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Ann Thorac Surg 1996;61:1532-1534
© 1996 The Society of Thoracic Surgeons
Weeks
Departments of Medicine, Pathology, and Surgery, Columbia-Presbyterian Medical Center, New York City, New York
Accepted for publication November 22, 1995.
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Abstract |
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weeks after operation that show that the channels do not maintain patency. Further work is needed to determine the frequency of channel patency and its relation to clinical benefit. |
Introduction |
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Transmyocardial laser revascularization (TMLR) is an experimental treatment for patients with angina that is refractory to medical therapy who are also unsuitable for treatment with coronary artery bypass grafting or angioplasty [1–3]. A high-energy laser is used to make 
1 mm channels through the myocardium into the left ventricular chamber. Although the epicardial region of the channel seals within a few moments after creation, it has been hypothesized that the remainder of the channel remains patent and that blood can flow from the left ventricular chamber to directly perfuse the myocardium, totally bypassing the epicardial vasculature [1, 4, 5].
Although results of clinical studies continue to suggest that this treatment is effective in relieving angina, data from animal studies have been mixed. Results of some studies have suggested that channels remain patent and protect against infarction [5], but other studies have challenged these primary hypotheses [6, 7]. Although limitations of clinically available techniques have made it impossible to test whether blood can flow through TMLR channels in the hearts of treated patients, histologic sections obtained at the time of autopsy have been interpreted by previous investigators as demonstrating patent channels weeks to months after the procedure [1, 2].
In this case report, we present autopsy results obtained from a patient who died 4 weeks after TMLR of complications unrelated to a failure of the treatment. The results show that the channels do not maintain patency in this patient.
The patient was a 71-year-old man with a history of diabetes, hypertension, and smoking. He suffered an inferior wall myocardial infarction 18 years ago (1977), after which he underwent three-vessel bypass grafting with vein grafts. He was free of angina for approximately 17 years. Six months before referral to Columbia-Presbyterian Medical Center, he reported a crescendo pattern of exertional and rest angina despite gradual increase in medical therapy, which ultimately included atenolol, diltizem, isosorbide dinitrate, furosemide, and lisinopril. Cardiac catheterization revealed a patent sequential graft to the first diagonal branch of the left anterior descending artery and first obtuse marginal artery, an occluded graft to the posterior descending artery, a totally occluded proximal right coronary artery, a very small left anterior descending artery, a small and diffusely diseased second obtuse marginal artery, and a long posterior descending artery (wrapping around the apex) with diffuse disease that filled via collaterals from the left circumflex artery. The diffuse nature of the disease in both the posterior descending and second obtuse marginal arteries rendered the patient unsuitable for treatment with either coronary artery bypass grafting or angioplasty, and it was decided to treat the patient medically. However, he continued to have symptoms of angina and was referred for consideration of TMLR in January 1995. An exercise thallium test was performed. He exercised 6 minutes on a modified Bruce protocol to a peak heart rate of 125 beats/min; he stopped exercising because of shortness of breath, but denied chest pains. Comparison of rest and exercise thallium scans revealed a fixed posterior defect and reversible defects in the inferoapical, anteroapical, and lateral walls.
Transmyocardial laser revascularization was performed on February 7, 1995, with The Heart Laser (PLC Systems, Inc, Milford, MA), which consisted of applying a total of 25 laser shots (40 J/channel) over the inferior, apical, and anterolateral regions of the heart. Twenty-four of these were confirmed to penetrate into the ventricular cavity as evidenced by visualization of bubbles filling the left ventricle on the transesophogeal echocardiogram. The patient did well after the operation and was discharged on the seventh postoperative day. However, he presented on postoperative day 24 after a bout of prolonged chest pain at rest. Cardiac catheterization was performed, which revealed a new critical stenosis in the previously patent saphenous vein graft. The lesion was dilated and a stent was placed with good result. A standard anticoagulation protocol was initiated. However, after the second warfarin dose (total of 20 mg), the prothrombin time became markedly elevated and remained elevated despite the discontinuation of heparin administration and, ultimately, the administration of fresh frozen plasma. The patient sustained a large, fatal intracerebral bleed. The family consented to an autopsy.
Numerous fibrous plaques were easily identified on the epicardial surface of the heart, which demarcated the sites at which laser channels had been created. Gross inspection of the endocardium also revealed fibrous plaques, presumably located at the original entry sites of the channels into the left ventricle, suggesting that any direct connection between the chamber and the myocardium was not patent. When the myocardium was cut from epicardium to endocardium in multiple transverse sections, channel regions were easily identified by eye as elliptical fibrous transmural scar extending from the epicardium to the endocardium. Microscopic examination was performed on nine of the channels; samples were chosen randomly from all portions of the treated regions (Fig 1
). Each channel consisted of fibrous scar, some of which included thin-walled capillaries in the central area of the channel remnant (see Fig 1A). No channel showed any residual patent central passage at any level through the myocardial wall.
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Comment |
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Although only about a third of the original channels were subjected to microscopic examination and it is possible that some of the channels that were not examined could have been patent, most of the channels were identified during gross inspection and all had the same appearance; any patent channels with diameter of about 1 mm would have been identified.
Thus, in contrast to previous histologic specimens, which have been interpreted as suggesting that TMLR channels remain patent several months after the procedure [1, 2, 4], the present results indicated that TMLR channels did not maintain patency in the present patient. Further work is needed to determine the frequency of channel patency in a larger number of patients and its relation to observed clinical benefit. We propose that mechanisms other than blood flow through patent channels should be considered.
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