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Are arterial grafts better or worse than applied physiology teaches?
Are Arterial Grafts Better or Worse Than Applied Physiology Teaches? Thomas A. Orszulak, MD Department of Thoracic and Cardiovascular Surgery, Mayo Clinic, Rochester, Minnesota The road to excess leads to the palace of wisdom William Blake, 1757-1827 English poet, artist
S
urgical revascularization of the myocardium has evolved into an extremely safe, predictable, longlasting, and life-prolonging procedure. Much has been learned regarding the timing, extent, method, risk factors, and limitations that direct the implementation of this procedure. We have learned that coronary artery bypass is not a cure for coronary atherosclerosis but merely a temporizing measure of control of the disease. This has been most evident in the increasing incidence of reoperations that are encountered in current surgical practice in this country and abroad [l, 21. We have also learned that the most common cause of recurrent angina and subsequent reoperation is graft disease and attrition, not progression of native coronary disease. The intuitive surgeon may reason: if a conduit would resist atherosclerosis and remain patent, the results would be better and last longer. It may be difficult to distinguish the motivational factors for improved patency: better patient survival or lower reoperation rates. See also page 951. Use of the internal thoracic artery (ITA) has been supported by superior patency rate and enhanced by evidence of its independence as a factor for survival in coronary revascularization [3,41. It is not surprising that complete coronary revascularization performed with arterial grafts is on the increase [5];if one is good, more must be better-right? Well, yes and no, to comply with current conventional wisdom and politically correct thought. To achieve complete revascularization with arterial grafts is a sound objective but is not applicable to all patients or clinical situations. Use of arterial grafts for myocardial revascularization may be necessary due to surgically absent or diseased saphenous veins, but the basic limitations imposed by arterial physiology and anatomy may not permit complete arterial revascularization. This is perhaps the thrust of the article by Tedoriya and associates [6]in this issue of The Annals of Thoracic Surgery. Tedoriya and associates have conducted an intriguing study in dogs comparing the flow and perfusion pressure of grafts originating in one of three progressively distal aortic locations. The anatomic origins are to correlate with Address reprint requests to Dr Orszulak, Department of Thoracic and Cardiovascular Surgery, Mayo Clinic, 200 First St SW, Rochester, MN 55905.
0 1993 by
The Society of Thoracic Surgeons
the proximal saphenous vein graft or free arterial grafts arising from the ascending aorta, the ITA, and the gastroepiploic artery. The construction of the arterial model includes three grafts (1ITA and 2 polytetrafluoroethylene) anastamosed in confluence to a canine femoral artery, which is in turn placed into the canine left anterior descending artery. Flows were measured with a fiberoptic transducer on the left anterior descending artery, and pressure was recorded from the femoral artery segment with an ultrasonic flow meter. Although the techniques of measurement may warrant discussion from the basic laboratory aspect, I am concerned about two factors in their model that diffuse the reliability of their conclusions when projected to clinical practice. One is the difference in diameter of the conduits. The 0.5-mm difference, when used in Poiseuille’s equation for flow, is raised to the fourth power and for the ITA (2.5mm) and polytetrafluoroethylene graft (3 mm) translate into factors of 39 and 81, respectively. Second, the rigidity and differing length of polytetrafluoroethylene may affect the flow and pressure measurement of this study, although perhaps not significantly enough to change the basic physiologic principle. It does cloud the correlation and application to clinical coronary operations. Tedoriya and associates’ endeavors are a variation of the basic physiology experiments performed in evaluating the regulation of pressure and flow and illustrated by Borelli more than 300 years ago, although the sophistication of present technology refines the experiment. As learned from basic physiology laboratories the farther away from the heart pressure is measured, the higher the systolic pressure and the lower the diastolic pressure becomes. Of perhaps little significance to visceral blood flow, this effect of lower diastolic pressure is important to the myocardium due to the heart’s diastolic dependence for flow. In steady state, at rest, this provides little concern because the mean diastolic pressure normally remains greater than 70 to 80 mm Hg. However, coronary artery grafts originating distal to the ascending aorta may experience alterations in flow. This concern may be amplified by the dynamic ability of arterial grafts to respond to pharmacologic or exertional stimuli [7-lo].The disparity in these concepts is that clinically, arterial coronary grafting has been very successful. Tedoriya and associates imply arterial grafts (those not directly anastomosed to the ascending aorta) carry inferior flow and cause myocardial hypoperfusion. One clinical reference quoted to substantiate this is an article by Jones and colleagues [ll], in which 5 of 712 patients undergoing consecutive bypass operations demonstrated hypoperfuAnn Thorac Surg 1993;56:809-11
0003-4975/93/$6.00
810
EDITORIAL ORSZULAK ARTERIAL GRAFTS
sion of myocardium grafted with ITAs. Before we can establish a legitimate cause and effect, we must closely examine the cases of "hypoperfusion." Three of the 5 were reoperations and had combinations of sequential, in situ, and free arterial grafts placed to diseased coronary arteries, and 2 of the 3 had their patent but diseased saphenous vein grafts ligated at the time of operation. The third case made no mention of ligation of grafts; however, the ITAs used were noted to be smaller than the target coronary arteries. The remaining 2 primary procedures involved the use of graft arteries smaller than their target vessels, and these were used for sequential grafts. These situations, as quoted in that reference, have since been rectified with prudent planning preoperatively and careful assessment of the ITA size and flow with flexibility in application of these arteries to minimize or eliminate the supply and demand mismatch. Tedoriya and colleagues have not developed nor defined a new principle with their article, and yet it seems that their concern has appropriate validity. What circumstances in arterial grafting lend themselves to problems and how can they be avoided? Problems may occur in legitimate surgical zeal to "cure" the disease or problem. The recurrence of coronary artery disease is predominantly manifest with graft attrition-eliminate the attrition, improve the result and thus longevity. Perhaps in the quest for immortality we have bypassed reason and have demanded too much of our procedures. Surgeons may be forced into total arterial revascularizations due to the prior use, absence, or disease of the venous system usually available for revascularization. Another less defensible, more defensive reason is as a marketing tool to acquire patients with claims of performing complete arterial revascularization. The desire for long-term patency with arterial grafts is admirable, but the application may be disastrous with the blame erroneously directed to the procedure, not the plan. It should not be difficult to avoid the potential mismatch described above. It requires constant willingness to adjust the operation to fit the situation that is dictated by the clinical presentation and the anatomy. It also requires the realization that little evidence currently exists to justify multiple arterial grafting. Loop and associates [3] and Cameron and co-workers [4] have independently described the improved survival imparted with the use of a single ITA. A recent update by Naunheim and associates [12] described improved freedom from subsequent myocardial infarction and recurrent angina with the use of bilateral ITAs, but there was no added improvement in survival with the addition of a second arterial graft. The update is somewhat marred by a 9% operative mortality, which was reported to have been reduced to 2.2% since 1985. Avoiding the possibility of hypoperfusion requires recognition of a potentially catastrophic situation. Replacing diseased but patent grafts rather than supplementing them requires a conduit (vein or artery) as large as the grafted artery or the original graft. Using an arterial conduit as a sequential graft if the graft itself is smaller than either target vessel may lead to ischemia, especially
Ann Thorac Surg 1993;56:809-11
in reoperations. This same graft may be very satisfactory as a single graft. The impact of myocardial hypertrophy greatly narrows the margin for error with arterial grafts. I do not believe arterial grafts are contraindicated in left ventricular hypertrophy if the ejection fraction is normal or the graft is large, but any decision must withstand close scrutiny for possible inadequate flow. One should be circumspect regarding preinfarction patients or patients in unstable condition. Our goal with these patients primarily is survival and myocardial preservation and secondarily, long-term patency. The forced fit of arterial grafts in patients with angina, electrocardiographic changes of ischemia or hemodynamic instability will lead to an increased risk of inadequate flow, "spasm," or infarction. Recognizing that the use of complete arterial grafting in this situation is excessive or inappropriate is one step closer to the clinical wisdom of arterial coronary grafting. I have not harvested the ITA on bypass in the situation of marked myocardial ischemia, although this is an option available if it is deemed mandatory to use arterial grafts in patients in severely unstable condition. The most frequent multiple arterial grafting done at our institution is bilateral ITAs, usually in the younger patient; in my practice, more than 92% of patients coming to coronary revascularization receive one or two ITAs. This includes the continuous increase in reoperations, approaching 15% to 18% for coronary procedures. We also encounter patients with multiple coronary and peripheral vascular procedures but are desirous of exhausting the greater and lesser saphenous veins before proceeding to the gastroepiploic or inferior epigastric arteries. My anecdotal experience with the gastroepiploic artery has been with in situ grafts and solely to the right posterior descending artery. The inferior epigastric arteries have only been used for grafts to the diagonal system as single grafts, again anecdotally. I believe we have learned that at the time of reoperation, with patent but diseased vein grafts, arterial grafts can add to but less likely replace the flow through a narrowed saphenous vein graft. Prior recommendations included the early ligation of diseased saphenous vein grafts, which may minimize or eliminate the opportunity of arterial grafting to that vessel but has diminished in concern with the improved protection of retrograde techniques for delivery of cardioplegia and flushing of debris [13]. If a patient is symptomatic from coronary artery disease to the point of requiring an operation or reoperation, the final application for arterial use can only be determined after review of the coronary arteriogram for possible placement and number of distal targets. This is followed by the arteriographic or intraoperative examination of the arterial graft in relation to size, length, and free flow. Discarding grafts, especially ITAS, is usually unnecessary unless they are damaged during harvesting. If the flow is unsatisfactory with papaverine bathing, a 1-mm probe may be passed proximally, reluctantly and gently. If still questionable, the graft may be divided at its origin or point of obstruction and used as a free graft if length permits. Unless the ITA caliber is sufficient as a sequential graft, it should be used only as a single graft. Patients entering the operating room in a
Ann Thorac Surg 1993;56809-11
stable state without evidence of ongoing ischemia will be better served with a patent ITA graft than a saphenous vein graft. This is based on the ability of the arterial grafts to increase in size with time and dependent on the demand of distal runoff. This capability has been noted by neurosurgeons (Thoralf Sundt, MD, personal communication) in their use of the superficial temporal artery for revascularization of the internal carotid artery. This growth potential is not immediate and must be recognized as a strength not a limitation of the arterial grafts. The enlarging capability has not yet been described with the gastroepiploic and inferior epigastric arteries; however, physiologically it could occur if distal run-off stimulates it. Tedoriya and associates have thus served an important service by refocusing our attention on the limitations, not prohibitions, of use of arterial grafts. It will, however, require the prudent surgeon to apply this information appropriately to each clinical situation encountered and decide the indications, need, and number of arterial grafts and more so the logistics of their harvest, origin, and insertion to achieve the most appropriate revascularization possible.
References 1. Laird-Meeter K, van Domburg R, Bos E, Hugenholtz PG. Incidence and outcome of reintervention after coronary bypass surgery. Adv Cardiol 1988;36:13W. 2. Lytle B, Loop F. Coronary reoperations. Surg Clin North Am 1988;68:55940.
EDITORIAL ORSZULAK ARTERIAL GRAFTS
811
3. Loop F, Lytle BW, Cosgrove DM, et al. Influence of the internal-mammary-artery graft on 10-year survival and other cardiac events. N Engl J Med 1986;314:1-6. 4. Cameron A, Davis KB, Green GE, Myers WO, Pettinger M. Clinical implications of internal mammary artery bypass grafts: the Coronary Artery Surgery Study experience. Circulation 1988;77:815-9. 5. Buche M, Schoevaerdts JC, Louagie Y, et al. Use of the inferior epigastric artery for coronary bypass. J Thorac Cardiovasc Surg 1992;103:665-70. 6. Tedoriya T, Kawasuji M, Ueyama K, Sakakibara N, Takemura H, Watanabe Y. Physiologic characteristics of coronary artery bypass grafts. Ann Thorac Surg 1993;56:951-6. 7. DiNardo J, Bert A, Schwartz MJ, Johnson RG, Thurer RL, Weintraub RM. Effects of vasoactive drugs on flows through left internal mammary artery and saphenous vein grafts in man. J Thorac Cardiovasc Surg 1991;102:730-5. 8. Jett GK, Arcidi JM Jr, Dorsey LM, Hatcher CR Jr, Guyton RA. Vasoactive drug effects on blood flow in internal mammary artery and saphenous vein grafts. J Thorac Cardiovasc Surg 1987;94:2-11. 9. Koike R, Suma H, Kondo K, et al. Pharmacological response of internal mammary artery and gastroepiploic artery. Ann Thorac Surg 1990;50:38&6. 10. Kawasuji M, Tsujiguchi H, Tedoriya T, Taki J, Iwa T. Evaluation of postoperative flow capacity of internal mammary artery. J Thorac Cardiovasc Surg 1990;99:696-702. 11. Jones E, Lattouf 0, Weintraub W. Catastrophic consequences of internal mammary artery hypoperfusion. J Thorac Cardiovasc Surg 1989;98:902-7. 12. Naunheim K, Barner H, Fiore A. Update: Results of internal thoracic artery grafting over 15 years: single versus double grafts. Ann Thorac Surg 1992;53:71&8. 13. Perrault L, et al. Morbidity and mortality of reoperation for coronary artery bypass grafting: significance of atheromatous vein grafts. Can J Cardiol 1991;49:427-30.
S
urgical revascularization of the myocardium has evolved into an extremely safe, predictable, longlasting, and life-prolonging procedure. Much has been learned regarding the timing, extent, method, risk factors, and limitations that direct the implementation of this procedure. We have learned that coronary artery bypass is not a cure for coronary atherosclerosis but merely a temporizing measure of control of the disease. This has been most evident in the increasing incidence of reoperations that are encountered in current surgical practice in this country and abroad [l, 21. We have also learned that the most common cause of recurrent angina and subsequent reoperation is graft disease and attrition, not progression of native coronary disease. The intuitive surgeon may reason: if a conduit would resist atherosclerosis and remain patent, the results would be better and last longer. It may be difficult to distinguish the motivational factors for improved patency: better patient survival or lower reoperation rates. See also page 951. Use of the internal thoracic artery (ITA) has been supported by superior patency rate and enhanced by evidence of its independence as a factor for survival in coronary revascularization [3,41. It is not surprising that complete coronary revascularization performed with arterial grafts is on the increase [5];if one is good, more must be better-right? Well, yes and no, to comply with current conventional wisdom and politically correct thought. To achieve complete revascularization with arterial grafts is a sound objective but is not applicable to all patients or clinical situations. Use of arterial grafts for myocardial revascularization may be necessary due to surgically absent or diseased saphenous veins, but the basic limitations imposed by arterial physiology and anatomy may not permit complete arterial revascularization. This is perhaps the thrust of the article by Tedoriya and associates [6]in this issue of The Annals of Thoracic Surgery. Tedoriya and associates have conducted an intriguing study in dogs comparing the flow and perfusion pressure of grafts originating in one of three progressively distal aortic locations. The anatomic origins are to correlate with Address reprint requests to Dr Orszulak, Department of Thoracic and Cardiovascular Surgery, Mayo Clinic, 200 First St SW, Rochester, MN 55905.
0 1993 by
The Society of Thoracic Surgeons
the proximal saphenous vein graft or free arterial grafts arising from the ascending aorta, the ITA, and the gastroepiploic artery. The construction of the arterial model includes three grafts (1ITA and 2 polytetrafluoroethylene) anastamosed in confluence to a canine femoral artery, which is in turn placed into the canine left anterior descending artery. Flows were measured with a fiberoptic transducer on the left anterior descending artery, and pressure was recorded from the femoral artery segment with an ultrasonic flow meter. Although the techniques of measurement may warrant discussion from the basic laboratory aspect, I am concerned about two factors in their model that diffuse the reliability of their conclusions when projected to clinical practice. One is the difference in diameter of the conduits. The 0.5-mm difference, when used in Poiseuille’s equation for flow, is raised to the fourth power and for the ITA (2.5mm) and polytetrafluoroethylene graft (3 mm) translate into factors of 39 and 81, respectively. Second, the rigidity and differing length of polytetrafluoroethylene may affect the flow and pressure measurement of this study, although perhaps not significantly enough to change the basic physiologic principle. It does cloud the correlation and application to clinical coronary operations. Tedoriya and associates’ endeavors are a variation of the basic physiology experiments performed in evaluating the regulation of pressure and flow and illustrated by Borelli more than 300 years ago, although the sophistication of present technology refines the experiment. As learned from basic physiology laboratories the farther away from the heart pressure is measured, the higher the systolic pressure and the lower the diastolic pressure becomes. Of perhaps little significance to visceral blood flow, this effect of lower diastolic pressure is important to the myocardium due to the heart’s diastolic dependence for flow. In steady state, at rest, this provides little concern because the mean diastolic pressure normally remains greater than 70 to 80 mm Hg. However, coronary artery grafts originating distal to the ascending aorta may experience alterations in flow. This concern may be amplified by the dynamic ability of arterial grafts to respond to pharmacologic or exertional stimuli [7-lo].The disparity in these concepts is that clinically, arterial coronary grafting has been very successful. Tedoriya and associates imply arterial grafts (those not directly anastomosed to the ascending aorta) carry inferior flow and cause myocardial hypoperfusion. One clinical reference quoted to substantiate this is an article by Jones and colleagues [ll], in which 5 of 712 patients undergoing consecutive bypass operations demonstrated hypoperfuAnn Thorac Surg 1993;56:809-11
0003-4975/93/$6.00
810
EDITORIAL ORSZULAK ARTERIAL GRAFTS
sion of myocardium grafted with ITAs. Before we can establish a legitimate cause and effect, we must closely examine the cases of "hypoperfusion." Three of the 5 were reoperations and had combinations of sequential, in situ, and free arterial grafts placed to diseased coronary arteries, and 2 of the 3 had their patent but diseased saphenous vein grafts ligated at the time of operation. The third case made no mention of ligation of grafts; however, the ITAs used were noted to be smaller than the target coronary arteries. The remaining 2 primary procedures involved the use of graft arteries smaller than their target vessels, and these were used for sequential grafts. These situations, as quoted in that reference, have since been rectified with prudent planning preoperatively and careful assessment of the ITA size and flow with flexibility in application of these arteries to minimize or eliminate the supply and demand mismatch. Tedoriya and colleagues have not developed nor defined a new principle with their article, and yet it seems that their concern has appropriate validity. What circumstances in arterial grafting lend themselves to problems and how can they be avoided? Problems may occur in legitimate surgical zeal to "cure" the disease or problem. The recurrence of coronary artery disease is predominantly manifest with graft attrition-eliminate the attrition, improve the result and thus longevity. Perhaps in the quest for immortality we have bypassed reason and have demanded too much of our procedures. Surgeons may be forced into total arterial revascularizations due to the prior use, absence, or disease of the venous system usually available for revascularization. Another less defensible, more defensive reason is as a marketing tool to acquire patients with claims of performing complete arterial revascularization. The desire for long-term patency with arterial grafts is admirable, but the application may be disastrous with the blame erroneously directed to the procedure, not the plan. It should not be difficult to avoid the potential mismatch described above. It requires constant willingness to adjust the operation to fit the situation that is dictated by the clinical presentation and the anatomy. It also requires the realization that little evidence currently exists to justify multiple arterial grafting. Loop and associates [3] and Cameron and co-workers [4] have independently described the improved survival imparted with the use of a single ITA. A recent update by Naunheim and associates [12] described improved freedom from subsequent myocardial infarction and recurrent angina with the use of bilateral ITAs, but there was no added improvement in survival with the addition of a second arterial graft. The update is somewhat marred by a 9% operative mortality, which was reported to have been reduced to 2.2% since 1985. Avoiding the possibility of hypoperfusion requires recognition of a potentially catastrophic situation. Replacing diseased but patent grafts rather than supplementing them requires a conduit (vein or artery) as large as the grafted artery or the original graft. Using an arterial conduit as a sequential graft if the graft itself is smaller than either target vessel may lead to ischemia, especially
Ann Thorac Surg 1993;56:809-11
in reoperations. This same graft may be very satisfactory as a single graft. The impact of myocardial hypertrophy greatly narrows the margin for error with arterial grafts. I do not believe arterial grafts are contraindicated in left ventricular hypertrophy if the ejection fraction is normal or the graft is large, but any decision must withstand close scrutiny for possible inadequate flow. One should be circumspect regarding preinfarction patients or patients in unstable condition. Our goal with these patients primarily is survival and myocardial preservation and secondarily, long-term patency. The forced fit of arterial grafts in patients with angina, electrocardiographic changes of ischemia or hemodynamic instability will lead to an increased risk of inadequate flow, "spasm," or infarction. Recognizing that the use of complete arterial grafting in this situation is excessive or inappropriate is one step closer to the clinical wisdom of arterial coronary grafting. I have not harvested the ITA on bypass in the situation of marked myocardial ischemia, although this is an option available if it is deemed mandatory to use arterial grafts in patients in severely unstable condition. The most frequent multiple arterial grafting done at our institution is bilateral ITAs, usually in the younger patient; in my practice, more than 92% of patients coming to coronary revascularization receive one or two ITAs. This includes the continuous increase in reoperations, approaching 15% to 18% for coronary procedures. We also encounter patients with multiple coronary and peripheral vascular procedures but are desirous of exhausting the greater and lesser saphenous veins before proceeding to the gastroepiploic or inferior epigastric arteries. My anecdotal experience with the gastroepiploic artery has been with in situ grafts and solely to the right posterior descending artery. The inferior epigastric arteries have only been used for grafts to the diagonal system as single grafts, again anecdotally. I believe we have learned that at the time of reoperation, with patent but diseased vein grafts, arterial grafts can add to but less likely replace the flow through a narrowed saphenous vein graft. Prior recommendations included the early ligation of diseased saphenous vein grafts, which may minimize or eliminate the opportunity of arterial grafting to that vessel but has diminished in concern with the improved protection of retrograde techniques for delivery of cardioplegia and flushing of debris [13]. If a patient is symptomatic from coronary artery disease to the point of requiring an operation or reoperation, the final application for arterial use can only be determined after review of the coronary arteriogram for possible placement and number of distal targets. This is followed by the arteriographic or intraoperative examination of the arterial graft in relation to size, length, and free flow. Discarding grafts, especially ITAS, is usually unnecessary unless they are damaged during harvesting. If the flow is unsatisfactory with papaverine bathing, a 1-mm probe may be passed proximally, reluctantly and gently. If still questionable, the graft may be divided at its origin or point of obstruction and used as a free graft if length permits. Unless the ITA caliber is sufficient as a sequential graft, it should be used only as a single graft. Patients entering the operating room in a
Ann Thorac Surg 1993;56809-11
stable state without evidence of ongoing ischemia will be better served with a patent ITA graft than a saphenous vein graft. This is based on the ability of the arterial grafts to increase in size with time and dependent on the demand of distal runoff. This capability has been noted by neurosurgeons (Thoralf Sundt, MD, personal communication) in their use of the superficial temporal artery for revascularization of the internal carotid artery. This growth potential is not immediate and must be recognized as a strength not a limitation of the arterial grafts. The enlarging capability has not yet been described with the gastroepiploic and inferior epigastric arteries; however, physiologically it could occur if distal run-off stimulates it. Tedoriya and associates have thus served an important service by refocusing our attention on the limitations, not prohibitions, of use of arterial grafts. It will, however, require the prudent surgeon to apply this information appropriately to each clinical situation encountered and decide the indications, need, and number of arterial grafts and more so the logistics of their harvest, origin, and insertion to achieve the most appropriate revascularization possible.
References 1. Laird-Meeter K, van Domburg R, Bos E, Hugenholtz PG. Incidence and outcome of reintervention after coronary bypass surgery. Adv Cardiol 1988;36:13W. 2. Lytle B, Loop F. Coronary reoperations. Surg Clin North Am 1988;68:55940.
EDITORIAL ORSZULAK ARTERIAL GRAFTS
811
3. Loop F, Lytle BW, Cosgrove DM, et al. Influence of the internal-mammary-artery graft on 10-year survival and other cardiac events. N Engl J Med 1986;314:1-6. 4. Cameron A, Davis KB, Green GE, Myers WO, Pettinger M. Clinical implications of internal mammary artery bypass grafts: the Coronary Artery Surgery Study experience. Circulation 1988;77:815-9. 5. Buche M, Schoevaerdts JC, Louagie Y, et al. Use of the inferior epigastric artery for coronary bypass. J Thorac Cardiovasc Surg 1992;103:665-70. 6. Tedoriya T, Kawasuji M, Ueyama K, Sakakibara N, Takemura H, Watanabe Y. Physiologic characteristics of coronary artery bypass grafts. Ann Thorac Surg 1993;56:951-6. 7. DiNardo J, Bert A, Schwartz MJ, Johnson RG, Thurer RL, Weintraub RM. Effects of vasoactive drugs on flows through left internal mammary artery and saphenous vein grafts in man. J Thorac Cardiovasc Surg 1991;102:730-5. 8. Jett GK, Arcidi JM Jr, Dorsey LM, Hatcher CR Jr, Guyton RA. Vasoactive drug effects on blood flow in internal mammary artery and saphenous vein grafts. J Thorac Cardiovasc Surg 1987;94:2-11. 9. Koike R, Suma H, Kondo K, et al. Pharmacological response of internal mammary artery and gastroepiploic artery. Ann Thorac Surg 1990;50:38&6. 10. Kawasuji M, Tsujiguchi H, Tedoriya T, Taki J, Iwa T. Evaluation of postoperative flow capacity of internal mammary artery. J Thorac Cardiovasc Surg 1990;99:696-702. 11. Jones E, Lattouf 0, Weintraub W. Catastrophic consequences of internal mammary artery hypoperfusion. J Thorac Cardiovasc Surg 1989;98:902-7. 12. Naunheim K, Barner H, Fiore A. Update: Results of internal thoracic artery grafting over 15 years: single versus double grafts. Ann Thorac Surg 1992;53:71&8. 13. Perrault L, et al. Morbidity and mortality of reoperation for coronary artery bypass grafting: significance of atheromatous vein grafts. Can J Cardiol 1991;49:427-30.