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Histology of internal mammary artery
CORRESPONDENCE
Histology of Internal Mammary Artery To the Editor: We would like to submit our comments on the recent article by van Son and associates [ l ] “Histological Study of the Internal Mammary Artery With Emphasis on Its Suitability as a Coronary Artery Bypass Graft.” From morphometric analysis of the internal thoracic artery (ITA) and the superior epigastric artery the conclusion was drawn that there is a correlation between the number of elastic lamellae and the observed intimal thickening. Furthermore, a correlation was noted between the absence of elastic lamellae and an increased number of discontinuities in the internal elastic lamina. Recently, we performed a study on the morphology of the inferior epigastric artery (IEA). Forty-five ITAs and IEAs were harvested at postmortem examinations. Sections at 1-cm intervals were stained with hematoxylin and eosin and with elastica van Gieson. Microscopy and morphometry showed an elastic pattern of the medial layer of the ITA and a muscular pattern of the media of the IEA. In contrast to van Son and associates’ findings for the ITA and the superior epigastric artery, we found significantly fewer fenestrations per millimeter of circumference for the IEA than for the ITA (4.00 t 1.60 versus 4.62 2 1.46; p < 0.05). Moreover, the intimal layer of the IEA was significantly thinner than the intima of the ITA ( p = 0.001) [2]. Our findings confirm results published previously on the morphology of the IEA [3]. We agree that arteries with few fenestrations within the internal elastic lamina seem to be protected from intimal hyperplasia. However, a muscular pattern with few elastic lamellae in the media is not correlated with intimal thickening or the number of fenestrations in the internal elastic lamina, at least in the IEA. It is of note that the radial artery exhibits a higher number of fenestrations of the internal elastic lamina [4] and has a high failure rate when used in myocardial revascularization [5]. But it should be appreciated that other factors, such as wall thickness, may also influence the patency rate [6].
Alexander Wahba, M D Klinik fur Herz-, Thorax- und Herznahe GefaJchirurgie des Klinikum Regensburg Franz-Josef-Straup-Allee I I 93053 Regensburg, FRG Kristin Offerdal, M D Abteilung fur Gefapchirurgie Klinikum rechts der Isar, Ismaningerstr. 22 8000 Miinchen 22, FRG
5. Curtis JJ, Stoney WS, Alford WC, Burrus GR, Thomas CS Jr. Intimal hyperplasia. Ann Thorac Surg 1975;20:62%35. 6. Chiu D-J. Why do radial artery grafts for aortocoronary bypass fail? A reappraisal. Ann Thorac Surg 1976;22:52&3.
Plasma C3a and C5a Concentrations During Cardiopulmonary Bypass To the Editor: We read with interest the review by Butler and associates [ l ] and the articles by Gillinov and associates [2] and Gu and associates [3] regarding the role of complement activation in the response to cardiopulmonary bypass (CPB) and we would like to add our preliminary experience. To assess the role of the C3a and C5a anaphylatoxins during CPB, we performed a preliminary study on 20 consecutive adult patients (mean age, 49.4 t 11.9 years) undergoing elective surgical procedures (8 myocardial revascularization, 4 aortic valve replacement, 3 mitral valve replacement, 3 mitral and aortic valve replacement, 2 mitral commissurotomy). All patients were operated on with the same anesthetic techniques and conventional extracorporeal circulation using a membrane oxygenator, a roller pump, moderate hypothermia, and coronary perfusion with a cold crystalloid cardioplegic solution. Blood samples required for radioimmunoassay determination of plasma C3a and C5a antigen levels [4] and complete blood counts were obtained from the arterial line at the following times: (1) anesthetic induction, (2) heparin administration, (3) 20 minutes after the beginning of CPB, (4) end of aortic cross-clamping, (5) end of CPB, and (6) 2 hours after the arrival of the patient in the intensive care unit. The values of C3a and C5a were calculated using the formula previously presented by Chenoweth and associates [5]. C3a levels were significantly higher ( p < 0.0001) at times 3, 4, 5, and 6 than preoperative levels. Plasma values of C5a did not change significantly during CPB. Moreover, we observed a 31% increase in the number of circulating neutrophils and a decrease in monocytes and eosinophils. Our results confirm that CPB promotes an increased formation of C3a and C5a anaphylatoxins, which cause pathophysiologic changes; nevertheless, the causal relation between these complement-derived inflammatory mediators and the “postperfusion syndrome” [6] has not been demonstrated.
Pasquale Mastroroberto, M D Massimo Chello, M D Antonietta R. Marchese, M D Cardiovascular Surge y Unit University Hospital Catanzaro, Italy
References References 1. Van Son JAM, Smedts F, de Wilde PCM, et al. Histological study of the internal mammary artery with emphasis on its suitability as a coronary artery bypass graft. Ann Thorac Surg 1993;55:10&13. 2. Wahba A, Offerdal LJ,v. Sommoggy S, Birnbaum DE. The morphology of the inferior epigastric artery has implications on its use as a conduit for myocardial revascularization. Eur J Cardiothorac Surg (in press). 3. Schwartz DS, Factor SM, Schwartz JD, et al. Histological evaluation of the inferior epigastric artery in patients with known atherosclerosis. Eur J Cardiothorac Surg 1992;643&41. 4. Sisto T. Atherosclerosis in internal mammary and related arteries. Scand J Thorac Cardiovasc Surg 1990;247-11.
0 1994 by The Society of Thoracic Surgeons
1. Butler J, Rocker GM, Westaby S. Inflammatory response to cardiopulmonary bypass. Ann Thorac Surg 1993;55:552-9. 2. Gillinov AM, DeValeria PA, Winkelstein JA, et al. Complement inhibition with soluble complement receptor type 1 in cardiopulmonary bypass. Ann Thorac Surg 1993;55:619-24. 3. Gu YJ, van Oeveren W, Akkerman C, Boonstra PW, Huyzen RJ, Wildevuur CRH. Heparin-coated circuits reduce the inflammatory response to cardiopulmonary bypass. Ann Thorac Surg 1993;55:917-22. 4. Hugli TE, Chenoweth DE. Biologically active peptides of complement: techniques and significance of C3a and C5a measurements. In: Nakamura RM, Dito WR, Tucker ES 111, eds. Future perspectives in clinical laboratory immunoassays. New York: Alan R. Liss, 1981:153-9. 5. Chenoweth DE, Cooper SW, Hugli TE, Stewart RW, Black-
Ann Thorac Surg 1994;57:781-6
-
0003-4975/94/$7.00
Histology of Internal Mammary Artery To the Editor: We would like to submit our comments on the recent article by van Son and associates [ l ] “Histological Study of the Internal Mammary Artery With Emphasis on Its Suitability as a Coronary Artery Bypass Graft.” From morphometric analysis of the internal thoracic artery (ITA) and the superior epigastric artery the conclusion was drawn that there is a correlation between the number of elastic lamellae and the observed intimal thickening. Furthermore, a correlation was noted between the absence of elastic lamellae and an increased number of discontinuities in the internal elastic lamina. Recently, we performed a study on the morphology of the inferior epigastric artery (IEA). Forty-five ITAs and IEAs were harvested at postmortem examinations. Sections at 1-cm intervals were stained with hematoxylin and eosin and with elastica van Gieson. Microscopy and morphometry showed an elastic pattern of the medial layer of the ITA and a muscular pattern of the media of the IEA. In contrast to van Son and associates’ findings for the ITA and the superior epigastric artery, we found significantly fewer fenestrations per millimeter of circumference for the IEA than for the ITA (4.00 t 1.60 versus 4.62 2 1.46; p < 0.05). Moreover, the intimal layer of the IEA was significantly thinner than the intima of the ITA ( p = 0.001) [2]. Our findings confirm results published previously on the morphology of the IEA [3]. We agree that arteries with few fenestrations within the internal elastic lamina seem to be protected from intimal hyperplasia. However, a muscular pattern with few elastic lamellae in the media is not correlated with intimal thickening or the number of fenestrations in the internal elastic lamina, at least in the IEA. It is of note that the radial artery exhibits a higher number of fenestrations of the internal elastic lamina [4] and has a high failure rate when used in myocardial revascularization [5]. But it should be appreciated that other factors, such as wall thickness, may also influence the patency rate [6].
Alexander Wahba, M D Klinik fur Herz-, Thorax- und Herznahe GefaJchirurgie des Klinikum Regensburg Franz-Josef-Straup-Allee I I 93053 Regensburg, FRG Kristin Offerdal, M D Abteilung fur Gefapchirurgie Klinikum rechts der Isar, Ismaningerstr. 22 8000 Miinchen 22, FRG
5. Curtis JJ, Stoney WS, Alford WC, Burrus GR, Thomas CS Jr. Intimal hyperplasia. Ann Thorac Surg 1975;20:62%35. 6. Chiu D-J. Why do radial artery grafts for aortocoronary bypass fail? A reappraisal. Ann Thorac Surg 1976;22:52&3.
Plasma C3a and C5a Concentrations During Cardiopulmonary Bypass To the Editor: We read with interest the review by Butler and associates [ l ] and the articles by Gillinov and associates [2] and Gu and associates [3] regarding the role of complement activation in the response to cardiopulmonary bypass (CPB) and we would like to add our preliminary experience. To assess the role of the C3a and C5a anaphylatoxins during CPB, we performed a preliminary study on 20 consecutive adult patients (mean age, 49.4 t 11.9 years) undergoing elective surgical procedures (8 myocardial revascularization, 4 aortic valve replacement, 3 mitral valve replacement, 3 mitral and aortic valve replacement, 2 mitral commissurotomy). All patients were operated on with the same anesthetic techniques and conventional extracorporeal circulation using a membrane oxygenator, a roller pump, moderate hypothermia, and coronary perfusion with a cold crystalloid cardioplegic solution. Blood samples required for radioimmunoassay determination of plasma C3a and C5a antigen levels [4] and complete blood counts were obtained from the arterial line at the following times: (1) anesthetic induction, (2) heparin administration, (3) 20 minutes after the beginning of CPB, (4) end of aortic cross-clamping, (5) end of CPB, and (6) 2 hours after the arrival of the patient in the intensive care unit. The values of C3a and C5a were calculated using the formula previously presented by Chenoweth and associates [5]. C3a levels were significantly higher ( p < 0.0001) at times 3, 4, 5, and 6 than preoperative levels. Plasma values of C5a did not change significantly during CPB. Moreover, we observed a 31% increase in the number of circulating neutrophils and a decrease in monocytes and eosinophils. Our results confirm that CPB promotes an increased formation of C3a and C5a anaphylatoxins, which cause pathophysiologic changes; nevertheless, the causal relation between these complement-derived inflammatory mediators and the “postperfusion syndrome” [6] has not been demonstrated.
Pasquale Mastroroberto, M D Massimo Chello, M D Antonietta R. Marchese, M D Cardiovascular Surge y Unit University Hospital Catanzaro, Italy
References References 1. Van Son JAM, Smedts F, de Wilde PCM, et al. Histological study of the internal mammary artery with emphasis on its suitability as a coronary artery bypass graft. Ann Thorac Surg 1993;55:10&13. 2. Wahba A, Offerdal LJ,v. Sommoggy S, Birnbaum DE. The morphology of the inferior epigastric artery has implications on its use as a conduit for myocardial revascularization. Eur J Cardiothorac Surg (in press). 3. Schwartz DS, Factor SM, Schwartz JD, et al. Histological evaluation of the inferior epigastric artery in patients with known atherosclerosis. Eur J Cardiothorac Surg 1992;643&41. 4. Sisto T. Atherosclerosis in internal mammary and related arteries. Scand J Thorac Cardiovasc Surg 1990;247-11.
0 1994 by The Society of Thoracic Surgeons
1. Butler J, Rocker GM, Westaby S. Inflammatory response to cardiopulmonary bypass. Ann Thorac Surg 1993;55:552-9. 2. Gillinov AM, DeValeria PA, Winkelstein JA, et al. Complement inhibition with soluble complement receptor type 1 in cardiopulmonary bypass. Ann Thorac Surg 1993;55:619-24. 3. Gu YJ, van Oeveren W, Akkerman C, Boonstra PW, Huyzen RJ, Wildevuur CRH. Heparin-coated circuits reduce the inflammatory response to cardiopulmonary bypass. Ann Thorac Surg 1993;55:917-22. 4. Hugli TE, Chenoweth DE. Biologically active peptides of complement: techniques and significance of C3a and C5a measurements. In: Nakamura RM, Dito WR, Tucker ES 111, eds. Future perspectives in clinical laboratory immunoassays. New York: Alan R. Liss, 1981:153-9. 5. Chenoweth DE, Cooper SW, Hugli TE, Stewart RW, Black-
Ann Thorac Surg 1994;57:781-6
-
0003-4975/94/$7.00