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Ann Thorac Surg 1998;66:721-725
© 1998 The Society of Thoracic Surgeons

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Original articles: Cardiovascular

Left ventricular functional improvement after transmyocardial laser revascularization

^a Feinberg Cardiovascular Research Institute, Northwestern University Medical School, Chicago, Illinois, USA

Address reprint requests to Dr Horvath, Northwestern University Medical School, 251 E Chicago Ave, Suite 1030, Chicago, IL 60611
e-mail: (khorvath{at}nmh.org)

Presented at the Poster Session of the Thirty-fourth Annual Meeting of The Society of Thoracic Surgeons, New Orleans, LA, Jan 26–28, 1998.

	Abstract

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Background. Transmyocardial laser revascularization has been used to treat patients with end-stage coronary artery disease that is not amenable to standard revascularization. Although there is evidence of angina relief and quality of life enhancement, there is little information concerning improvement in myocardial contractility. The purpose of this study was to determine whether transmyocardial laser revascularization improves myocardial function in chronically ischemic myocardium.

Methods. In a model of chronic ischemia by Ameroid occlusion of the circumflex artery, domestic pigs (n = 8) were treated with transmyocardial laser revascularization. Before laser treatment, segmental contraction was assessed at rest and with dobutamine stress echocardiography. Myocardium subtended by the occlusion was compared with that remote from the occlusion. Six weeks after transmyocardial laser revascularization, the animals were restudied at rest and with stress, and then sacrificed. Sham-treated control animals (n = 4) underwent the same procedures but were not treated with transmyocardial laser revascularization. Control animals did not demonstrate significant recovery of function.

Results. Transmyocardial laser revascularization improved resting function in chronically ischemic myocardium by 100%.

Conclusions. Transmyocardial laser revascularization significantly improves the function of chronically ischemic myocardium. These data may help explain the mechanisms by which transmyocardial laser revascularization is clinically effective.

	Introduction

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Transmyocardial laser revascularization (TMR) is a relatively new therapy for treating patients with end-stage coronary artery disease. Because of the diffuse nature of their disease, these patients are not candidates for coronary artery bypass grafting or angioplasty and are experiencing severe angina refractory to medical management.

Since 1993, more than 4,000 patients have been treated worldwide with TMR using a CO₂ laser to create transmural channels as sole therapy for their disabling angina [1–5]. Clinical results have been encouraging: 75% to 80% of the patients have improved by at least two angina classes, and 30% are angina-free 1 year after TMR. In addition to the symptomatic improvement, there is a reduction in ischemia and enhanced blood flow as evidenced by single-photon emission computed tomography and positron emission tomography myocardial perfusion scans after TMR [1–3].

In a large-animal model of acute myocardial ischemia, TMR has previously been shown to reduce infarct size and improve myocardial contractility [6, 7]. Histologically, the ischemic area in the laser-treated animals had evidence of transmural blood-filled channels extending into neighboring sinusoids and interstitium with minimal thermal damage and viable myocardium around the channels. However, whether TMR improves the function of chronically ischemic myocardium is unknown. This is an important distinction because patients treated with TMR have chronic rather than acute ischemia.

Clinical studies to determine the improvements in function after TMR are important but will undoubtedly include a heterogeneous mix of patients, medications, and myocardium. The purpose of this study was to determine the effect of TMR on myocardial function in chronically ischemic myocardium.

	Material and methods

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Animal model
Animals received humane care as approved by the Center for Experimental Animal Research at Northwestern University and in compliance with the "Guide for the Care and Use of Laboratory Animals" published by the National Institutes of Health (NIH publication 85-23, revised 1985).

To accurately mimic the clinical scenario, we employed the standard model of chronic myocardial ischemia (Ameroid occlusion of the circumflex artery). For these experiments, the animals underwent three operative procedures over a 12-week period (Fig 1). In the first operation, an occluder that slowly constricts the circumflex coronary artery was placed. Six weeks later, the animals were studied at rest and with stress. During this second operation, the ischemic zone was left alone (control group) or treated with TMR. At 12 weeks after the first operation, the animals were restudied and sacrificed.

View larger version (38K): [in this window] [in a new window]   Fig 1. The experimental protocol. The animals underwent three operations as illustrated by this timeline. (TMR = transmyocardial laser revascularization.)

Operation 1
With use of sterile technique, the heart was exposed through a small left thoracotomy and the pericardium was opened. The proximal left circumflex coronary artery was dissected free of surrounding tissue for a length of 1 to 1.5 cm. An Ameroid constrictor (Research Instruments Mfg, Corvallis, OR) with an internal diameter of 2.5 mm was placed around the origin of the left circumflex artery. The pericardium and chest were then closed and the animal was allowed to recover. The animals were ambulatory before leaving the operating room suite and were monitored daily by a veterinarian and his staff as well as the surgical team. Adequate food and water were provided and intake as well as weights were measured daily. Antibiotics were administered intramuscularly for 3 days postoperatively. Pain medications were also given intramuscularly until the animals were ambulating without difficulty and exhibited normal levels of activity.

The Ameroid constrictor was sized to provide a close but nonconstrictive fit over the artery. The constrictor is a C-shaped metal cylinder lined with a hydrophilic material that swells over time and slowly occludes (4 to 6 weeks) the artery, rendering the circumflex territory ischemic. There were no acute electrocardiographic changes after Ameroid placement.

Operation 2
Through a larger left thoracotomy, the pericardium was opened and the heart reexposed. Continuous blood pressure monitoring via an arterial line placed in the left internal mammary artery as well as electrocardiographic monitoring was employed. Using an epicardial echocardiography probe (7.5 MHz; model 128; Acuson, Inc, Mountainview, CA), we assessed regional and global function at rest and with dobutamine stress echocardiography. Dobutamine was administered intravenously starting at 5 µg · kg^-1 · min^-1 and titrated to a maximum infusion rate of 50 µg · kg^-1 · min^-1 to achieve at least a 50% increase in heart rate. This dobutamine stress was performed to verify that the ischemic zone was viable and not infarcted. The echocardiographic images were recorded onto -inch videotape. Hearts were then allowed to recover from the dobutamine stress echocardiography. Once echocardiographic data confirmed the presence of chronic ischemia of the circumflex distributions, the circumflex territory (ischemic zone) was then treated with TMR (n = 8). Control animals (n = 4) underwent the same protocol but were not treated with TMR. Transmural channels (22 ± 1) were created in a distribution of one channel per square centimeter in each TMR-treated animal. Transmural penetration by the laser was confirmed by echocardiogram. The thoracotomies were then closed and the animals allowed to recover. The aforementioned postoperative care was repeated.

Operation 3
Six weeks later, the animals underwent repeat thoracotomy. Repeat epicardial echocardiography was performed at rest and with dobutamine stress as per the protocol described for operation 2.

Echocardiographic analysis
End-diastolic and end-systolic short-axis images were then digitized off-line from the videotape with a dedicated software package (Prism Lite for Windows, v5.14; Tomtec Imaging Systems, Broomfield, CO). The digitized images were spatially calibrated and the endocardial and epicardial contours were traced. The software then automatically calculated the wall motion along the 100 evenly distributed lines of site around the contour. By standard segmental contraction analysis, the mean wall motion score for each segment was obtained (48 segments for each short axis image). Segmental contraction was defined as the change in wall thickness between systole and diastole as measured in centimeters. Echocardiographic analysis was performed by an independent observer blinded to the treatment that the animal received. Segmental contraction was compared in all segments at all times using each animal as its own control. As an additional control, the data from the untreated animals were compared with those of the TMR treated animals.

Segmental contraction data (as measured by wall thickening) at baseline and at follow-up was compared with the use of a paired t test and one-way analysis of variance using SigmaStat for Windows v2.0 (SPSS Inc, Chicago, IL). Differences were considered significant at p less than 0.05. When necessary, a Bonferroni correction for repeated measures at multiple time points was used. The p values listed are two-sided p values. Results are expressed as mean ± standard deviation.

	Results

Top Abstract Introduction Material and methods Results Comment Acknowledgments References

 
All animals underwent the same degree of stress at each operation. There was no significant difference in the resting heart rates at operation 2 (6 weeks after Ameroid placement) or operation 3 (12 weeks after Ameroid placement) (103 ± 22 versus 85 ± 8; p = 0.6). Similarly, there was no significant difference between the stress heart rates at operations 2 and 3 (181 ± 28 versus 155 ± 19; p = 0.4). This yielded an average of a 75% increase in the resting heart rate when stressed at operation 2, and an 82% increase in the resting heart rate when stressed at operation 3. Mean arterial pressures demonstrated a modest increase with stress, and there was no significant difference between the resting and the stressed blood pressure measurements for operation 2 versus operation 3.

Echocardiographic measurements of segmental contraction 6 weeks after placement of the Ameroid constrictor demonstrated hypokinesis of the ischemic zone of myocardium subtended by the occlusion (Fig 2). Segmental contraction was significantly decreased after Ameroid placement (Fig 3). At operation 2, the segmental contractility in the ischemic zone was 0.26 ± 0.05 cm (mean ± standard deviation) (see Fig 3). These values in animals that were subsequently treated with TMR were similar to the contractility in the ischemic zone of the sham-treated control animals (0.32 ± 0.06 cm). In contrast, the nonischemic zone had resting contractility of 0.63 ± 0.08 cm. After treatment with TMR, the resting segmental contraction in the ischemic zone improved to 0.50 ± 0.04 cm. The resting contractility in the untreated nonischemic zone was unchanged, at 0.62 ± 0.03 cm. Control animals showed no improvement in resting contractility in the ischemic zone (0.37 ± 0.07 cm).

View larger version (61K): [in this window] [in a new window]   Fig 2. Representative echocardiographic images and analysis of segmental contractility. These short axis myocardial contour tracings demonstrate the amount of contractility at rest. The inner line represents myocardial wall position at end-systole. The outer line represents end-diastole. Segmental wall motion in the ischemic zone is diminished before transmyocardial laser revascularization (TMR) (A) and improves after TMR (B).

View larger version (33K): [in this window] [in a new window]   Fig 3. Echocardiographic measurements of segmental contraction. Wall thickening (in centimeters) for all segments in the transmyocardial laser revascularization (TMR)-treated ischemic zone (dash/dot line) compared with the nonischemic zone in the same animals (dashed line). The wall thickening in the ischemic zone of the control animals (solid line) shows the same decrease in resting function after Ameroid placement without recovery over time.

	Comment

Top Abstract Introduction Material and methods Results Comment Acknowledgments References

Clinically, TMR has primarily been used in the treatment of chronic myocardial ischemia. To optimize clinical relevance, a model of chronic myocardial ischemia was used in the present study. This model provides a reproducible area of collateral-dependent tissue as a result of the Ameroid constriction. Historically, this model establishes an ischemic zone that has diminished function at rest and with stress [15, 16]. This preparation is stable over time (up to 16 weeks) and may show some improvement in resting function at that interval. To account for this, we have employed two types of controls. Each animal serves as its own control in that the segmental contraction of the nonischemic zone is compared with that of the ischemic zone over time. Additionally, a group of animals that underwent the same coronary occlusion were not treated with the laser. These control animals showed a decrease in resting function that did not significantly change over the 6-week interval.

One potential limitation is that the echocardiographers could bias the results, as they are not blinded to the treatment the animals received. Similarly, points of acquisition of echo images may be variable at different times. We attempted to diminish bias by having the analysis performed by a different observer who was blinded to the treatment the animals received. The variability in this analysis on a frame-by-frame basis was less than 5%.

Myocardium responds to acute and chronic ischemia in different ways. For example, it is quite common to see an increase in collateral circulation on a patient’s angiogram in response to chronic ischemia. These collaterals are not as extensive in a more acutely ischemic heart and are nonexistent in normal myocardium. Similarly, one would not expect the laser channels or ensuing collateral development as a result of TMR to occur in normal myocardium or to be as extensive in acutely ischemic myocardium. The functional response to chronically and acutely ischemic myocardium is different as well. Significant and sometimes permanent dysfunction is seen with acute ischemia. The same coronary occlusion developed chronically may lead to minimal dysfunction depending on the degree of collateral development. This is particularly true in the resting state.

Donovan and associates [17] recently reported that dobutamine stress echocardiography before and after TMR demonstrated improvement in inducible ischemia during stress in laser treated segments. An improvement in resting contractile function after TMR was also noted. Donovan and associates concluded the reduction in ischemic wall motion during peaked dobutamine stress echocardiography indicates an improvement in local perfusion to these regions. There are several differences between this clinical study and our experimental work. Most importantly, the patients had multivessel disease and were taking a number of different medications. The advantage of the present study is the ability to control the many variables, such as extent of ischemia and medications, that are present in a clinical study. Additionally, measurements were made at 6 weeks as compared with 12 weeks for the clinical study. It is unknown whether the improvement at rest would translate into an improvement with stress if given more time.

In summary, the results of the present study show an improvement in function of chronically ischemic myocardium after TMR. Whether this is due to an increase in perfusion as a result of new blood vessels after TMR requires further experimentation.

	Acknowledgments

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Support for this research was provided by a grant from the A. Ward Ford Memorial Institute, Inc, Wausau, WI.

	References

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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): Keith A. Horvath David A. Fullerton Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Horvath, K. A. Articles by Fullerton, D. A. Search for Related Content PubMed PubMed Citation Articles by Horvath, K. A. Articles by Fullerton, D. A.