK, Flege JB. Minimally invasive direct coronary artery bypass using “H” graft for pleural symphysis. Ann Thorac Surg 1999;68:234–5. 2. Coulson AS, Bakhshay SA, Borges M. Modification of minimally invasive coronary artery bypass surgery for high-risk patients. Surg Rounds 1998;21:126–38. 3. Coulson AS, Bakhshay SA, Spohn P, Borges M. Truly minimally invasive coronary artery bypass: the TRUCAB [Letter]. J Thorac Cardiovasc Surg 1998;116:181. 4. Coulson AS, Bakhshay SA. The “T-MIDCAB” procedure. Use of extension grafts from the undisturbed internal mammary artery in high-risk patients. Heart Surg Forum 1998;1:54 –9.
Anaphylactic Aprotinin Reaction To the Editor: We refer to the article by Cohen and colleagues [1] presenting the unusual case of a 3.5-year-old boy with a near-fatal reaction to a test dose of aprotinin administered intravenously before complete surgical repair of tetralogy of Fallot. The boy survived thanks to resuscitation using cardiopulmonary bypass support. An enzyme-linked immunosorbent assay (ELISA) revealed aprotinin-specific IgE. Former contacts or cross-sensitizations seemed to be disclosed. We congratulate the authors for managing this near-fatal situation and saving the boy’s life, but question some details of the case. The history as presented does not disclose previous aprotinin contacts. However, formation of aprotinin-specific IgE is very improbable without former antigen contacts. As intravenous contacts and cross-sensitizations are ruled out, hidden local contacts by fibrin tissue adhesives have to be considered. Most commercially available fibrin sealants contain small doses of aprotinin which can induce temporarily detectable levels of specific IgE as we have observed in a study of 49 children [2]. Even self-made fibrin glues may contain aprotinin [3]. Repeated local contacts can also cause generalized allergic reactions [4]. In the present case report we miss a statement on the possibility of former local aprotinin contacts although it had not been documented. The formation of allergen-specific antibodies is a timedependent dynamic process. Antibody screening tests must be interpreted with regard to the time lapse between the last allergen contact and the time of antibody screening. Concerning aprotinin, we have made some observations, which could con© 2000 by The Society of Thoracic Surgeons Published by Elsevier Science Inc
Ann Thorac Surg 2000;69:1295–1302
tribute to the discussion of the present case. Aprotinin-specific IgE may become detectable 1 week after primary aprotinin contact [2]. Consequently, only positive IgE tests dating from before or immediately after the reaction indicate preexistent sensitization. If the highly positive IgE test in this boy dates from later than a few days after the reaction, it can also be due to the primary immune response to the test dose. Then the adverse reaction would not have been IgE mediated and thus not anaphylactic. However, this consideration does not rule out aprotinin from being the causative agent, because there is still the possibility of an antibody-independent anaphylactoid reaction. For precise assessment of the actual mechanism of the case presented, the authors need to report the exact time lapse between the incriminated aprotinin administration and the time of IgE testing thereafter. According to our experience, it is extremely difficult to obtain reproducible ELISA results for aprotinin-specific IgE as the authors did. This is due to the extremely low amount of specific serum IgE. Therefore we rely on a fluorescence enzyme immunoassay, which is more sensitive for allergen-specific IgE. We do agree with Cohen and colleagues that the possibility of an allergic reaction should be considered whenever aprotinin is used. But we have doubts concerning the interpretation of the present case as an anaphylactic reaction due to a primary exposure. Wolfram Beierlein, MD Albertus M. Scheule, MD Gerhard Ziemer, MD, PhD Division of Thoracic, Cardiac and Vascular Surgery Eberhard-Karls-University Tu¨bingen Hoppe-Seyler-Str 3 D-72076 Tu¨bingen, Germany
References 1. Cohen DM, Norberto J, Cartabuke R, Ryu G. Severe anaphylactic reaction after primary exposure to aprotinin. Ann Thorac Surg 1999;67:837– 8. 2. Scheule AM, Beierlein W, Wendel HP, Eckstein FS, Heinemann MK, Ziemer G. Fibrin sealant, aprotinin, and immune response in children undergoing operations for congenital heart disease. J Thorac Cardiovasc Surg 1998;115:883–9. 3. Spotnitz WD. Fibrin sealant in the United States: clinical use at the University of Virginia. Thromb Haemost 1995;74:482–5. 4. Beierlein W, Scheule AM, Antoniadis G, Braun C, Schosser R. An immediate allergic skin reaction to aprotinin after reexposure to fibrin sealant. Transfusion (in press).
Collagen-Thrombin-Plasma Composite Hemostat To the Editor: In connection with the paper: “A sprayable hemostat containing fibrillar collagen, bovine thrombin, and autologous plasma,” I would like to sound a serious caveat. As the paper illustrates, microfibrillar collagen is a needle-shaped substance with a small diameter and a considerable length. We have also found it (mixed with plasma components) to be most effective in inducing hemostasis [1]. Our studies, however, also revealed that if shed blood, which contains microfibrillar collagen, is reintroduced into the circulation, such as it may occur through cellsaver devices, it has a high potential of causing severe organ, 0003-4975/00/$20.00