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J Thorac Cardiovasc Surg 2000;120:642-650
© 2000 The American Association for Thoracic Surgery

Surgery for Acquired Cardiovascular Disease

The effect of leukocyte-depleted blood cardioplegia in patients with severe left ventricular dysfunction: A randomized, double-blind study

From the Departments of Thoracic and Cardiovascular Surgery^a and Anesthesiology,^b Kerckhoff-Clinic Foundation, Bad Nauheim, and the Department of Cardiology,^c Heart Center Baden, Lahr, Germany.

Address for reprints: Matthias Roth, MD, Department of Thoracic and Cardiovascular Surgery, Kerckhoff-Clinic Foundation, Benekestr 2-8, 61231 Bad Nauheim, Germany (E-mail: Matthias.Roth{at}kerckhoff.med.uni-giessen.de).

	Abstract

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Background: The propensity for leukocytes to cause reperfusion injury in patients undergoing heart surgery is widely accepted. Reperfusion injury may result in myocardial damage and unfavorable operative outcome, especially in patients with severely reduced ejection fractions. This study was performed to evaluate the impact of leukocyte filtration on the postoperative course of patients undergoing coronary bypass surgery.
Methods: Thirty-two patients with coronary artery disease and left ventricular ejection fraction less than 35% were included in this double-blind, randomized study. Two serial leukocyte removal filters (Pall BC1B filter [Pall Biomedical, Portsmouth, England], group F, 15 patients) or two dummy filters (group C, 17 patients) were connected to the blood cardioplegia line. Leukocyte count, hemodynamic measurement, and transesophageal echocardiography were performed before and after cardiopulmonary bypass. Cardiac-specific enzymes were analyzed from arterial blood during the first 72 hours and from coronary sinus blood 30 and 60 minutes after aortic unclamping.
Results: Patient characteristics were similar in the two groups (ejection fraction 20.9% ± 4.3% in group C and 21.1% ± 4.8% in group F; P = .773). No early death or perioperative myocardial infarction occurred. Leukocyte count, hemodynamic parameters, cardiac troponin T, cardiac troponin I, and creatine kinase MB mass levels in arterial blood were similar in the two groups. Group F showed lower release of cardiac troponin T from the coronary sinus 30 minutes after unclamping of the aorta (group F, 0.263 ± 0.12 ng/mL; group C, 0.6 ± 0.32 ng/mL; P = .005). Lower doses of dopamine were necessary after cardiopulmonary bypass (group F, 0.36 ± 0.11 mg · kg^–1 · min^–1; group C, 0.49 ± 0.14 mg · kg^–1 · min^–1; P = .003). A moderate increase in ejection fraction was observed at 30 minutes in both groups (group F, 30.3% ± 6.2%; group C, 28.0% ± 6.3%; P = .239) and a significant increase at 60 minutes in group F (group F, 32.5% ± 6.0%; group C, 27.4% ± 7.5%; P = .012).
Conclusions: These results indicate that serial leukocyte filters connected to the blood cardioplegia line decrease myocardial cell injury and may therefore help to improve outcome of patients with severely depressed ejection fractions undergoing coronary artery bypass grafting.

	Introduction

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Leukocyte depletion during cardiopulmonary bypass (CPB) and its effect on reperfusion injury and postoperative lung dysfunction have been thoroughly investigated over the past several years. ^1-6 Leukocyte depletion has been shown to prevent myocardial edema, to decrease the incidence of ventricular arrhythmias, and to reduce free radical–mediated lung injury ⁷ and cardiac reperfusion injury in animal models. Neutrophil granulocytes may cause myocardial stunning due to production of oxygen-derived free radicals, ^8,9 which may damage cell membranes, sarcoplasmic reticulum, and different enzymes. Furthermore, granulocytes can plug capillaries during ischemia; after their degranulation, cell membranes may be damaged by different cell enzymes. ^10-15 Temporary reduction of circulating activated neutrophils by leukocyte-depleting filters during the early period of reperfusion after ischemia may decrease release of free oxygen radicals and therefore reduce endothelial injury (eg, endothelial adherence, capillary plugging, no-reflow phenomenon). ^10,13

Several reports describe leukocyte depletion in human beings. A broad spectrum of indications for leukocyte depletion in cardiac surgery is reported, such as myocardial ischemia, ^16,17 heart transplantation, ^18,19 depressed left ventricular function, ²⁰ left ventricular hypertrophy, ²¹ cyanotic heart disease, and different elective cardiac procedures. ^22-25

This study was performed in patients undergoing coronary artery bypass grafting (CABG) with severely depressed left ventricular function. The blood cardioplegic solution and initial reperfusion blood volume were depleted of leukocytes only. This management combines the advantages of leukocyte depletion during the initial period of CPB and ischemia and the early period of reperfusion. ²⁶ On the other hand, the technical problems of filtration of the total arterial blood volume could be avoided.

	Methods

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Patients
The study includes 32 male patients undergoing CABG during a 5-month period. The inclusion criteria were left ventricular ejection fraction (LVEF) less than 35%, age younger than 75 years, and elective or urgent CABG. Patients with anemia, immunodeficiency, leukocytopenia, or thrombocytopenia and reoperations were excluded from the study. The patients were divided into two groups: group C (15 control patients, who did not receive leukocyte-depleted blood cardioplegic solution) and group F (17 patients, who did receive leukocyte-depleted blood cardioplegic solution [Pall BC1B filter; Pall Biomedical, Portsmouth, England]). In group C, two "dummy filters" were placed within the cardioplegia line, and in group F, two leukocyte removal filters were inserted. The study design was randomized and double blind. The perfusionist incorporated two Pall BC1B leukocyte removal filters or two empty dummy filters within the blood cardioplegia line according to the random list. Neither the surgeon nor the anesthesiologist was informed of the type of leukocyte removal filter. All operations were performed by one surgeon and one anesthesiologist, who handled transesophageal echocardiography and hemodynamic measurements.

Surgical protocol
Patients were premedicated with flunitrazepam by mouth (1 mg for those weighing < 70 kg or 2 mg for those weighing > 70 kg) the evening before the operation. Before the operation, patients received their usual morning dose of antianginal medication and 2 mg of flunitrazepam. Total intravenous anesthesia with sufentanil citrate (250-500 µg), pancuronium bromide (12-16 mg), and propofol (500-1000 mg) was used. The first dose of cefazolin (2 g) was given intravenously for infection prophylaxis during introduction of anesthesia and the second dose (1 g) was given after completion of CPB. After endotracheal intubation, patients received mechanical ventilation with an oxygen (FIO₂: 0.5) and air mixture. Radial artery and thermodilution pulmonary artery catheters (7F True Size thermodilution catheter; Baxter Healthcare Corp, Irvine, Calif) were placed for hemodynamic measurements. CPB was administered with the use of a hollow-fiber membrane oxygenator (Bard HF 5701, Bard, Inc, Haverhill, Mass) with a venous cardiotomy reservoir. A roller pump (Multiflow, Stöckert, Munich, Germany) was used with a standard nonpulsatile flow rate of 2.4 L · min^–1 · m^–2. A 40-µm heparin-coated arterial filter (Bentley, Irvine, Calif) was placed within the arterial line. Standard cannulation technique was used with cannulas placed in the ascending aorta and right atrium (2-stage venous cannula). After systemic heparinization (500 units/kg), CPB was initiated. Additional heparin was added during CPB to maintain the activated clotting time over 400 seconds. The left ventricle was vented via the aortic root. A 14F retrograde cannula (RC-014; Research Medical, Midvale, Utah) was placed into the coronary sinus. Distal anastomoses of the grafts were performed during aortic crossclamping, and proximal anastomoses were made after unclamping. Patients were weaned from CPB as usual. When necessary, dopamine (Dopamin; Giulini, Hannover, Germany) was given to maintain the arterial blood pressure over 80 mm Hg. If additional cardiac support was necessary, enoximone (Perfan I.V.; Myogen, Westminster, Colo) was administered. The consumption of inotropic drugs after aortic unclamping up to the end of the operation was expressed in milligrams per kilogram per minute. After completion of CPB, heparin was neutralized by administration of protamine sulfate (1 mg/100 units of heparin) to achieve an activated clotting time of ±10% of baseline value.

A prime solution comprising 1600 mL of Ringer solution (Braun Schiwa B. GmbH & Co KG, Glandorf, Germany), 100 mL of mannitol 20%, 100 mL of sodium bicarbonate 8.4%, and 5000 units of heparin was used. Acid-base balance was managed according to the alpha-stat concept. Two million units of aprotinin (Trasylol; Bayer AG, Leverkusen, Germany) was added in the priming solution and an additional dose of 1 million units after initiation of rewarming. For myocardial preservation, two cold blood cardioplegic solutions (4°C; 1:4 ratio of blood to cardioplegic solution) were administered at a rate of 250 mL · min^–1 for 4 minutes. The composition of the two solutions was as follows: solution I contained sodium chloride, 1.006 g; sodium hydroxide, 0.290 g; citric acid in water, 0.690 g; potassium chloride, 2.631 g; and glucose, 16.832 g; solution II contained sodium chloride, 1.043 g; sodium hydroxide, 0.298 g; citric acid in water, 0.723 g; potassium chloride, 0.909 g; and glucose, 17.45 g (BC-Card I and BC-Card II; Planer, Graz, Austria). Solution I was used initially until cardiac arrest and solution II thereafter. Repeated doses (50 mL · min^–1) were given every 20 minutes. Solution II was then infused as the final cardioplegic solution ("hot shot," 34.5°C) for 4 minutes immediately before aortic unclamping. For the next 6 minutes, either leukocyte-depleted or non–leukocyte-depleted blood (50 mL · min^–1) was administered. All patients received a combination of antegrade and retrograde infusion of cardioplegic solution. Fifty percent of the cardioplegic solution was given antegradely and 50% retrogradely. A heat exchanger for blood cardioplegia (Eurosets Vision; HMT, Fürstenfeldbrück, Germany) was incorporated in the cardioplegia line. Patients were not actively cooled, but their systemic temperature was allowed to drop to 33°C ± 1°C. Rewarming was started 10 minutes before release of the aortic clamp.

Sample collection
Blood samples were collected proximal and distal to the filters 2 minutes after the first doses of cardioplegic solution were begun and 2 minutes after the terminal dose of cardioplegic solution was started. For hematologic testing, blood samples were taken from the radial artery before initiation of CPB, 30 minutes after aortic crossclamping, and 1, 30, and 60 minutes and 6, 12, 24, and 48 hours after completion of CPB. Samples for cardiac troponin T (cTnT), troponin I (cTnI), and creatine kinase MB (CK-MB) mass were taken from the coronary sinus before initiation of CPB, 30 minutes after aortic crossclamping, and 1, 30, and 60 minutes after completion of CPB. Samples for cTnT, cTnI and CK-MB mass were taken from the radial artery before initiation of CPB, 30 minutes after aortic crossclamping, and 1, 30, and 60 minutes and 6, 12, 24, 48, and 72 hours after completion of CPB.

Leukocyte count
Blood cell counts were immediately determined with the use of a counter (K-1000; Sysmex Corporation of America, Long Grove, Ill) and differential cell counting for neutrophils in Nageotte chambers with a dilution of 1:100.

Biochemical assays
Blood samples were taken for biochemical assays after defined time intervals. The blood samples were centrifuged for 10 minutes at 2000g. The serum was frozen in aliquots and stored at –80°C until subsequent analysis. CTnT was measured by means of the Troponin T STAT immunoassay Elecsys 2010 Analyser (Roche Diagnostics GmbH, Mannheim, Germany). CTnI was quantified by means of the Axsym Troponin I System (Abbott, Wiesbaden, Germany). CK activity (CK-NAC; Boehringer Mannheim, Division of Roche), CK-MB activity (Boehringer Mannheim, Division of Roche), and CK-MB mass (Sandwich immunoassay test) were calculated. Analysis was done at one laboratory and without knowledge of the patients' outcomes.

Hemodynamic measurements
Heart rate, mean arterial blood pressure, and pulmonary capillary wedge pressure were measured. Cardiac output was measured with the thermodilution technique. Cardiac index, stroke index, and left ventricular stroke work index were measured before initiation of CPB (I), 30 minutes after completion of CPB (II), 60 minutes after completion of CPB (III), and 12 hours after admission to the intensive care unit (IV).

Echocardiography
Intraoperative transesophageal echocardiography was performed with a Hewlett-Packard Sonos 2500 system and a 3.7/5.0-MHz phased-array omniplane transducer (Hewlett-Packard Company, Andover, Mass). Left ventricular ejection fraction (LVEF) was calculated as follows: (End-diastolic volume – End-systolic volume)/End-diastolic volume. Left ventricular end-diastolic and end-systolic volumes were estimated by acoustic quantification (echocardiographic automatic border detection) in the transverse 4-chamber view by means of the method of discs (according to Simpson's rule).

These echocardiographic data were measured before initiation of CPB (I) and 30 minutes (II) and 60 minutes after completion of CPB (III).

Data analysis
Patients were randomized by means of a computer-generated series of random numbers. The patients were assigned to either leukocyte-depleted blood cardioplegia or non–leukocyte-depleted blood cardioplegia. The results were reported as the mean ± the standard deviation of the mean. The Mann-Whitney U test or Wilcoxon rank-sum test for difference in medians was used for comparisons of nominal data.

Ethics
All patients gave written informed consent, and the study was performed according to the guidelines of the institutional ethical committee.

	Results

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Clinical results
Preoperative LVEF measured by transthoracic echocardiography was 21.5% ± 4.2% in group C and 21.1% ± 4.8% in group F (P = .773). There were no significant differences regarding preoperative data and risk factors, surgical data, and patient outcomes between group C and group F(Table I). All patients survived and one patient with preoperative and postoperative ventricular fibrillation received a defibrillator. Intensive care unit stay in group F was shorter, but not significantly so (group C, 67.3 ± 102 hours; group F, 40.6 ± 38.6 hours; P = .081).

View larger version (17K): [in this window] [in a new window]   Fig. 1. Leukocyte count proximal and distal to two Pall BC1B filters (group F) and proximal and distal to the dummy filters (during first and terminal dose of blood cardioplegia).

View larger version (16K): [in this window] [in a new window]   Fig. 2. Measurement of cardiac enzymes (cTnT, cTnI, CK mass) preoperatively and during the first 72 hours after the operation. *Peak level; cTnT, cardiac troponin T, P = .371; cTnI, cardiac troponin I, P = .178; CK mass, creatinine mass, P = .562; 1 to 11, time points 1 to 11 (see "Sample collection" in the "Methods" section).

View larger version (11K): [in this window] [in a new window]   Fig. 3. Troponin T (cTnT) release from coronary sinus 30 and 60 minutes after unclamping of the aorta.

View larger version (12K): [in this window] [in a new window]   Fig. 4. Requirement for dopamine for weaning from CPB.

View larger version (14K): [in this window] [in a new window]   Fig. 5. Ejection fractions (EF) estimated by transesophageal echocardiography in group F and group C. I, Before initiation of CPB; II, 30 minutes after completion of CPB; III, 60 minutes after completion of CPB.

	Discussion

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These results are consistent with our observations. We found a significant decrease of cTnT levels in coronary sinus blood 30 minutes after unclamping the aorta when using leukocyte filters. Only a moderate decrease of cTnT levels in coronary sinus blood could be seen after 60 minutes. When looking at the peak levels of cTnT, cTnI, and CK-MB mass in the systemic circulation during the first 72 hours, we saw no significant differences between the groups. Sawa and associates ^17,21 demonstrated a better outcome in patients with acute myocardial ischemia or left ventricular hypertrophy treated with leukocyte-depleted terminal blood cardioplegia; they measured a lower release of malondialdehyde as a marker of lipid peroxidation, lower release of CK-MB, significantly lower postoperative inotropic support and, in patients with left ventricular hypertrophy, lower myocyte damage and endothelial cell damage of capillaries. In patients with cardiogenic shock, ¹⁷ the same group observed a significantly lower requirement for dopamine for weaning from CPB in patients treated with leukocyte-depleted blood cardioplegic solutions, as observed by our group. Mihaljevic and coworkers ²⁴ stated that the use of a leukocyte-depleting filter in the arterial line (Leuko-Guard-6; Pall Biomedical, Portsmouth, England) during CPB did not reduce the number of circulating leukocytes at any time during or after filtration (flow 1.8 L · min^–1 · m^–2). Mair and coworkers ²⁷ could not achieve effective leukocyte depletion using an arterial line filter (LG6). However, Sawa and associates ^17,21 showed more than 95% leukocyte depletion in the coronary circulation during terminal blood cardioplegia reperfusion (Cellsorba-80P, Asahi Medical, Tokyo, Japan) (300 mL · min^–1 for 10 minutes).

In our study we used two leukocyte filters during blood cardioplegia and terminal reperfusion and achieved more than 96% reduction of leukocytes in the coronary circulation. This is consistent with the results published by Suzuki and colleagues, ²⁵ who used the same filter system (98.1% total leukocyte reduction through the filter). Pala and coworkers ²⁰ tested leukocyte-depleted blood cardioplegia in patients with an LVEF lower than 35% or greater than 45%. They could not observe an effect in patients with an LVEF greater than 45%, but they found better myocardial protection measured by glutathione redox ratio in patients with an LVEF lower than 35%. We found a significant increase of LVEF in the group with leukocyte depletion 60 minutes after CPB (P = .012).

There were several hints that leukocyte depletion with leukocyte filters effectively reduced myocardial cell damage in our patients. First, the level of cTnT was reduced in group F. As we know, this enzyme is a sensitive marker for myocardial tissue damage, which is up-regulated shortly after ischemia. We assume that cTnI, another specific marker for myocardial damage, was not up-regulated significantly due to the small number of patients enrolled in this study. Second, the requirement for dopamine and enoximone was lower in these patients. Obviously, these leukocyte filters even have a positive hemodynamic effect on left ventricular function. Transesophageal echocardiography objectively confirmed these data. We are unable to explain whether leukocyte filters may decrease early mortality in patients with poor LVEF, since mortality was zero in both groups.

	Study limitations

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The two groups were identical concerning preoperative infarction rate. However, viability testing by either positron emission tomography or stress echocardiography was not carried out. This, in theory, could show differences regarding extent of viable myocardium that could influence the results. Yet, since the groups were properly randomized, we can assume that myocardial viability of infarcted areas was nearly identical. Endothelial markers were not investigated. However, such markers could influence expression of free oxygen radicals and therefore influence the results.

	References

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