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Histologic Findings of Transmyocardial Laser Channels After Two Hours
CASE REPORTS
Histologic Findings of Transmyocardial Laser Channels After Two Hours Georg Lutter, MD, Jirka Schwarzkopf, MD, Christoph Lutz, MD, Juergen Martin, MD, and Friedhelm Beyersdorf, MD Departments of Cardiovascular Surgery and Pathology, University of Freiburg, Freiburg, Germany
Histologic examination of the human myocardium has been performed several days, weeks, and months after transmyocardial laser revascularization. We performed microscopic examinations 2 hours postoperatively. In addition to the patent channel (diameter, 1 mm) and a 1to 2-mm rim of necrosis, a 1- to 3-mm zone of myofibrillary degeneration was found. This additional reversible injury immediately after transmyocardial laser revascularization could explain the higher mortality rate in patients with reduced left ventricular function. (Ann Thorac Surg 1998;65:1437–9) © 1998 by The Society of Thoracic Surgeons
T
ransmyocardial laser revascularization (TMLR) is a relatively new surgical technique of indirect revascularization for patients with symptomatic end stage coronary artery disease. Transmyocardial laser revascularization creates transmural channels in ischemic viable myocardium via laser ablation. Hypothetically this allows direct perfusion from the left ventricular cavity via the channels to the myocardium. Postmortem microscopic examinations have been performed days, weeks, or months postoperatively. Here we report the histologic appearance of human myocardium 2 hours after TMLR. A 69-year-old man was transferred to our clinic for the consideration of revascularization with a history of hyperlipidemia, hyperuricemia, hypertension, smoking and multiple cerebral infarctions in 1984. He suffered two inferior myocardial infarctions in 1978 and 1979. In 1982 he underwent three-vessel coronary bypass grafting with vein grafts. Since 1990 he had angina under maximal medical treatment. Coronary angiography revealed small-vessel disease with proximal total occlusion of the circumflex and right coronary arteries and partial collateralization of the posterior descending artery from the left side with diffuse disease. The left anterior descending artery was a diffuse vessel with occlusion distal to the first diagonal branch and filled via collaterals with multiple distal stenoses; the diagonal branch showed multiple proximal stenoses and was occluded distally. Two vein grafts were occluded, and the third graft to the posteroAccepted for publication Nov 19, 1997. Address reprint requests to Dr Lutter, Department of Cardiovascular Surgery, University of Freiburg, 55 Hugstetter St, D-79106 Freiburg, Germany (e-mail: [email protected]).
© 1998 by The Society of Thoracic Surgeons Published by Elsevier Science Inc
lateral branches was subtotally occluded with only minimal flow. The left ventricular diastolic pressure was 39 mm Hg, and the ejection fraction was 0.20. The small-vessel disease rendered the patient unsuitable for conventional revascularization, and he was treated medically. However, crescendo angina developed. The patient was given intravenous nitrates, and preparations for TMLR were performed. Positron emission tomography and sestamibi scan showed two old inferolateral and apical myocardial infarctions with surrounding mismatch of perfusion and metabolism. All other regions were fully vital. Echocardiography demonstrated a hypokinesia to akinesia of the inferior wall and hypokinesia of the anterior wall (ejection fraction, 0.20). Via left anterolateral thoracotomy, 41 transmural microchannels (40 J/channel; 1 mm in diameter) in the inferior, apical, and anterolateral regions were performed by a 800-watt CO2 laser (PLC Systems, Milford, MA) in May 1996. At the end of this operation the patient required moderate inotropic support. One hour postoperatively low cardiac output (cardiac index, 1.4 L z min21 z m22) developed and the patient needed high inotropic support. One hour later an electromechanical dissociation developed and he died of left ventricular failure. The family consented to an autopsy. The gross inspection revealed massive ischemic heart disease with eccentric myocardial hypertrophy (heart weight, 660 g; thickness of the left ventricular wall, 1.6 cm), myocardial scars in the inferior and anterior wall, highly narrowed atherosclerotic coronary arteries, and old thrombotic almost complete occlusions of the bypass grafts. All transmyocardial laser channels were identified to be open (1 mm in diameter) by viewing the endocardium and serial transverse sections. In the subepicardium, only clotting of the channels could be seen. Histologic examination of the channels (1 mm in diameter) showed patent channels, which were bordered by a 1- to 2-mm broad rim of carbonization and necrosis (Fig 1), followed by a 1- to 3-mm rim of myofibrillary degeneration and edema with a beginning focal demarcation by granulocytes (Fig 2). The early myofibrillary degeneration and edema could be clearly identified by Lie (see Fig 2) and Luxol fast blue staining, in contrast to hematoxylin and eosin staining (see Fig 1). The residual myocardium demonstrated no further pathologic changes. Direct communications were observed between some of the channels, the native myocardial vessels, and the ventricular cavity. Each of the 15 analyzed channels was partially filled with blood. No fibrin thrombi could be seen. Planimetric analysis showed that 41% of the left ventricular volume consisted of myocardial scars. Of the residual vital myocardium (59%), one third (20% of total myocardium) was affected by TMLR. A small zone was irreversibly injured by creating tissue-ablated channels (diameter, 1 mm) surrounded by a zone of carbonization and necrosis (diameter, 1 to 2 mm). Outside this central zone, an additional area of potentially reversible injury by myofibrillary degeneration and edema [1] was detected (diameter, 1 to 3 mm). 0003-4975/98/$19.00 PII S0003-4975(98)00161-1
1438
CASE REPORT LUTTER ET AL HISTOLOGY OF TRANSMYOCARDIAL LASER CHANNELS
Fig 1. Hematoxylin and eosin staining shows an open laser channel (C) 1 mm in diameter bordered by a 1- to 2-mm broad rim of necrotic, carbonized myocardium (lower third of figure). (3200 before 38% reduction.)
Comment Controversial reports exist concerning channel patency several months after TMLR in postmortem examinations. Some authors report open [2] and others occluded chan-
Ann Thorac Surg 1998;65:1437–9
nels [3–5]. The same discrepancy was found in experimental studies [6, 7]. Does channel patency correlate with the efficacy of TMLR? The mechanism of TMLR is unknown. In the present case one would expect the typical features of CO2 laser channels, with marginal necrotic and thermal damage as described by Hardy and associates [8] in 1987. However a broader damage zone was found 2 hours postmortem. Using the same CO2 laser, Krabatsch and colleagues [4] reported occluded laser channels (except one) with a diameter of 1 mm and a small zone of 0.5 mm of carbonization and necrosis in a postmortem study 2 days postoperatively. A further zone of myofibrillary degeneration and edema was not described by Krabatsch and colleagues. In contrast, Gassler and coworkers [5] found this zone after TMLR (to a lesser extent than in our report) in their postmortem examination on day 3 of a patient who was treated with the same laser regimen: The total maximal lesion size was 2 mm in closed laser channels. It might be speculated that the differences between their study and our report are caused by (1) the use of the Lie staining in our study, which is specialized to detect the total extent of the ischemic and degenerated myocardium immediately postoperatively and (2) the reversibility of the myofibrillary degeneration and edema zone within 24 hours [1, 4, 5]. In the present case, decline of the left ventricular function does not correlate with channel patency. Lie or Luxol fast blue staining was the only appropriate staining to define the total extent of the thermal damage after TMLR, because hematoxylin and eosin staining did not reveal the myofibrillary degeneration and edema zones. The acute loss of left ventricular contractility could be caused by laser carbonization, necrosis, myofibrillary degeneration, and edema in the border zone of the microchannels. These histologic and our clinical data [9] support our concept of starting preoperative intraaortic balloon counterpulsation in patients with reduced left ventricular contractile reserve (ejection fraction ,0.35) to provide cardiac support during the phase of reversible myocardial damage induced by TMLR. Further studies about channel patency, thermal damage, biochemistry, and viability of the surrounding myocardium after TMLR are necessary. Doctor Lutter is supported by the Clinical Cardiovascular Research Center II at the University of Freiburg, Freiburg, Germany.
References Fig 2. Lie staining reveals an open laser channel (C) bordered by a 1- to 2-mm broad rim of necrotic myocardium (lower third of figure), followed by a 1- to 3-mm rim of myofibrillated degeneration (MFD) and edema with a beginning focal demarcation by granulocytes (middle third) and normal myocardium (N) (upper third). (3200 before 38% reduction.)
1. Matsuda M, Fujiwara H, Onodera T, et al. Quantitative analysis of infarct size, contraction band necrosis, and coagulation necrosis in human autopsied hearts with acute myocardial infarction after treatment with selective intracoronary thrombolysis. Circulation 1987;76:981–9. 2. Cooley DA, Frazier OH, Kadipasaoglu KA, Pehlivanoglu S, Shannon RL, Angelini P. Transmyocardial laser revascular-
Ann Thorac Surg 1998;65:1439 – 41
3.
4. 5.
6.
7. 8. 9.
ization: anatomic evidence of long-term channel patency. Tex Heart Inst J 1994;21:220– 4. Burkhoff D, Fisher PE, Apfelbaum M, Kohmoto T, DeRosa CM, Smith CR. Histologic appearance of transmyocardial laser channels after 41⁄2 weeks. Ann Thorac Surg 1996;61: 1532–5. Krabatsch T, Scha¨per F, Leder C, Tu¨lsner J, Thalmann U, Hetzer R. Histological findings after transmyocardial laser revascularization. J Card Surg 1996;11:326–31. Gassler N, Wintzer HO, Stubbe HM, Wullbrand A, Helmchen U. Transmyocardial laser revascularization. Histological features in human nonresponder myocardium. Circulation 1997; 95:371–5. Horvath KA, Smith WJ, Laurence RG, Schoen FJ, Appleyard RF, Cohn LH. Recovery and viability of an acute myocardial infarct after transmyocardial laser revascularization. J Am Coll Cardiol 1995;25:258– 63. Whittaker P, Kloner RA, Przyklenk K. Laser-mediated transmural myocardial channels do not salvage acutely ischemic myocardium. J Am Coll Cardiol 1993;22:302–9. Hardy RI, Kevin EB, James FW, Kaplan S, Goldman L. A histologic study of laser-induced transmyocardial channels. Lasers Surg Med 1987;6:563–73. Lutter G, Saurbier B, Nitzsche E, et al. Transmyocardial laser revascularization (TMLR) in patients with unstable angina and low ejection fraction. Eur J Cardiothorac Surg 1998;13: 21– 6.
Thoracoscopic Transmyocardial Laser Revascularization Keith A. Horvath, MD Division of Cardiothoracic Surgery, Northwestern University Medical School, Chicago, Illinois
Transmyocardial laser revascularization has been used to treat patients with end-stage coronary artery disease and severe disabling angina. Typically, the operative approach is through a left anterior thoracotomy. I report a case of transmyocardial laser revascularization performed thoracoscopically. (Ann Thorac Surg 1998;65:1439 – 41) © 1998 by The Society of Thoracic Surgeons
A
minimally invasive technique for transmyocardial laser revascularization is described. Employing a thoracoscope and standard instruments, the procedure can be performed safely and should decrease postoperative pain and length of stay. Transmyocardial laser revascularization has been used for more than 6 years to treat patients with end-stage coronary artery disease. These patients who are not amenable to standard revascularization techniques and suffer severe angina refractory to medical therapy have shown improvement in angina class and myocardial perfusion after transmyo-
Accepted for publication Jan 28, 1998. Address reprint requests to Dr Horvath, Northwestern University Medical School, Wesley Tower #1030, 251 E Chicago Ave, Chicago, IL 60611 (e-mail: [email protected]).
© 1998 by The Society of Thoracic Surgeons Published by Elsevier Science Inc
CASE REPORT HORVATH THORACOSCOPIC TMR
1439
cardial laser revascularization [1]. The operative approach for these patients has been through an 18- to 20-cm anterior thoracotomy in the fifth intercostal space. The pericardium is then opened and the left ventricular free wall is drilled with a high-powered laser. The 1-mm channels are created in a distribution of one per square centimeter. The majority of these patients are extubated in the operating room. Because of the severe nature of their coronary artery disease, postoperative pain control after their thoracotomy is critical. A thoracic epidural anesthetic has been used to provide local anesthesia but, in at least 1 case, has caused a perioperative death [1]. Occasionally, the difficulty in recovering from a thoracotomy has also increased the patient’s length of stay. The average length of stay for this procedure has been reported at 8 days [1]. My colleagues and I [2] have previously described the performance of thoracoscopic transmyocardial laser revascularization in an animal model. In an effort to decrease the morbidity of the procedure, the thoracoscopic approach was recently employed clinically. A 67-year-old woman who had two myocardial infarctions in 1996 had been treated previously with angioplasty and stenting of her left anterior descending coronary artery and her first obtuse marginal artery. Her course was complicated by flash pulmonary edema requiring intraaortic balloon pump assistance and a cerebral bleed requiring surgical evacuation. Six months later, she suffered a third myocardial infarction. A repeat angiography revealed that her stents were open and there was little change in her diffusely diseased coronary arteries. Since that time, she experienced significant substernal chest pressure, which occurred often after eating and with minimal exertion. Despite maximal medical therapy (including warfarin), she remained significantly symptomatic. Dual-isotope perfusion scanning demonstrated a large area of reversible ischemia involving the left anterior descending and left circumflex coronary artery regions. Under general anesthesia with a double-lumen endotracheal tube in a right lateral decubitus position, a thoracoscopic port was placed in her fifth intercostal space along the midaxillary line (Fig 1A). The heart was easily visualized and the pericardium was opened. Endoscopic graspers were used to hold the pericardium, and standard Metzenbaum scissors were used to open the pericardium through an additional 4-cm incision in Doctor Horvath has been compensated for time and travel expenses by PLC Medical Systems for proctoring various surgeons who are starting transmyocardial laser revascularization programs at their institutions. No funding was provided for the performance of the reported case or other operations.
0003-4975/98/$19.00 PII S0003-4975(98)00143-X
Histologic Findings of Transmyocardial Laser Channels After Two Hours Georg Lutter, MD, Jirka Schwarzkopf, MD, Christoph Lutz, MD, Juergen Martin, MD, and Friedhelm Beyersdorf, MD Departments of Cardiovascular Surgery and Pathology, University of Freiburg, Freiburg, Germany
Histologic examination of the human myocardium has been performed several days, weeks, and months after transmyocardial laser revascularization. We performed microscopic examinations 2 hours postoperatively. In addition to the patent channel (diameter, 1 mm) and a 1to 2-mm rim of necrosis, a 1- to 3-mm zone of myofibrillary degeneration was found. This additional reversible injury immediately after transmyocardial laser revascularization could explain the higher mortality rate in patients with reduced left ventricular function. (Ann Thorac Surg 1998;65:1437–9) © 1998 by The Society of Thoracic Surgeons
T
ransmyocardial laser revascularization (TMLR) is a relatively new surgical technique of indirect revascularization for patients with symptomatic end stage coronary artery disease. Transmyocardial laser revascularization creates transmural channels in ischemic viable myocardium via laser ablation. Hypothetically this allows direct perfusion from the left ventricular cavity via the channels to the myocardium. Postmortem microscopic examinations have been performed days, weeks, or months postoperatively. Here we report the histologic appearance of human myocardium 2 hours after TMLR. A 69-year-old man was transferred to our clinic for the consideration of revascularization with a history of hyperlipidemia, hyperuricemia, hypertension, smoking and multiple cerebral infarctions in 1984. He suffered two inferior myocardial infarctions in 1978 and 1979. In 1982 he underwent three-vessel coronary bypass grafting with vein grafts. Since 1990 he had angina under maximal medical treatment. Coronary angiography revealed small-vessel disease with proximal total occlusion of the circumflex and right coronary arteries and partial collateralization of the posterior descending artery from the left side with diffuse disease. The left anterior descending artery was a diffuse vessel with occlusion distal to the first diagonal branch and filled via collaterals with multiple distal stenoses; the diagonal branch showed multiple proximal stenoses and was occluded distally. Two vein grafts were occluded, and the third graft to the posteroAccepted for publication Nov 19, 1997. Address reprint requests to Dr Lutter, Department of Cardiovascular Surgery, University of Freiburg, 55 Hugstetter St, D-79106 Freiburg, Germany (e-mail: [email protected]).
© 1998 by The Society of Thoracic Surgeons Published by Elsevier Science Inc
lateral branches was subtotally occluded with only minimal flow. The left ventricular diastolic pressure was 39 mm Hg, and the ejection fraction was 0.20. The small-vessel disease rendered the patient unsuitable for conventional revascularization, and he was treated medically. However, crescendo angina developed. The patient was given intravenous nitrates, and preparations for TMLR were performed. Positron emission tomography and sestamibi scan showed two old inferolateral and apical myocardial infarctions with surrounding mismatch of perfusion and metabolism. All other regions were fully vital. Echocardiography demonstrated a hypokinesia to akinesia of the inferior wall and hypokinesia of the anterior wall (ejection fraction, 0.20). Via left anterolateral thoracotomy, 41 transmural microchannels (40 J/channel; 1 mm in diameter) in the inferior, apical, and anterolateral regions were performed by a 800-watt CO2 laser (PLC Systems, Milford, MA) in May 1996. At the end of this operation the patient required moderate inotropic support. One hour postoperatively low cardiac output (cardiac index, 1.4 L z min21 z m22) developed and the patient needed high inotropic support. One hour later an electromechanical dissociation developed and he died of left ventricular failure. The family consented to an autopsy. The gross inspection revealed massive ischemic heart disease with eccentric myocardial hypertrophy (heart weight, 660 g; thickness of the left ventricular wall, 1.6 cm), myocardial scars in the inferior and anterior wall, highly narrowed atherosclerotic coronary arteries, and old thrombotic almost complete occlusions of the bypass grafts. All transmyocardial laser channels were identified to be open (1 mm in diameter) by viewing the endocardium and serial transverse sections. In the subepicardium, only clotting of the channels could be seen. Histologic examination of the channels (1 mm in diameter) showed patent channels, which were bordered by a 1- to 2-mm broad rim of carbonization and necrosis (Fig 1), followed by a 1- to 3-mm rim of myofibrillary degeneration and edema with a beginning focal demarcation by granulocytes (Fig 2). The early myofibrillary degeneration and edema could be clearly identified by Lie (see Fig 2) and Luxol fast blue staining, in contrast to hematoxylin and eosin staining (see Fig 1). The residual myocardium demonstrated no further pathologic changes. Direct communications were observed between some of the channels, the native myocardial vessels, and the ventricular cavity. Each of the 15 analyzed channels was partially filled with blood. No fibrin thrombi could be seen. Planimetric analysis showed that 41% of the left ventricular volume consisted of myocardial scars. Of the residual vital myocardium (59%), one third (20% of total myocardium) was affected by TMLR. A small zone was irreversibly injured by creating tissue-ablated channels (diameter, 1 mm) surrounded by a zone of carbonization and necrosis (diameter, 1 to 2 mm). Outside this central zone, an additional area of potentially reversible injury by myofibrillary degeneration and edema [1] was detected (diameter, 1 to 3 mm). 0003-4975/98/$19.00 PII S0003-4975(98)00161-1
1438
CASE REPORT LUTTER ET AL HISTOLOGY OF TRANSMYOCARDIAL LASER CHANNELS
Fig 1. Hematoxylin and eosin staining shows an open laser channel (C) 1 mm in diameter bordered by a 1- to 2-mm broad rim of necrotic, carbonized myocardium (lower third of figure). (3200 before 38% reduction.)
Comment Controversial reports exist concerning channel patency several months after TMLR in postmortem examinations. Some authors report open [2] and others occluded chan-
Ann Thorac Surg 1998;65:1437–9
nels [3–5]. The same discrepancy was found in experimental studies [6, 7]. Does channel patency correlate with the efficacy of TMLR? The mechanism of TMLR is unknown. In the present case one would expect the typical features of CO2 laser channels, with marginal necrotic and thermal damage as described by Hardy and associates [8] in 1987. However a broader damage zone was found 2 hours postmortem. Using the same CO2 laser, Krabatsch and colleagues [4] reported occluded laser channels (except one) with a diameter of 1 mm and a small zone of 0.5 mm of carbonization and necrosis in a postmortem study 2 days postoperatively. A further zone of myofibrillary degeneration and edema was not described by Krabatsch and colleagues. In contrast, Gassler and coworkers [5] found this zone after TMLR (to a lesser extent than in our report) in their postmortem examination on day 3 of a patient who was treated with the same laser regimen: The total maximal lesion size was 2 mm in closed laser channels. It might be speculated that the differences between their study and our report are caused by (1) the use of the Lie staining in our study, which is specialized to detect the total extent of the ischemic and degenerated myocardium immediately postoperatively and (2) the reversibility of the myofibrillary degeneration and edema zone within 24 hours [1, 4, 5]. In the present case, decline of the left ventricular function does not correlate with channel patency. Lie or Luxol fast blue staining was the only appropriate staining to define the total extent of the thermal damage after TMLR, because hematoxylin and eosin staining did not reveal the myofibrillary degeneration and edema zones. The acute loss of left ventricular contractility could be caused by laser carbonization, necrosis, myofibrillary degeneration, and edema in the border zone of the microchannels. These histologic and our clinical data [9] support our concept of starting preoperative intraaortic balloon counterpulsation in patients with reduced left ventricular contractile reserve (ejection fraction ,0.35) to provide cardiac support during the phase of reversible myocardial damage induced by TMLR. Further studies about channel patency, thermal damage, biochemistry, and viability of the surrounding myocardium after TMLR are necessary. Doctor Lutter is supported by the Clinical Cardiovascular Research Center II at the University of Freiburg, Freiburg, Germany.
References Fig 2. Lie staining reveals an open laser channel (C) bordered by a 1- to 2-mm broad rim of necrotic myocardium (lower third of figure), followed by a 1- to 3-mm rim of myofibrillated degeneration (MFD) and edema with a beginning focal demarcation by granulocytes (middle third) and normal myocardium (N) (upper third). (3200 before 38% reduction.)
1. Matsuda M, Fujiwara H, Onodera T, et al. Quantitative analysis of infarct size, contraction band necrosis, and coagulation necrosis in human autopsied hearts with acute myocardial infarction after treatment with selective intracoronary thrombolysis. Circulation 1987;76:981–9. 2. Cooley DA, Frazier OH, Kadipasaoglu KA, Pehlivanoglu S, Shannon RL, Angelini P. Transmyocardial laser revascular-
Ann Thorac Surg 1998;65:1439 – 41
3.
4. 5.
6.
7. 8. 9.
ization: anatomic evidence of long-term channel patency. Tex Heart Inst J 1994;21:220– 4. Burkhoff D, Fisher PE, Apfelbaum M, Kohmoto T, DeRosa CM, Smith CR. Histologic appearance of transmyocardial laser channels after 41⁄2 weeks. Ann Thorac Surg 1996;61: 1532–5. Krabatsch T, Scha¨per F, Leder C, Tu¨lsner J, Thalmann U, Hetzer R. Histological findings after transmyocardial laser revascularization. J Card Surg 1996;11:326–31. Gassler N, Wintzer HO, Stubbe HM, Wullbrand A, Helmchen U. Transmyocardial laser revascularization. Histological features in human nonresponder myocardium. Circulation 1997; 95:371–5. Horvath KA, Smith WJ, Laurence RG, Schoen FJ, Appleyard RF, Cohn LH. Recovery and viability of an acute myocardial infarct after transmyocardial laser revascularization. J Am Coll Cardiol 1995;25:258– 63. Whittaker P, Kloner RA, Przyklenk K. Laser-mediated transmural myocardial channels do not salvage acutely ischemic myocardium. J Am Coll Cardiol 1993;22:302–9. Hardy RI, Kevin EB, James FW, Kaplan S, Goldman L. A histologic study of laser-induced transmyocardial channels. Lasers Surg Med 1987;6:563–73. Lutter G, Saurbier B, Nitzsche E, et al. Transmyocardial laser revascularization (TMLR) in patients with unstable angina and low ejection fraction. Eur J Cardiothorac Surg 1998;13: 21– 6.
Thoracoscopic Transmyocardial Laser Revascularization Keith A. Horvath, MD Division of Cardiothoracic Surgery, Northwestern University Medical School, Chicago, Illinois
Transmyocardial laser revascularization has been used to treat patients with end-stage coronary artery disease and severe disabling angina. Typically, the operative approach is through a left anterior thoracotomy. I report a case of transmyocardial laser revascularization performed thoracoscopically. (Ann Thorac Surg 1998;65:1439 – 41) © 1998 by The Society of Thoracic Surgeons
A
minimally invasive technique for transmyocardial laser revascularization is described. Employing a thoracoscope and standard instruments, the procedure can be performed safely and should decrease postoperative pain and length of stay. Transmyocardial laser revascularization has been used for more than 6 years to treat patients with end-stage coronary artery disease. These patients who are not amenable to standard revascularization techniques and suffer severe angina refractory to medical therapy have shown improvement in angina class and myocardial perfusion after transmyo-
Accepted for publication Jan 28, 1998. Address reprint requests to Dr Horvath, Northwestern University Medical School, Wesley Tower #1030, 251 E Chicago Ave, Chicago, IL 60611 (e-mail: [email protected]).
© 1998 by The Society of Thoracic Surgeons Published by Elsevier Science Inc
CASE REPORT HORVATH THORACOSCOPIC TMR
1439
cardial laser revascularization [1]. The operative approach for these patients has been through an 18- to 20-cm anterior thoracotomy in the fifth intercostal space. The pericardium is then opened and the left ventricular free wall is drilled with a high-powered laser. The 1-mm channels are created in a distribution of one per square centimeter. The majority of these patients are extubated in the operating room. Because of the severe nature of their coronary artery disease, postoperative pain control after their thoracotomy is critical. A thoracic epidural anesthetic has been used to provide local anesthesia but, in at least 1 case, has caused a perioperative death [1]. Occasionally, the difficulty in recovering from a thoracotomy has also increased the patient’s length of stay. The average length of stay for this procedure has been reported at 8 days [1]. My colleagues and I [2] have previously described the performance of thoracoscopic transmyocardial laser revascularization in an animal model. In an effort to decrease the morbidity of the procedure, the thoracoscopic approach was recently employed clinically. A 67-year-old woman who had two myocardial infarctions in 1996 had been treated previously with angioplasty and stenting of her left anterior descending coronary artery and her first obtuse marginal artery. Her course was complicated by flash pulmonary edema requiring intraaortic balloon pump assistance and a cerebral bleed requiring surgical evacuation. Six months later, she suffered a third myocardial infarction. A repeat angiography revealed that her stents were open and there was little change in her diffusely diseased coronary arteries. Since that time, she experienced significant substernal chest pressure, which occurred often after eating and with minimal exertion. Despite maximal medical therapy (including warfarin), she remained significantly symptomatic. Dual-isotope perfusion scanning demonstrated a large area of reversible ischemia involving the left anterior descending and left circumflex coronary artery regions. Under general anesthesia with a double-lumen endotracheal tube in a right lateral decubitus position, a thoracoscopic port was placed in her fifth intercostal space along the midaxillary line (Fig 1A). The heart was easily visualized and the pericardium was opened. Endoscopic graspers were used to hold the pericardium, and standard Metzenbaum scissors were used to open the pericardium through an additional 4-cm incision in Doctor Horvath has been compensated for time and travel expenses by PLC Medical Systems for proctoring various surgeons who are starting transmyocardial laser revascularization programs at their institutions. No funding was provided for the performance of the reported case or other operations.
0003-4975/98/$19.00 PII S0003-4975(98)00143-X