Eur J Cardiothorac Surg 1999;16:135-143
© 1999 Elsevier Science NL
Transventricular non-transmural laser treatment of hypoperfused porcine myocardium acutely reduces left ventricular contractile function
Georgios K. Kanellopoulosa,b,
Aud Svindlandc,
Arnfinn Ilebekka,
Ingeborg Goverudc,
Knut Kvernebob
a Institute for Experimental Medical Research, Ullevaal University Hospital, University of Oslo, Oslo, Norway
b Department of Cardiothoracic Surgery, Ullevaal University Hospital, University of Oslo, Oslo 0407, Norway
c Department of Pathology, Ullevaal University Hospital, University of Oslo, Oslo, Norway
Corresponding author. Tel.: +47-22-119500; fax: +47-22-117470.
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Abstract
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Objective: Creation of non-transmural myocardial channels by lasers transmitted through endovascular fiberoptics is a novel therapeutic option in the management of patients with coronary artery disease. The acute effect of transventricular laser treatment (TvL) on coronary blood flow, myocardial metabolism and left ventricular function are not well established. Methods: In five anesthetized pigs, flow in the proximal left anterior descending coronary artery (LAD) was reduced and maintained at 70% of baseline. A venous shunt had previously been established draining the hypoperfused region. At 30 min of ischemia, non-transmural myocardial channels were created through the endocardium using a Ho:YAG laser. We measured (a) left ventricular, central venous and arterial pressures, (b) ascending aortic, LAD and coronary venous blood flows, as well as (c) lactate concentration and blood gases in arterial and coronary venous blood, prior to ischemia (baseline), before and 30 min after TvL. Data (given as mean±SD) were analyzed with repeated measures ANOVA. Results: Reduction of LAD blood flow resulted in reduced regional coronary venous blood flow and myocardial oxygen consumption, conversion of regional myocardial lactate uptake to release and adaptation of left ventricular contractility to a lower level. Following transventricular laser, the peak left ventricular systolic pressure declined from 86±12 to 77±11 mmHg (P<0.05), its maximal first positive derivative (LV dP/dt) declined from 900±221 to 763±127 mmHg/s (P<0.05) and the stroke volume decreased from 19.2±4.1 to 16.4±5.4 ml (P<0.05). The changes in regional coronary venous flow, myocardial oxygen consumption and myocardial lactate release after TvL were not significant compared to before TvL. Significant intramural hematomas and tissue destruction were found around the channels at autopsy and by histologic examination. Conclusion: Transventricular laser treatment of hypoperfused myocardium decreased left ventricular contractility in the acute phase, possibly due to development of perichannel hematomas and disruption of the wall architecture. In addition, TvL did not alter the regional myocardial oxygen supply/demand balance. These results call for caution in the treatment of patients with coronary artery disease by transventricular Ho-YAG laser when there is significant impairment of the left ventricular contractile function.
Key Words: Metabolism • Myocardial ischemia • Coronary circulation • Oxygen consumption • Regional blood flow • Pig • Angina pectoris
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1. Introduction
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Laser treatment of the myocardium is a novel procedure whose place in the management of patients with coronary artery disease is under investigation. Laser treatment of the myocardium may be achieved not only by open or thoracoscopic approaches, but also by the transventricular approach following percutaneous transluminal insertion of a laser probe in the left ventricular cavity. The latter procedure, which involves the creation of non-transmural myocardial channels through the endocardium, is considered attractive because it requires neither general anesthesia nor thoracotomy. The fist report from a feasibility study on the use of percutaneous laser myocardial ‘revascularization’ for treatment of patients with angina pectoris has been published recently [1].
Laser treatment of the myocardium was initially developed on the premise that laser-created transmural channels directly augmented nutritive perfusion of the myocardium by conducting blood from the ventricular cavity [2,3]. The effect of a series of transmural channels on left ventricular wall structure, perfusion, metabolism and contractile function have been examined in a number of animal and in vitro studies. On the other hand, the effect of non-transmural laser channels created by the transventricular approach have received limited attention [4–7]. The objective of this study was to assess the acute effect of transventricular non-transmural laser treatment on regional coronary venous flow, regional myocardial metabolism and left ventricular contractility. For this purpose we used a well-characterized porcine model of acute myocardial hibernation [8,9]. We performed this study in the pig because native collaterals in this species are very sparse [10] and, therefore, it would not be necessary to include collateral flow in the interpretation of the results.
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2. Materials and methods
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2.1. Animal preparation
Five male domestic pigs weighing 28–33 kg were used in this study. Animal care and procedures complied with institutional guidelines and with conditions set by the European Convention on Animal Care. The animals were anesthetized with injection of pentobarbital sodium, 40 mg/kg, intraperitoneally; a satisfactory depth of anesthesia was maintained during the experiment by continuous administration of pentobarbital sodium 5–20 mg/kg per h, intravenously. The animals were intubated through a tracheostoma and were ventilated with a 50% oxygen/50% air mixture by a volume regulated ventilator (model 101; Princeton Medical Instruments, Natick, MA, USA). The ventilation rate and volume were adjusted to maintain normal pCO2. The left femoral artery was cannulated for pressure monitoring (model P23 Gb; Gould Instruments, Hato Rey, PR, USA) and for obtaining arterial blood samples. The left femoral vein was also cannulated for fluid replacements. A microtip pressure transducer catheter (model PC-470; Millar Instruments, Houston, TX, USA) was introduced into the left ventricular cavity via the right common carotid artery. A polyethylene cannula was passed through the right internal jugular vein into the superior vena cava for monitoring central venous pressure. Three-lead electrocardiogram was used to monitor heart rate and rhythm. A urinary catheter was introduced into the bladder through a cystostoma. Constant intra-abdominal temperature was maintained between 37 and 39°C throughout the experimental protocol by using an electric heated mattress and drapes. A midline sternotomy was performed and the pericardium was incised vertically to expose the heart. An electromagnetic flow probe was placed around the ascending aorta for measuring aortic flow (model 376; Nycotron, Drammen, Norway). Two adjacent segments of the left anterior descending artery (LAD), each about 0.5 cm in length, were dissected close to the origin of the artery form the left main coronary artery (Fig. 1). A transit time flow probe (Transonics Inc., Ithaca, NY, USA) was placed around the most distal segment for measuring blood flow in the LAD (Doppler Master VF-1; Crystal Biotech, Holliston, MA, USA). The cuff of a hydraulic occluder was placed around the most proximal segment. Heparin sulfate, 400 IU/kg was administered by intra-arterial injection and this was followed by continuous heparin infusion, 60 IU/kg per h, intravenously. A shunt from the anterior interventricular vein to the right atrium was established according to a previously described technique [11,12] (Fig. 1). The anterior interventricular vein was ligated at a suitable level distal to the level of the hydraulic occluder cuff on the LAD and the one end of a polyvinyl shunt (internal diameter of 5 mm) was inserted distal to the ligature in the retrograde direction. The other end of the shunt (internal diameter of 7 mm) was introduced in the right atrium. A transit time flow probe (Transonics Inc., Ithaca, NY, USA) was placed around the shunt tube and connected to the same flow meter as the LAD flow probe. A side branch with a three-way stopcock attached to its end was incorporated in the shunt.
2.2. Experimental protocol
A period of stabilization followed the end of the surgical preparation during which none of the monitored hemodynamic parameters deviated more than 10% of the baseline for at least 30 min (Fig. 2). Baseline measurements and blood samples were obtained in the end of this period. Subsequently, the flow in the LAD was reduced and maintained at approximately 70% of the baseline till the end of the experiment. It has previously been shown in our laboratory that the shunt drains the ischemic myocardial region [12]. A second set of data was obtained 30 min after the establishment of reduced flow in the LAD (referred to as ‘before transventricular laser (TvL)’). Then, a Holmium-yttrium-aluminum garnet (Ho-YAG) laser (Cardiogenesis, Sunnyvale, CA, USA) was used to create non-transmural channels through the endocardium in the myocardial region drained by the venous shunt by a technique similar to the one used in a previous study [13]. The laser probe (ITMR probe, Cardiogenesis, USA), was introduced in the left ventricular cavity through the posterolateral wall of the ventricle avoiding visible epicardial vessels and the posterior papillary muscle. The probe was advanced and its tip, which had a diameter of 1.75 mm, was easily stabilized against the endocardial aspect of the anterior wall by gentle pressure. The position of the laser fiber tip against the anterior left ventricular wall was accurately located by observing the bright red light produced by the aiming Helium-Neon laser beam transilluminating through the myocardial wall. One laser burst, synchronized with the R-wave of the electrocardiogram, was used for each channel; 6 J were released with each burst in three pulses delivered at a frequency of 16 Hz. Approximately 15 non-transmural myocardial channels were created within the region drained by the coronary venous shunt over a period of about 1 min. Transmural penetration did not occur. Following the creation of the channels, a fingertip was applied on the transmural channel which was used for the entry of the laser probe in the left ventricle to prevent blood loss; bleeding from the entry channel ceased promptly in all animals. A third set data was obtained 30 min after the end of the laser procedure (referred to as ‘after TvL’). At the end of the experiment, the LAD was completely occluded and the blood flow in the shunt was recorded. Finally, the animals were killed by intracardiac injection of potassium chloride and the heart was harvested for histology.
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Fig. 2. Time diagram illustrating the experimental protocol used. A period of at least 30 min was allowed for stabilization after completion of the surgical preparation and prior to reduction of blood flow in the left anterior descending coronary artery (LAD). The period of reduced blood flow in LAD is shaded. The period of transventricular laser treatment of the myocardium is shown in black. Arrows indicate the time points when blood samples for metabolic measurements were taken.
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2.3. Hemodynamic measurements
The heart rate, arterial blood pressure, central venous pressure, left ventricular pressure as well as the blood flow in the ascending aorta, the LAD and the coronary venous shunt were continuously monitored. The maximal positive value of the first derivative of the left ventricular pressure and the stroke volume were electronically calculated from the left ventricular pressure and aortic flow signals, respectively. The systemic vascular resistance was calculated by dividing the difference between mean arterial and mean central venous pressures by the aortic flow. All hemodynamic variables were continuously recorded by an eight-channel galvanometric recorder (Hewlett-Packard, model 7758 B). The output of the recorder was sampled periodically at 100 Hz and the signals were transformed and stored in digital form.
2.4. Biochemical measurements and calculations
In order to monitor changes in biochemical indicators of myocardial metabolism, blood samples were simultaneously obtained from both the femoral artery and the coronary venous shunt at baseline, after 30 min of myocardial hypoperfusion (referred to as ‘before TvL’) and 30 min after transventricular laser treatment (referred to as ‘after TvL’). Special care was taken not to reverse the direction of blood flow in the venous shunt (determined with Doppler flowmetry) during sampling of blood from the venous shunt; this ensured that the sample was free of contamination by blood from the right atrium. The blood samples were used for measurements of blood gases, blood pH, hemoglobin concentration, oxygen saturation, packed cell volume and serum lactate. Duplicate samples were obtained anaerobically using cold syringes containing heparin sulfate; the final value for each parameter was the average of the two measurements. Blood gases, hemoglobin concentration and oxygen saturation were assessed immediately by an automatic blood gas analyzer (model OMNI 945; AVL List GmbH, Graz, Austria) and an automatic hemoximeter (model OSM3; Radiometer, Copenhagen, Denmark). Packed cell volume (PCV) was measured using microhematocrit tubes. Samples for analysis of the plasma lactate concentration were temporarily stored on ice; they were centrifuged within 30 minutes and the plasma was stored in the freezer at -20°C. The plasma lactate concentration was determined by an enzymatic spectrophotometric method [14] within 2 days of the collection of specimens.
The oxygen consumption (MVO2, in ml of O2 per min) in the myocardial region drained by the coronary venous shunt was computed by multiplying the arterio-coronary venous difference in oxygen content by venous shunt flow determined with the flowmeter probe. Oxygen content in the arterial and the venous shunt blood (in milliliters of oxygen per deciliter of blood) was calculated as (hemoglobin concentration (g/dl)x1.34 (ml/g)xoxygen saturation (decimal value))+(PO2 (mmHg)x0.0031 (ml/dl per mmHg)).
The lactate release (in µmol/min) in the myocardial region drained by the venous shunt was calculated by the following formula: (coronary venous lactate concentration-arterial lactate concentration)xCBFx(1-PCV), where concentrations are given in µmol/ml, CBF is venous shunt blood flow in ml/min and PCV is packed cell volume. A negative value was interpreted as lactate extraction and a positive value as lactate release.
2.5. Histological analysis
The anterior left ventricular wall region with laser-created channels was fixed in buffered paraformaldehyde solution for at least 5 days. Representative myocardial slices were subsequently cut perpendicular to the heart apex to basis axis and were embedded in paraffin. Sections 5 µm in thickness were stained with hematoxylin and eosin (H&E) and with acid fuchsin orange G (AFOG).
2.6. Statistical analysis
Data are reported as mean±SD. Each animal served as its own control. One way repeated measurements ANOVA followed by post hoc testing with Student–Newman-Keuls method was used for the comparison of measurements obtained at baseline, before TvL and after TvL. A P value of less than 0.05 was accepted as indicating a significant difference in mean values.
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3. Results
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3.1. Blood flow in the LAD and the coronary venous shunt
By partial inflation of the cuff of the hydraulic occluder, blood flow in the LAD was reduced from 27±8 ml/min to 18±6 (68±4% of baseline, P<0.001; Fig. 3). This was associated with a drop of the blood flow in the venous shunt from 18±8 ml/min to 13±6 (74±14% of baseline, P<0.05). At 30 min after TvL, the coronary venous blood flow was 14±8 ml/min (P=0.8 compared to before TvL) with constant blood flow in the LAD. Blood flow in the venous shunt was only 1±2 ml/min (4±6% of baseline) during complete occlusion of the LAD in the end of the experiment, indicating that the shunt almost exclusively drained the myocardial region subjected to ischemia.
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Fig. 3. Blood flow in the left anterior descending artery (LAD) and the coronary venous shunt as well as oxygen saturation in regional coronary venous blood at baseline, at 30 min after induction of reduced blood flow in the LAD (before TvL) and at 30 min after transventricular laser treatment (after TvL). Values are means, vertical bars represent standard deviations; n=5; *P<0.05.
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3.2. Left ventricular contractility and hemodynamic parameters
Peak left ventricular systolic pressure (LVSP) adapted within 1 min after reduction of blood flow in the LAD and remained stable for the following 30 min. The LVSP was reduced from 95±15 mmHg at baseline to 86±12 at 30 min of low flow (P<0.05; Fig. 4). Similarly, the maximal positive value of the first derivative of the left ventricular pressure (LV dP/dt) was reduced from 1038±311 mmHg/s to 900±221 (P<0.05). At 30 min after TvL, the LVSP and the LVP dP/dt were further reduced to 77±11 mmHg and 763±127 mmHg, respectively (P<0.05 compared to before TvL for both parameters). There were associated significant decreases of the mean arterial blood pressure and stroke volume (Fig. 4). No significant changes were observed in heart rate and central venous pressure between baseline, before and after TvL (Fig. 4).
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Fig. 4. Hemodynamic variables at baseline, at 30 min after induction of reduced blood flow in the LAD (before TvL) and at 30 min after transventricular laser treatment (after TvL). Values are means, vertical bars represent SDs; n=5; *P<0.05.
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3.3. Blood gases, blood pH, hemoglobin concentration and oxygen saturation
The differences in partial pressures for O2 and CO2, pH, the hemoglobin concentration and the oxygen saturation in both arterial and coronary venous blood were not statistically different before and after TvL (Table 1 and Fig. 3). In four out of five animals, the oxygen saturation in the venous shunt blood after TvL was higher than before TvL. In two animals, the coronary venous oxygen saturation after TvL (24.5 and 19%) was even higher than baseline values (22.5 and 14.75%, respectively).
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Table 1. Blood gases, pH, hemoglobin concentration in arterial and coronary venous shunt at baseline, before and after transventricular laser treatmenta
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3.4. Regional myocardial oxygen consumption and lactate release
The mean oxygen consumption in the myocardial region drained by the coronary venous shunt (MVO2) decreased from 1.98±0.93 ml/min at baseline to 1.58±0.71 at 30 min of hypoperfusion (P<0.05 vs. baseline) (Fig. 5). Thirty minutes after TvL, the MVO2 was 1.56±0.84 ml/min (P=0.75 vs. before TvL). The myocardial region of interest took up lactate at 8.50±9.90 µmol/min at baseline conditions. After coronary flow restriction, myocardial lactate release ensued, amounting to 0.18±7.42 µmol/min (P=0.11 vs. baseline). Thirty minutes after TvL, lactate was again taken up by the myocardium at 1.90±6.51 µmol/min (P=0.49 vs. before TvL).
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Fig. 5. Oxygen consumption and lactate release at the myocardial region drained by the coronary venous shunt at baseline, at 30 min after induction of reduced blood flow in the LAD (before TvL) and at 30 min after transventricular laser treatment (after TvL). Values are means, vertical bars represent SDs; n=5; *P<0.05.
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3.5. Morphological outcomes
Intramural hematomas, visible through the epicardium, developed in the treated myocardial region early after TvL (Fig. 6a). At autopsy, the endocardial openings of the laser-created channels into the left ventricular cavity were apparent at the areas between ventricular trabeculae. A narrow rim of subendocardial hematoma was occasionally seen around the channel opening. The length of the laser channels ranged between 0.8 and 1.2 cm, whereas the thickness of the left ventricular wall at the treated area was approximately 1.8 cm. The blind end of the channels was often dilated forming a cavity whose longest diameter was occasionally more than 5 mm (Figs. 6b and 7a). Significant intramural hematomas radiating from the blind end of the channels were found on sectioning the treated region (Fig. 6b). On histologic examination, the laser channels were seen as non-transmural tissue defects (Fig. 7a) that contained varying amounts of blood. All channels had a patent connection to the ventricular cavity. The cavity of the channels was surrounded by a zone of necrosis, which was often followed by a thin zone with pyknotic cardiomyocytes (Fig. 7b). In addition, a widespread zone of tissue injury, characterized by extravasated erythrocytes and widening of the connective tissue planes (Fig. 7c) was found mainly around the dilated blind end of the channels.
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Fig. 6. (a) Photograph of a porcine heart in vivo taken a few minutes after transventricular laser treatment of the hypoperfused anterior left ventricular wall. Significant intramural hematomas are apparent at the treated area. (b) Gross appearance of a section through a paraformaldehyde -fixed specimen obtained from the left ventricular wall area wall 30 min after transventricular laser treatment. The arrows point to the dilated intramural end of a laser-created channel, which is surrounded by tissue hematoma.
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Fig. 7. (a) Myocardial channel created by transventricular laser in the hypoperfused anterior left ventricular wall of a porcine heart. The arrow points to the dilated intramural blind end of the channel. The section was obtained at 30 min after laser treatment. (Acid fuchsin orange G staining, x2.5). (b,c) High power views of the tissue adjacent to the channel lumen (Acid fuchsin orange G staining, x25). Distinct zones of tissue damage around the channel lumen are seen in (b). Disruption of the normal tissue architecture (arrow) extending beyond the damaged tissue immediately adjacent to the channel lumen may be seen in (c).
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4. Discussion
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The main finding of the present study is that marked deterioration of left ventricular contractility occurred early after laser treatment of hypoperfused myocardium using the transventricular approach. This was associated with intramural bleeding and disruption of the tissue architecture mainly around the blind end of the laser-created channels, but not with impaired metabolism of the ischemic myocardium.
4.1. Model considerations
In the present study we used a previously described model of the so-called short-term myocardial hibernation in the open-chest anesthetized pig. Sustained matching of the myocardial metabolism [9,15] and contractility [8] to the reduced coronary blood flow is a main characteristic of this model. More specifically, left ventricular contractility [8] as well as regional myocardial metabolic parameters, such as oxygen extraction [9], oxygen consumption, ATP level, and lactate uptake/release [15] adapt to acute reduction of LAD flow to 50–80% of baseline and remain stable for at least 30–60 min. In the current study, we opened approximately 15 non-transmural channels in the anterior wall of the left ventricle through the endocardium following introduction of the laser probe in the ventricular cavity through the postero-lateral wall of the left ventricle. Similar techniques for transventricular laser treatment of the anterior left ventricular wall have previously been used in open-chest animal preparations by us [13] and other investigators [5,6].
4.2. Left ventricular function after transventricular laser treatment
Transventricular laser treatment (TvL) of the anterior left ventricular wall resulted in significant acute deterioration of the global left ventricular function as indicated by the 10±4% reduction in peak left ventricular systolic pressure (LVSP) and 14±9% reduction in LV dP/dt at 30 min after TvL. The reduced contractile function resulted in 16±14% and 13±5% reductions in stroke volume and mean arterial blood pressure, respectively. It is likely that TvL-induced damage of the treated left ventricular wall caused regional contractile dysfunction and reduced left ventricular function. Specific acute histopathologic changes were found in the treated wall indicating damage of the tissue between the laser-created channels, which could have contributed to the contractile dysfunction after TvL. Further studies are needed to determine the evolution of the LV contractile function with time after TvL. Although there may be important differences in the effects between transmyocardial and transventricular laser treatment approaches, it is interesting to note that transmyocardial laser treatment of patients with impaired LV function resulted in acute deterioration of the LV function that was reversible within 6 h [16].
4.3. Regional coronary venous blood flow and myocardial metabolism after transventricular laser
The regional coronary venous flow decreased by 26±14% following reduction of the LAD flow by 32±4%. There was an associated decrease in the partial pressure for oxygen in the regional coronary venous blood indicating increased oxygen extraction by the hypoperfused myocardium. In addition, the regional myocardial oxygen consumption decreased by 17±18%, whereas the myocardial lactate extraction was converted to release. Thirty minutes after TvL, there was a small increase of the coronary venous flow, which was accompanied by an increase in the partial pressure of oxygen in the regional coronary venous blood in four out of the five animals despite constant blood flow in the LAD. However, the oxygen consumption remained unaltered and there was no significant change in the rate of myocardial lactate release in the myocardial region drained by the coronary venous shunt at 30 min after TvL. Accordingly, the transventricular laser procedure failed to improve oxygen delivery to the hypoperfused myocardium despite the mild increases in regional coronary venous flow and coronary venous oxygen concentration. The increased coronary venous flow in some animals early after TvL may therefore represent shunting of blood from the ventricular cavity into post-capillary venous channels bypassing the myocardial microcirculation. Our results are consistent with findings from another study on isolated dog hearts, in which non-transmural channels created through the endocardium using a Holmium YAG laser failed to improve nutritive perfusion to ischemic myocardium in the acute phase [4].
4.4. Morphology of heart wall after transventricular laser treatment
In this study we observed significant gross and microscopic changes in the left ventricular wall acutely after treatment by TvL. More specifically, we found dilatation of the blind intramural ends of the laser-created channels with marked tissue disruption and hematomas radiating around these dilatations. Localized dilatations of the channel lumens with damage of the tissue surrounding them have not to our knowledge been described in studies that examined histologic changes within hours following creation of either transmural channels from the epicardial surface [17] or non-transmural channels through the endocardium [6]. However, the presence of dilated intramural channel ends containing blood is consistent with striking radiological images obtained during contrast ventriculography early after TvL; in a previous study, injection of contrast material in the left ventricle of dogs early after TvL demonstrated distinct intramural ‘lakes’ of contrast with dispersion of the contrast into adjacent myocardial tissue [7]. The acute damage of tissue between the channels may be responsible for the associated development of acute left ventricular contractile dysfunction after TvL in the present study.
The thermal and acoustic tissue effects of lasers are probably important in the pathogenesis of the acute tissue damage after TvL [18–20]. The extent of myocardial damage depends on the type of laser light used [20,21]. In this study we used the Holmium-YAG laser because it is one of the lights that can be delivered through an optical fiber and that has been used for the creation of non-transmural myocardial channels through the endocardial surface in patients [1]. The pronounced damage around the blind ends of the laser-created channels suggests that there might be additional factors capable of augmenting the laser-induced thermoacoustic damage in these areas. One such factor might be the development of abnormal intramural pressures acutely after TvL secondary to myocardial contraction around incompressible blood volumes trapped within the channel cavities. Transmission of left ventricular cavity pressures inside the LV wall through patent channel openings could also alter the normal intramural pressure profile in the acute phase after TvL. Administration of heparin, which was given to the animals in accordance to the clinical practice, might have been a factor contributing to the development of intramural hematomas after TvL. This view is supported by the findings from a subsequent study on two additional pigs, where treatment of an hypoperfused myocardial region by transventricular Ho-YAG laser without administration of heparin resulted in decreased acute intramural hematomas.
Creation of non-transmural channels through the endocardium using lasers is an emerging technique in the management of patients with ischemic heart disease, which does not require general anesthesia or thoracotomy. The criteria for the selection of patients to undergo transventricular laser treatment have not been clearly defined yet. In this study, we found that significant reduction of the left ventricular function occurred in the acute phase after transventricular laser of hypoperfused myocardium in an open-chest porcine model. These findings indicate that caution should be employed in the treatment of patients with ischemic heart disease and moderately to severely impaired left ventricular function by transventricular laser.
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Acknowledgments
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The authors would like to thank Professor O.M. Sejersted for his support of this work; Gerd Torgersen for her assistance during the perioperative period; Turid Verpe for help in the use of electronic and technical equipment; Hilde Dishington and Bjorg Austbo for performing the measurements of lactate concentration. This work was financially supported by grants from Forskningsforum Ullevaal Hospital, from the Anders Jahre's Fund for the Promotion of Science and from the Rakel and Otto Kr. Bruun's Legacy Fund.
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Footnotes
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This paper was presented at the 12th Annual Meeting of the European Association for Cardio-thoracic Surgery, Brussels, Belgium, September 20–23, 1998.
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Received December 7, 1998;
received in revised form April 26, 1999;
accepted May 4, 1999.
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Abstract
1. Introduction
