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Right arrow Extracorporeal circulation

Eur J Cardiothorac Surg 2003;23:1046-1050
© 2003 Elsevier Science NL

Heart surgery with extracorporeal circulation leads to platelet activation at the time of hospital discharge

Alexander Wahbaa*, Vibeke Videmb

a St. Elisabeth Heart Centre, Norwegian University of Science and Technology, 7018 Trondheim, Norway
b Department of Immunology and Transfusion Medicine/Institute of Laboratory Medicine, Norwegian University of Science and Technology, 7018 Trondheim, Norway

Received 29 September 2002; received in revised form 15 February 2003; accepted 6 March 2003.

* Corresponding author. Tel.: +47-7386-7000, fax: +47-7386-7029
e-mail: alexander.wahba{at}rit.no


   Abstract
Top
 Abstract
1. Introduction
 2. Material and methods
 3. Results
 4. Discussion
 References
 
Objective: Heart surgery with extracorporeal circulation has a marked effect on platelet function and coagulation accounting for abnormal blood loss and allegedly a low incidence of thromboembolic complications. Little is known about platelet function at the time of hospital discharge of routine patients. Methods: Blood samples from 91 patients undergoing elective heart surgery were drawn before surgery and prior to discharge. Thirty-seven patients underwent coronary artery surgery and 54 an aortic valve implantation. The mean age of patients was 69±9 years. Fifty patients were male and 41 female. Platelet function was evaluated using plasma ß-thromboglobulin quantification in enzyme-linked immunosorbent assay. In addition, flow cytometric analysis of platelet–monocyte conjugates and platelet–neutrophil conjugates was performed. Results: The platelet count before discharge was significantly increased (265±86 vs. 212±61x109/l preoperatively). ß-Thromboglobulin was significantly increased (176±127 vs. 79±70 ng/ml preoperatively) and flow cytometry proved a significant increase in monocyte–platelet aggregates (8.3±5.4% vs. 5.3±2.6% preoperatively) indicating platelet activation at the time of hospital discharge. There were no significant differences among the three subgroups coronary surgery, mechanical valve insertion and biological valve insertion. Conclusions: Heart surgery with extracorporeal circulation leads to significant platelet activation and a reactive increase in platelet count before discharge. This is in contrast to the reduced platelet function immediately postoperatively.

Key Words: Platelet function • Cardiopulmonary bypass • Coronary artery surgery • Heart valve surgery • Flow cytometry


   1. Introduction
Top
 Abstract
 1. Introduction
2. Material and methods
 3. Results
 4. Discussion
 References
 
Although clinically detected thromboembolic complications following heart surgery are uncommon, there is a significant incidence of subclinical deep venous thrombosis and pulmonary embolism [1]. This may seem surprising, because cardiopulmonary bypass (CPB) has well-documented effects of on coagulation and blood platelets that may protect against thromboembolic complications. CPB leads to dilution of coagulation factors and furthermore to activation of fibrinolysis [2–4]. In addition, platelet function is altered [5,6]. However, it is unknown whether CPB has effect on platelet function beyond the first 48 h following cardiac procedures. The aim of the present study was to investigate platelet function and platelet–monocyte interactions upon discharge from the cardiothoracic unit in patients undergoing heart surgery.


   2. Material and methods
Top
 Abstract
 1. Introduction
 2. Material and methods
3. Results
 4. Discussion
 References
 
The study was a prospective investigation of platelet function in patients undergoing open heart surgery with the use of CPB. Consecutive patients undergoing elective coronary artery bypass grafting with CPB or aortic valve replacements were included. Emergency cases, patients with acquired or congenital coagulation defects, as well as, patients on subcutaneous or intravenous heparin until 1 week before surgery were excluded. A total of 91 patients within a period of 1 year were included. Thirty-seven patients underwent coronary artery bypass grafting, 54 patients received aortic valve replacement (25 mechanical, 29 biological). In 26 patients the valve operation was an isolated procedure whereas 28 patients suffered from coronary heart disease as well and received coronary grafts in addition to the valve replacement. The study was approved by the local ethics committee. Informed oral and written consent was obtained from all individuals included in the study.

A standard anaesthetic technique with morphine and scopolamine for premedication, and fentanyl, thiopental, diazepam and pancuronium for induction was used. Anaesthesia was maintained with nitrous oxide (before bypass), isoflurane and small additional doses of fentanyl as necessary (total dose of fentanyl approximately 10 µg/kg). During CPB anaesthesia was maintained with diazepam and/or midazolam. The blood pressure was controlled with glyceryl trinitrate before and after bypass, and with sodium nitroprusside during CPB.

Before CPB heparin 300 U/kg (Leo, Copenhagen, Denmark) was given through a central venous line to achieve a celite activated clotting time of more than 480 s. The activated clotting time (ACT) was measured in duplicate, and additional heparin was given when needed to keep the ACT above the target. During CPB the ACT was monitored every 20 min. The perfusion circuit was primed with 1800 ml of Ringer's acetate solution to which 7500 units of heparin were added. A membrane oxygenator without heparin coating was used. Cold crystalloid hyperkalaemic antegrade cardioplegia and moderate hypothermia to 34 °C were employed during CPB. The pump flow was 2.4 l/m2 during normothermia and 2.0–2.4 l/m2 at 34 °C. The patient was warmed to a rectal temperature of at least 36 °C before termination of CPB. After CPB 1 mg of protamine sulphate for every 100 units of previously administered heparin (prime heparin not included) was given to achieve an ACT within 10% of the baseline value. Additional doses of protamine were given when necessary.

A standard surgical technique was used in all patients. Coronary surgery was performed with a left internal mammary graft to the left anterior descending coronary artery in all patients and vein grafts to other territories. Distal anastomoses were constructed first and proximal anastomoses were sewn with use of a partial aortic clamp. The decision whether to implant a biological or mechanical valve was discussed with patients individually. However, most patients over 70 years of age received a biological valve. The Medtronic Mosaic stented tissue valve (Medtronic Inc., Minneapolis, MN) was used as biological prosthesis and the Sulzer Carbomedics valve (Sulzer Carbomedics Inc., Austin, TX) was the mechanical valve used. All valve patients were anticoagulated with warfarin beginning with a dose of 10 mg of warfarin on the day after surgery. The target international normalized ratio (INR) was 2.5–3.5. In the postoperative course red blood cells were transfused when haemoglobin was below 80 g/l. None of the patients received Macrodex or plasma or platelet transfusions.

Blood samples were drawn on the day before surgery and on the day of hospital discharge. Hospital discharge was between postoperative day 4 and 7. Ninety percent of patients were discharged on days 5, 6 or 7. Citrate theophylline adenosine dipyridamole (CTAD) tubes (Vacutainer, Becton Dickinson, San José, CA) were used to collect samples for ß-thromboglobulin (BTG) measurements in plasma. Samples were stored briefly on ice until centrifuged for 20 min at 3000xg. Thereafter, samples were stored at -70 °C until analysis. Samples for flow cytometry were drawn in citrate tubes (Vacuette, Greiner Labortechnik, Austria). Fifty micrograms of blood were immediately transferred into an Eppendorff tube containing 200 µl Tyrode buffer with 0.35% human serum albumin and 250 µl formaldehyde 1%. At the same time an additional sample was drawn in ethylenediaminetetraacetic acid tubes (Vacuette, Greiner Labortechnik, Austria) for determination of platelet count and mean platelet volume in an automated haematology instrument (K-1000, Sismex, Kobe, Japan).

2.1. Flow cytometry
In the present study whole blood flow cytometry was used to investigate platelet activation. Preliminary experiments using dual colour flow cytometry as described previously [7] for determination of P-selectin (CD 62P) expression on the platelet surface were performed in samples of the first 30 patients undergoing valvular heart surgery. Platelets were identified by their expression of GP IX (CD 42a) and platelet activation was quantified based on the increased surface expression of P-selectin. Since no significant activation was found, this assay was not performed in the remaining patients.

In addition, platelet–monocyte and platelet–neutrophil conjugates were measured according to Furman et al. with slight modifications [8]. One hundred microliters of the fixed and diluted blood sample was incubated with a saturating concentration of PE-labelled anti-GP IIb (CD 41, clone 5B12, DAKO, Glostrup, Denmark) at room temperature for 15 min. Thereafter the reaction was stopped with 5 ml distilled water. A FACScan flow cytometer (Becton Dickinson) was used. List mode data were acquired in a monocyte or neutrophil gate. The PE fluorescence of the brightly expressed antigen GP IIb was used as a marker for detection of platelet–monocyte and platelet–neutrophil conjugates in the diluted whole blood. Thus monocytes and neutrophils positive for platelet antigen represent platelet–monocyte and platelet–neutrophil conjugates. Dividing the number of aggregates by the number of cells (monocytes or neutrophils) within the gate and multiplication with 100 yields the percentage of platelet–monocyte or platelet–neutrophil aggregates stated within the paper.

2.2. Statistics
When planning the study, sample size calculations were performed. Assuming that a 5% difference between groups (coronary surgery, valve surgery) would represent a clinically meaningful result, and {alpha}=0.05 a sample size of 30 patients for each group was needed to achieve a power of 90%. Data are given as mean±SD. Data were entered into a Microsoft Excel 2000 spreadsheet and analysed using the SPSS (Statistical Product and Service Solutions) for Windows version 10.0 statistical software on a personal computer. Analysis of data revealed non-normal distribution and thus statistical comparison of data between groups and within groups was performed using non-parametric tests, namely Mann–Whitney and Kruskal–Wallis test. A P-value below 0.05 was termed statistically significant.


   3. Results
Top
 Abstract
 1. Introduction
 2. Material and methods
 3. Results
4. Discussion
 References
 
Patient characteristics are summarized in Table 1. The mean age of patients was 69±9 years (range 38–82 years). Fifty patients were male and 41 female. The postoperative samples were drawn between the fourth and the seventh postoperative day (median day 6). As shown in Table 2, the platelet count was elevated and the mean platelet volume reduced before hospital discharge in the valve group but not in the coronary bypass group.


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  		Table 1. Patient characteristics

 

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  		Table 2. Results from the two groups

 
However, there was evidence for platelet activation in both groups. BTG was significantly elevated (Fig. 1) and platelet–monocyte conjugates were significantly increased before discharge both in the valve and the bypass group (Fig. 2) . Platelet–neutrophil conjugates were not significantly changed following surgery in either group. There was no significant difference between groups with regard to platelet count and volume, BTG, platelet–monocyte and platelet–neutrophil conjugates preoperatively or before discharge (Table 2).



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  		Fig. 1. Plasma ß-thromboglobulin levels in patients undergoing coronary surgery (white bars) and valve surgery (black bars) the day before surgery and the day of hospital discharge. *P<0.05.

 


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  		Fig. 2. Platelet–monocyte conjugates levels in patients undergoing coronary surgery (white bars) and valve surgery (black bars) the day before surgery and the day of hospital discharge. *P<0.05.

 

   4. Discussion
Top
 Abstract
 1. Introduction
 2. Material and methods
 3. Results
 4. Discussion
References
 
In this study flow cytometry and plasma BTG measurements were performed to assess platelet activation before discharge from the cardiac surgical unit in patients undergoing various heart surgical procedures. We found an increase in platelet count on the day of hospital discharge in the valve group and a significant increase in plasma BTG release a significant elevation of platelet–monocyte conjugates, indicating platelet activation in both groups.

It seems intriguing to assume that difference in platelet count and mean platelet volume between coronary surgery and valve surgery may be due to the significantly longer CPB times and greater operative trauma in the valve group. However, we have no data to prove this hypothesis. Reactive thrombocytosis following heart surgery has been described previously in a subset of 19.5% of patients investigated [9]. No difference in operative data between patients with thrombocytosis compared to those without was found. However, Schmuziger et al. [9] suggested that hyperlipidaemia, smoking and previous myocardial infarction were contributing factors. Moreover, patients with thrombocytosis had a significantly higher incidence of late vein graft occlusion and myocardial infarction. However, platelet activation was not analysed in these patients. The number of patients in our study is too small to investigate whether thrombocytosis is significantly correlated to platelet activation in our patients.

A number of methods are used to assess platelet activation. Flow cytometry is advantageous over other methods, because it analyses surface antigens on individual platelets, independent of platelet-to-platelet interaction and platelet concentration [10]. However, flow cytometry focuses on the state of activation of circulating cells, but does not give information on cells that have left the circulation prior to blood sampling. Flow cytometric analysis of platelet surface P-selectin expression is an accepted measure of platelet activation in vivo [10,11]. The effect of CPB on P-selectin expression has been addressed in several studies [6,12,13]. In this study no significant change in P-selectin expression was noted when comparing preoperative and predischarge measurements. This may be due to a rapid loss of surface P-selectin in vivo in circulating degranulated platelets that continue to circulate and function [14,15]. Our study thus supports the conclusion of Michelson et al. that P-selectin is not an ideal marker for circulating activated platelets in all circumstances [16].

Platelet–monocyte conjugates may be a more sensitive marker of platelet activation in vivo [16]. An increase in circulating platelet–monocyte conjugates has been shown in coronary artery disease and CPB [8,17]. Formation of platelet–monocyte conjugates is dependent on platelet activation. It is mediated by P-selectin expressed on circulating platelets, which binds to the P-selectin glycoprotein ligand on leukocytes [18–20]. Platelet–monocyte conjugates may be more stable than P-selectin expression on the platelet surface. However, to date this has not been proven.

In this study we found a significant increase in monocyte–platelet conjugates before discharge following coronary artery surgery and heart valve replacement, suggesting prolonged platelet activation. Platelet–monocyte conjugates might induce tissue factor expression by monocytes leading to activation of inflammatory cells and generation of cytokines [21].

Platelet–neutrophil conjugates were not significantly changed in this study. This is in accordance with findings in patients with stable coronary artery disease [8] and venous stasis ulcers [22]. It appears that platelet–monocyte conjugates are a better indicator of platelet activation in cardiac surgical patients as well. Furthermore, the clinical significance of platelet–neutrophil conjugates is unclear [23].

Significantly increased plasma BTG levels in our patients support our conclusion of platelet activation. Plasma BTG was shown to be markedly increased immediately following heart surgery. Harker et al. found a progressive increase in BTG during CPB and a decrease following surgery [2]. Values had returned to baseline at 24 h [2]. This was supported by others [24]. The observed significant increase in plasma BTG concentrations before discharge compared to baseline suggest that the observed platelet activation takes place some time after the completion of surgery.

Platelet activation more than 1 week following major surgery has been reported recently. Bunesco et al. found a significant increase in monocyte–platelet complexes and BTG [23]. In addition, a significant correlation between these two measures of platelet activation was found. A correlation of markers of platelet activation with activation of coagulation was also found. According to the findings of this study, CPB does not seem to have a modulating effect on platelet activation several days following surgery. Apparently the difference between valve procedures and coronary surgery was not significant, but our study was small and this may be a false-negative finding.

It has been suggested that continued activation of the haemostatic system several days following major surgery may be triggered by the inflammatory process of wound healing or existence of subclinical thrombi [23]. It is not known whether the observed activation of platelets or in general the activation of haemostasis following major surgery as observed by Bunesco et al. are related to clinical events such as thromboembolic complications [23]. None of the patients included in this study showed clinical signs of venous thromboembolism or early bypass occlusion. However, it is known that the risk for bypass occlusion following coronary surgery is significant early following surgery [25]. In addition, there is a significant risk of thromboembolic events following heart operations [1]. Known risk factors for venous thromboembolism are immobilization and postoperative congestive heart failure [1]. It is believed that platelet active medication reduces the incidence of thromboembolic events and early bypass occlusion [1]. Thus postoperative thromboembolic events may well coincide with the observed platelet activation before discharge described in this report. Larger trials are required to elucidate this issue and to assess the predictive value of increased platelet–monocyte conjugates for the development of early bypass occlusion, pulmonary emboli and other thromboembolic events.


   Acknowledgments
 
This work was supported by a grant of the SINTEF Unimed research foundation. The authors would like to express their thanks to the bioengineers of the Department of Immunology and Transfusion Medicine for their invaluable help with the laboratory work.


   Footnotes
 
Presented at the 16th Annual Meeting of the European Association for Cardio-thoracic Surgery, Monte Carlo, Monaco, September 22–25, 2002.


   References
Top
 Abstract
 1. Introduction
 2. Material and methods
 3. Results
 4. Discussion
 References
 

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