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Anesth Analg 1999;89:580
© 1999 International Anesthesia Research Society

CARDIOVASCULAR ANESTHESIA

Use of abciximab-Modified Thrombelastography in Patients Undergoing Cardiac Surgery

S. C. Kettner, MD*,{ddagger}, O. P. Panzer, MD*, S. A. Kozek, MD*, F. A. Seibt, MD*,{ddagger}, B. Stoiser, MD{dagger}, J. Kofler, MD{dagger}, G. J. Locker, MD{dagger}, and M. Zimpfer, MD*,{ddagger}

*Department of Anesthesiology and General Intensive Care and the {dagger}Department of Internal Medicine I, University of Vienna, General Hospital Vienna; and {ddagger}Ludwig Boltzmann Institute of Clinical Anesthesiology and Intensive Care, Vienna, Austria

Address correspondence and reprint requests to Stephan C. Kettner, MD, Department of Anesthesiology and General Intensive Care, General Hospital Vienna, 18-20 Währinger Gürtel, A-1090 Vienna, Austria. Address e-mail to stephan.kettner{at}akh-wien.ac.at


   Abstract
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 Abstract
Introduction
 Methods
 Results
 Discussion
 References
 
Thrombelastography (TEG) is a reliable coagulation monitoring system that can guide blood product transfusion in cardiac surgery. The maximum amplitude (MA) of TEG measures clot strength, which is dependent on both fibrinogen level and platelet function. Inhibition of platelet function with abciximab-fab is suggested to permit quantitative assessment of the contribution of fibrinogen to clot strength. We hypothesized that abciximab-modified TEG permits prediction of plasma fibrinogen levels and that the difference of standard MA and abciximab-modified MA ({Delta}MA) is a correlate for platelet function. We correlated abciximab-modified MA with plasma fibrinogen levels and {Delta}MA with platelet count in patients undergoing coronary revascularization. Correlation between plasma fibrinogen levels and abciximab-modified MA was significant (adjusted r2: 0.8; P < 0.0001). Correlation of {Delta}MA with platelet count was not significant when calculated in millimeters (adjusted r2: 0.04; P = 0.73). However, when {Delta}MA was calculated in dynes per square centimeter ({Delta}GMA), it correlated significantly with platelet count (adjusted r2: 0.51;

P < 0.0001). We conclude that abciximab-modified TEG may therefore help to discriminate between hypofibrinogenemia and platelet dysfunction as a cause of decreased MA.

Implications: We examined the use of abciximab-modified thrombelastography in patients undergoing cardiac surgery. Modification of thrombelastography with abciximab-fab allows prediction of fibrinogen levels, despite coagulation altered by cardiac surgery. The difference of standard maximum amplitude and abciximab-modified maximum amplitude correlates with platelet function when expressed in dynes per square centimeter.


   Introduction
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 Abstract
 Introduction
Methods
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 Discussion
 References
 
Bleeding complications after cardiac surgery can require reexploration or correction of hemostatic abnormalities to restore adequate coagulation. Rapid assessment of coagulation abnormalities is essential to decide if bleeding complications should be treated with transfusion therapy or by reexploration.

Thrombelastography (TEG) correlates with blood loss after cardiopulmonary bypass (CPB), and heparinase-modified TEG is able to predict coagulation status after heparin reversal (1–3). The greatest accuracy of predicting hemorrhage from abnormal results after CPB was achieved with TEG, compared with activated clotting time, coagulation screen, Sonoclot measurements, or platelet activating factor-modified activated clotting time (3).

TEG is a global assessment of hemostatic function documenting the interaction of platelets with the protein coagulation cascade from the time of the initial fibrin-forming, through platelet aggregation, clot strengthening, and fibrin cross-linkage to eventual clot lysis (4). To assess these processes, TEG measures different variables including maximum amplitude (MA). MA measures the maximum clot strength, which is dependent on platelet function and fibrinogen level. Thus, a decrease in MA can indicate the requirement for either platelet therapy or administration of cryoprecipitate.

The inhibition of platelets in TEG measurements may allow discrimination between platelet dysfunction or decreased fibrinogen levels. abciximab-fab is an antibody fragment against platelet integrin glycoprotein IIb/IIIa (5). The interaction of platelets with fibrinogen is mediated via this receptor and is sufficiently inhibited by the antibody fragment (5–7). Consequently, the resulting MA may depend mainly on fibrinogen level, and modification of TEG with abciximab might allow an estimation of plasma fibrinogen levels (8,9). When the resulting MA of abciximab-modified TEG is an estimation for the contribution of fibrinogen to clot strength, the difference of standard MA and abciximab-modified MA may be a correlate for platelet function.

We hypothesized that abciximab-modified TEG permits prediction of plasma levels of fibrinogen and that the difference of standard MA and abciximab-modified MA is a correlate for platelet function. Accordingly, we correlated abciximab-modified MA with plasma fibrinogen levels, and the difference of standard MA and abciximab-modified MA with platelet count in patients undergoing CPB.


   Methods
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 Abstract
 Introduction
 Methods
Results
 Discussion
 References
 
After obtaining local Ethics Committee approval and informed consent, 56 patients scheduled for elective primary coronary revascularization using CPB were investigated. Patients were randomly assigned into four groups, and each group was studied at different perioperative intervals: the day before surgery, after surgery, and at the first and third days after surgery.

Exclusion criteria were preexisting bleeding disorders, renal dysfunction, diabetes with severe peripheral vascular complications, and platelet or coagulation altering medications, such as coumadin, nonsteroidal antiinflammatory drugs, and dipyridamole within 1 week before or during surgery.

The extracorporeal circuit consisted of a membrane oxygenator with polyvinyl chloride tubing, nonocclusive roller pumps, and a cardiotomy reservoir. The oxygenator was primed with 2,000 mL crystalloid solution, 100 mL of 20% mannitol, containing 8,000 IU unfractionated heparin, and 1 million KIU aprotinin (TRASYLOL®, Bayer, Leverkusen, Germany). CPB was performed with a flow rate of 2.5 L · min-1 · m-2 and moderate hypothermia.

Blood samples were obtained in the first group the day before surgery, in the second group immediately after admission to the intensive care unit, and on the first and third days after surgery in Groups 3 and 4, respectively. Samples of 4.5 mL were collected in silicone-coated glass tubes, containing 0.5 mL of 0.129 M buffered sodium citrate (VACUTAINER®, Becton Dickinson, Meylan, France). TEG was performed with 300 µL citrated whole blood after incubation with 4 IU/mL heparinase (Hemoscope, Skokie, IL). Samples were recalcified with 40 µL of 0.645% CaCl2. TEG tracings were performed on samples with and without addition of 5 µL of 2 mg/mL abciximab antibody-fragment (ReoPro®, Centocor, Leiden, The Netherlands). A Thrombelastograph D® (Hemoscope, Skokie, IL) was used for this investigation. The MA of each TEG tracing was documented. Plasma fibrinogen levels were measured using a photometric coagulation analyzer (STA Gerinnungsanalyzer®, Böehringer, Mannheim, Germany).

We calculated the difference of standard MA and abciximab-modified MA ({Delta}MA = standard MA - abciximab-modified MA). Based on the original work of Hartert (10), we also calculated the elastic shear modulus of standard MA and abciximab MA. The elastic share modulus of MA was estimated as follows: G = (5,000 MA)/(100 - MA), where G is the elastic shear modulus in dynes per square centimeter. The difference of standard MA and abciximab MA was calculated accordingly by: {Delta}GMA = (5,000 standard MA)/(100 - standard MA) - (5,000 abciximab MA)/(100 - abciximab MA).

Linear regression analysis was performed to determine the correlation of plasma fibrinogen levels with standard MA or abciximab-modified MA, and of platelet count with standard MA, {Delta}MA, and {Delta}GMA. To test the difference between correlations of standard MA with plasma fibrinogen levels and abciximab-modified MA with plasma fibrinogen levels, a Z-transformation was performed to compare the resulting r2 values. All values are expressed as means ± SD.


   Results
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 Abstract
 Introduction
 Methods
 Results
Discussion
 References
 
We studied 56 patients (14 patients in each group; 49 males, 7 females; age 64.4 [range 40–80] yr; height 174.1 ± 9.5 cm; weight 84.5 ± 10.8 kg).

abciximab-fab decreased clot strength of TEG tracings (Fig. 1). The correlation between plasma fibrinogen levels and standard MA was significant(P < 0.0001), with an adjusted r2 value of 0.5 and a regression line defined as fibrinogen = -494.2 + 14.868 x standard MA (Fig. 2). The correlation of abciximab-modified MA with plasma fibrinogen levels was significantly better, leading to an adjusted r2 value of 0.8 and a regression line defined as fibrinogen = -53.86 + 21.626 x abciximab-modified MA (P < 0.0001) (Fig. 2). The standard error of the estimate was 3.85. Fibrinogen levels ranged between 132 to 866 mg/dL (421.5 ± 203.5 mg/dL). Time necessary to reach MA of abciximab-modified TEG was 32.5 ± 5.1 min.



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  		Figure 1. Typical standard thrombelastogram (top) and the corresponding thrombelastogram with abciximab-fab modification (bottom).

 


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  		Figure 2. Correlation between plasma fibrinogen levels and standard maximum amplitude (top; P < 0.0001, adjusted r2: 0.5, fibrinogen = -494.2 + 14.868 * abciximab-modified maximum amplitude) or abciximab-modified maximum amplitude (bottom; P < 0.0001, adjusted r2: 0.8, fibrinogen = -53.86 + 21.626 * standard maximum amplitude) (regression line and 95% confidence intervals).

 
The correlation of standard MA with platelet count revealed an adjusted r2 of 0.37 (P < 0.0001). {Delta}MA did not correlate with platelet count (r2: 0.04, P = 0.73). The correlation of {Delta}GMA with platelet count was significant, with an adjusted r2 of 0.51 (P < 0.0001) (Table 1). Mean values for platelet count were 159,000 ± 39,900/µL and for hematocrit 29.8% ± 3.2%.


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  		Table 1. Correlation of Platelet Count with TEG Variables
 
Of note, in one subject, high plasma levels of fibrinogen lead to MAs corresponding to normal values of standard TEG, despite inhibition of platelet function (Fig. 3).



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  		Figure 3. Thrombelastogram of a subject with hypercoagulation at the third postoperative day (top). The corresponding abciximab-modified maximum amplitude reaches the normal range of standard maximum amplitude because of high plasma levels of fibrinogen (866 mg/dL) (bottom).

 

   Discussion
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 Abstract
 Introduction
 Methods
 Results
 Discussion
References
 
The use and correct interpretation of TEG may reduce blood product usage and surgical reexploration rate in cardiac patients (1–3). Our results show correlation between MA and plasma fibrinogen levels. Whereas the correlation between standard MA and fibrinogen levels was significant, but weak (adjusted r2: 0.5; P < 0.0001), the modification of TEG with abciximab-fab led to a better correlation between fibrinogen levels and abciximab-modified MA (adjusted r2: 0.8; P < 0.0001). Because the resulting MA of abciximab-modified TEG is an estimation for the contribution of fibrinogen to clot strength, the difference of standard MA and abciximab-modified MA ({Delta}MA) may primarily reflect platelet function. Therefore, we correlated {Delta}MA with the platelet count. The resulting r2 of 0.04 was not significant (P = 0.73). This result is probably because elastic shear modulus increases exponentially in proportion to MA. The absolute elastic shear modulus of MA can be estimated as G = (5,000 MA)/(100 - MA). Thus, when an abciximab MA of 17 mm is subtracted from a standard MA of 67 mm, the resulting {Delta}MA of 50 mm underestimates the contribution of platelets to clot strength; a decrease in MA of 67 mm to 50 mm is equivalent to a twofold decrease in the elastic shear modulus. Accordingly, the difference of standard MA and abciximab MA was calculated by: {Delta}GMA = (5,000 standard MA)/(100 - standard MA) - (5,000 abciximab MA)/(100 - abciximab MA). The correlation of the resulting {Delta}GMA with platelet count was significant with an adjusted r2 of 0.51 (P < 0.0001) and suggests that {Delta}GMA may correlate with platelet function. These findings suggest that the use of abciximab may further increase the role of TEG in the management of perioperative hemostasis in patients with complex coagulopathies. In postoperative patients at risk of hemostatic and surgical bleeding, rapid and reliable assessment of the patient's coagulation status is crucial for rational treatment. The average time for reaching the MA in a celite-activated abciximab-modified TEG was 32.5 ± 5.1 min. Thus, abciximab-modified TEG and comparison with standard TEG provided rapid, on-site estimation of plasma fibrinogen levels and provides a correlate for platelet function. This time may be further reduced by the use of tissue factor instead of celite for activation of TEG measurements. However, in a series of measurements correlating native, celite-activated, and tissue factor-activated abciximab-modified TEG values with plasma levels of fibrinogen, we found the highest accuracy for celite-activated TEG (11). Therefore, we used celite-activated TEG in this study.

TEG permits a global assessment of hemostatic function correlating to routine coagulation tests and, most importantly, to postoperative blood loss. In standard TEG tracings, MA measures clot strength, which is dependent on both fibrinogen level and platelet function (4). Liquid whole blood transmits little or no torque in TEG, producing no amplitude on the TEG tracing even in blood samples with high viscosity. As the blood clots, fibers composed of fibrin and platelets form, producing an increasing amplitude. Platelets provide a phospholipid surface for coagulation reactions in the standard TEG tracing and thus promote the formation of fibrin (12). Furthermore, platelets bind to fibrinogen (13) and modulate the viscoelastic properties of the clot via the specific platelet surface receptor glycoprotein IIb/IIIa (14). Fibrinogen is soluble until thrombin binds to the central region, which produces proteolysis at the N-terminus releasing fibrinopeptide A and B and fibrin monomer. This release process exposes other regions of the molecule to interact with other activated fibrin molecules for polymerization of the fibrin network. The end point of this cascade is fibrin. The MA of the TEG tracing increases with higher levels of fibrinogen and greater platelet number in the blood sample (12). The use of standard TEG to distinguish between hypofibrinogenemia or platelet dysfunction as the cause of hypocoagulation is therefore ambiguous, because a decrease in MA can indicate either decreased plasma fibrinogen levels or reduced overall platelet function. Inhibition of platelet function allows quantitative assessment of the contribution of fibrinogen to clot strength (5,7). abciximab-fab is an antibody fragment that binds to platelet glycoprotein IIb/IIIa and blocks the interaction of platelets with fibrin in TEG (14). Our data show that the blockade of platelet function by abciximab-fab antibody fragments enables prediction of fibrinogen levels, and {Delta}GMA correlates with platelet number. {Delta}GMA and abciximab MA can therefore help to distinguish between fibrinogen deficiency and platelet dysfunction and could guide transfusion of cryoprecipitate and platelets. Although {Delta}GMA correlates with platelet count in our study, we have not investigated whether {Delta}GMA correlates with other platelet tests or surgical blood loss. Further studies are necessary to investigate whether {Delta}GMA could serve as a platelet test.

In patients with decreased platelet function, decreased MA can be compensated by increased plasma fibrinogen levels (Fig. 3). Decreased plasma fibrinogen levels may theoretically be compensated by increased platelet function, resulting in a normal or near-normal MA. {Delta}GMA and abciximab MA may help differentiate between these coagulation changes that may not be apparent with use of routine TEG.

Studies investigating other populations of patients showed better correlations between abciximab-modified MA and plasma fibrinogen levels or standard MA and platelet count than our results. In healthy volunteers, the correlation of abciximab-modified MA with fibrinogen levels reached an r2 value of 0.97 (9). In patients undergoing a variety of elective surgery, this correlation reached an r2 value of 0.87 (8). However, in the latter study, subjects undergoing cardiothoracic procedures were excluded. The correlation of standard MA and platelet count reached an r2 value of 0.59 in subjects undergoing liver transplantation (12).

We investigated subjects in the perioperative period of cardiac surgery because of the anticipated wide range of plasma fibrinogen levels (132–866 mg/dL) and because of other alterations of the coagulation system. The coagulation system of these subjects is affected by multiple factors, such as extracorporeal circulation, use of heparin and protamine, hemodilution, transfusion of blood and blood components, and surgery per se (15). Furthermore, the priming solution of CPB contained 106 KIU of aprotinin. Even in small doses, aprotinin reduces binding of heparin to platelets and preserves platelet function in patients undergoing CPB (16,17). The administered aprotinin may have also altered the interaction of glycoprotein IIb/IIIa with abciximab. Finally, the use of heparinase in our TEG measurements may have also contributed to the weaker correlation between abciximab-modified MA and fibrinogen levels, compared with other investigations. We used heparinase to exclude residual heparin effects that may occur after CPB (18). Heparinase per se can alter TEG measurement and may have affected the estimation of fibrin levels or the correlation between MA and platelet count (19).

Nevertheless, our results demonstrate that abciximab-modified TEG permits quantitative estimation of plasma fibrinogen levels, even in patients with alterations of the coagulation system. Thus, abciximab-modified-TEG and comparison with standard TEG could provide a rational guide to hemostatic therapy, even in patients with complex coagulopathies.

A limitation of the present study is that no patients with severe hypofibrinogenemia were studied. We cannot prove that abciximab-modified MA predicts very low fibrinogen levels as accurately as the levels we measured (132–866 mg/dL). Therefore, comparison of abciximab-modified MA with correspondingly lower fibrinogen levels remains to be evaluated.

In conclusion, abciximab-modified MA can be used to predict fibrinogen levels. The difference of elastic shear modulus between standard MA and its corresponding abciximab-modified MA correlates with platelet number. Thus, measurement of abciximab-modified TEG and comparison with standard TEG could provide a rational guide to hemostatic therapy when evaluating hypofibrinogenemia and platelet dysfunction as causes of coagulopathy.


   References
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 Abstract
 Introduction
 Methods
 Results
 Discussion
 References
 

  1. Tuman KJ, Spiess BD, McCarthy RJ, et al. A comparison of viscoelastic measurements of coagulation after cardiopulmonary bypass. Anesth Analg 1989;69:69–75.[Abstract/Free Full Text]
  2. Tuman KJ, McCarthy RJ, Djuric M, et al. Evaluation of coagulation during cardiopulmonary bypass with a heparinase-modified thrombelastographic assay. J Cardiothorac Vasc Anesth 1994;8:144–9.[Medline]
  3. Spiess BD, Tuman KJ, McCarthy RJ, et al. Thrombelastography as an indicator of post-cardiopulmonary bypass coagulopathies. Clin Monitor 1987;3:25–30.
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  6. Khurana S, Mattson JC, Westley S, et al. Monitoring platelet glycoprotein IIb/IIIa-fibrin interaction with tissue factor-activated thromboelastography. J Lab Clin Med 1997;130:401–11.[ISI][Medline]
  7. Konstantopoulos K, Kamat SG, Schafer AI, et al. Shear-induced platelet aggregation is inhibited by in vivo infusion of an anti-glycoprotein IIb/IIIa antibody fragment, c7E3 Fab, in patients undergoing coronary angioplasty. Circulation 1995;91:1427–31.[Abstract/Free Full Text]
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Accepted for publication May 21, 1999.




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Lippincott, Williams & Wilkins Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins with the assistance of Stanford University Libraries' HighWire Press®. Copyright 2006 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999 HighWire Press