Asian Cardiovasc Thorac Ann 2003;11:157-159
© 2003 Asia Publishing EXchange Ltd
Myocardial Laser Coagulation for Free Wall Rupture Following Acute Infarction
Tetsuo Mizutani, MD,
Hitoshi Suzuki, MD,
Jin Tanaka, MD
Department of Cardiovascular Surgery, Mie General Medical Center, Yokkaichi, Mie, Japan
For reprint information contact: Tetsuo Mizutani, MD Tel: 81 593 45 2321 Fax: 81 593 47 3500 email: ttjr-f{at}cty-net.ne.jp Department of Cardiovascular Surgery, Mie General Medical Center, 5450-132 Hinaga, Yokkaichi, Mie 510-8561, Japan.
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ABSTRACT
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A 73-year-old woman was diagnosed with ventricular free wall rupture following acute myocardial infarction. The lesion was repaired with laser coagulation, fibrinogen–thrombin glue application, and patch reinforcement. Five years after surgery, the patient was in New York Heart Association class I.
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INTRODUCTION
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Free wall rupture after acute myocardial infarction can be fatal because of left ventricular (LV) diastolic disturbance due to hemopericardium and systolic pump failure due to myocardial damage. LV free wall rupture occurs in 1% to 4.6% of acute myocardial infarction1,2 and accounts for 12% to 21% of cardiac deaths following acute myocardial infarction.3 Diagnosis is not difficult by careful assessment of symptoms such as chest pain and restlessness, electromechanical dissociation, and pericardial effusion on the transthoracic echocardiogram. Nevertheless, operative mortality is still high because most patients have circulatory collapse and the ruptured myocardium is extremely fragile for direct closure.2 We introduce a procedure to control bleeding and to repair the ruptured site.
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CASE REPORT
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A 73-year-old female was admitted with severe chest pain. Her blood pressure was 140/90 mm Hg, and heartbeat was regular at 94 min-1. Biochemical analysis showed raised serum levels of creatine phosphokinase MB (835 IU•L-1), glutamic-oxaloacetic transaminase (383 IU•L-1), and lactate dehydrogenase (1,533 IU•L-1). Her cardiothoracic ratio on the chest radiograph was 55%, and the electrocardiogram showed sinus rhythm with ST elevation of 6 mm in I, aVL, and V1–6 leads. Acute myocardial infarction of the anteroseptal, anterolateral, and apica1 walls was suspected, and emergent coronary angiography was performed. There was no stenosis in the circumflex artery, but the proximal segment of the left anterior descending artery was completely occluded with delayed filling of the distal segment supplied by the septal branches of the right coronary artery. Percutaneous transluminal coronary angioplasty for segment 6 was tried with a balloon of 2.75-mm diameter, but 90% stenosis remained. Dilatation to the angioplasty site was performed with a Palmaz-Schatz stent (Johnson & Johnson, Warren, NJ, USA), and the stenosis was completely relieved. Intravenous administration of dobutamine hydrochloride was started together with intraaortic balloon pumping (IABP). Heparin was initiated intravenously at 600 U•h-1 to control activated coagulation time at between 160 and 180 seconds. Oral warfarin was added the next day, and IABP was ceased on day 3. The patient complained of chest discomfort on day 7, and her systolic blood pressure fell below 90 mm Hg. The echocardiogram showed a 2-cm-wide free pericardial space, and chest computed tomography revealed hemopericardium. These changes strongly suggested LV free wall rupture resulting in cardiac tamponade. Emergent surgery was performed.
During general anesthesia induction, blood pressure fell to 44/30 mm Hg. Immediate pericardiotomy relieved cardiac tamponade with an elevation of blood pressure to 110/56 mm Hg. Extracorporeal circulation was started, with total bypass flow of 2.4 L•min-1•m-2 at 32°C without cardiac arrest. The apical myocardium between the left anterior descending artery and the 2nd diagonal branch was edematous and reddish, and continuous blood effusion was clearly observed (Figure 1A
). A 15-watt Nd:YAG laser (CL 50; SLT Japan, Kofu, Japan) of 1.064 µm wavelength, transmitted through a surgical rod holder (SRH 4; SLT Japan, Kofu, Japan), was directed at the ruptured myocardium, turning it into coagulative and degenerative tissue (Figure 1B). A thin layer of fibrinogen–thrombin glue was sprayed on the treated area to cover and seal it (Figure 1C). The site was then covered with a 0.1-mm thick polytetrafluoroethylene patch, which was firmly sutured to the normal myocardium around the infarct (Figure 1D). Finally, the fibrinogen–thrombin glue was injected into the space between the epicardium and the patch. The patient was easily weaned from extracorporeal circulation without the assistance of IABP.
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Figure 1. (A) Continuous blood effusion from the apical wall. (B) Noncontact laser directed at the hemorrhagic myocardium. (C) Fibrinogen–thrombin glue sprayed over the coagulated site. (D) Patch reinforcement of the site.
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Postoperatively, dopamine hydrochloride and amrinone were intravenously administered to maintain the cardiac index at above 2.1 L•min-1•m-2 during the first 48 hours. Mechanical ventilation was stopped the next day, and ventricular fibrillation was converted to sinus rhythm by electrical conversion on day 4. The patient was discharged without complications on day 30. Since the operation, she had been taking orally enalapril maleate, carvedilol, furosemide, aspirin, and simvastatin, and had been in New York Heart Association functional class I. Her LV ejection fraction on the echocardiogram was 38% 5 years postoperatively.
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DISCUSSION
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The traditional surgical treatment of free wall rupture following acute myocardial infarction is infarctectomy with Dacron patch closure using pledgeted sutures.3 However, this procedure has technical limitations and produces poor results. Sutureless techniques using biological or cyanoacrylate glue to repair the lesion has been reported.3–5 The glue is effective for binding 2 different tissues but ineffective for hemostasis with single use. In our procedure, laser is applied to the lesion to bring about coagulation, tissue degeneration, and vessel shrinkage. Nd:YAG laser–tissue interaction of the vascular system was found to produce 0.2-mm-deep carbonization, 0.5 mm of coagulation, and 1.5 mm of denaturation.6 Another advantage of laser coagulation is the noncontact approach to the necrotic myocardium. Laser energy is transmitted to the beating heart without contact, which is preferable to the contact method of electrical cautery.
We conclude that myocardial laser coagulation with fibrinogen–thrombin glue application effectively repairs free wall rupture, and patch reinforcement of the lesion prevents rerupture.
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REFERENCES
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- Mizutani T, Suzuki H, Katayama Y. New application of a bipolar Nd-YAG handpiece in laser cardiac surgery. In: Anderson RR, Bartels KE, Bass LS, Gregory KW, Harris DM, Lui H, et al., editors. Lasers in surgery: advanced characterization, therapeutics, and systems VII. Proceedings of SPIE. Vol. 2970. Washington: SPIE, 1997:69–79.
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