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Ann Thorac Surg 1998;65:1437-1439
© 1998 The Society of Thoracic Surgeons

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Case Reports

Histologic Findings of Transmyocardial Laser Channels After Two Hours

^a Department of Cardiovascular Surgery, University of Freiburg, Freiburg, Germany
^b Department of Pathology, University of Freiburg, Freiburg, Germany

Accepted for publication November 19, 1997.

Address reprint requests to Dr Lutter, Department of Cardiovascular Surgery, University of Freiburg, 55 Hugstetter St, D-79106 Freiburg, Germany
e-mail: (lutter{at}ch11.ukl.uni-freiburg.de)

	Abstract

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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 1- to 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.

	Introduction

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Transmyocardial 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 posterolateral 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 · min^-1 · m^-2) 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).

View larger version (154K): [in this window] [in a new window]   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). (x200 before 38% reduction.)

View larger version (152K): [in this window] [in a new window]   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). (x200 before 38% reduction.)

	Comment

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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.

	Acknowledgments

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Doctor Lutter is supported by the Clinical Cardiovascular Research Center II at the University of Freiburg, Freiburg, Germany.

	References

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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;76:981-989.[Abstract/Free Full Text]
2. Cooley D.A., Frazier O.H., Kadipasaoglu K.A., Pehlivanoglu S., Shannon R.L., Angelini P. Transmyocardial laser revascularization: anatomic evidence of long-term channel patency. Tex Heart Inst J 1994;21:220-224.[Medline]
3. Burkhoff D., Fisher P.E., Apfelbaum M., Kohmoto T., DeRosa C.M., Smith C.R. Histologic appearance of transmyocardial laser channels after 4 weeks. Ann Thorac Surg 1996;61:1532-1535.[Abstract/Free Full Text]
4. Krabatsch T., Schäper F., Leder C., Tülsner J., Thalmann U., Hetzer R. Histological findings after transmyocardial laser revascularization. J Card Surg 1996;11:326-331.[Medline]
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6. Horvath K.A., Smith W.J., Laurence R.G., Schoen F.J., Appleyard R.F., Cohn L.H. Recovery and viability of an acute myocardial infarct after transmyocardial laser revascularization. J Am Coll Cardiol 1995;25:258-263.[Abstract]
7. Whittaker P., Kloner R.A., Przyklenk K. Laser-mediated transmural myocardial channels do not salvage acutely ischemic myocardium. J Am Coll Cardiol 1993;22:302-309.[Abstract]
8. Hardy R.I., Kevin E.B., James F.W., Kaplan S., Goldman L. A histologic study of laser-induced transmyocardial channels. Lasers Surg Med 1987;6:563-573.[Medline]
9. 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;13:21-26.

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This Article Abstract Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): Georg Lutter Christoph Lutz Juergen Martin Friedhelm Beyersdorf Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Lutter, G. Articles by Beyersdorf, F. Search for Related Content PubMed PubMed Citation Articles by Lutter, G. Articles by Beyersdorf, F.