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Role of Thromboelastography Platelet Mapping and International Normalized Ratio in Defining “Normocoagulability” During Anticoagulation for Mechanical Circulatory Support Devices: A Pilot Retrospective Study

Volod, Oksana; Lam, Lee D.; Lin, Gloria; Kam, Clarice; Kolyouthapong, Kristica; Mac, Jessica; Mirocha, James; Ambrose, Peter J.; Czer, Lawrence S. C.; Arabia, Francisco A.

doi: 10.1097/MAT.0000000000000445
Adult Circulatory Support
Free

Thromboembolic (TE) events and hemorrhagic complications continue to remain as frequent adverse events and causes of death after mechanical circulatory support device (MCSD) implantation. To counterbalance this postimplant multifactorial hypercoagulable state, antithrombotic therapy given postimplant must be individually tailored to keep patient adequately anticoagulated yet normocoagulable. Prior studies describing different anticoagulation protocols do not define normocoagulability for patients on MCSDs. We evaluated the role of thromboelastography platelet mapping (TEG PM) in defining “normocoagulability” for MCS patients on anticoagulant (warfarin) and antiplatelet agents. Ninety-eight MCSD patients who underwent TEG PM assay at our institution from 2012 to 2014 were included for retrospective analysis. Eleven (11.2%) subjects developed at least one TE event during the study period. Of the 13 TE events, 8 occurred in patients with total artificial heart (TAH). TEG parameters closest to the event or when patient was clinically adequately anticoagulated and corresponding international normalized ratio (INR) were measured. Thromboelastography coagulation index (CI) appears to be the single most statistically significant parameter that can be used to designate a patient as normocoagulable. Based on our results, patients with HeartMate II (HM II) and Heart Ware (HW) devices should be maintained at a CI value of less than or equal to 1.5 whereas patients with TAH devices should be maintained at a CI less than or equal to 1.2. The CI should be correlated with the degree of Vitamin K-dependent coagulation factor inhibition that is achieved using device-specific goal INR ranges. A recent modification, TEG PM assesses the effects of antiplatelet drug. Maximal amplitude arachidonic acid (MA-AA) < 50 and maximal amplitude adenosine diphosphate (MA-ADP) < 50 are desired for normocoagulable state.

From the *Department of Pathology, Cedars Sinai Medical Center, Los Angeles, California; Cedars-Sinai Comprehensive Transplant Center, Cedars Sinai Medical Center, Los Angeles, California; §School of Pharmacy, University of California, San Francisco, California; and Cedars - Sinai Research Institute (CSHI), Cedars Sinai Medical Center, Los Angeles, California.

† Deceased.

Submitted for consideration December 2015; accepted for publication in revised form September 2016.

Disclosures: Oksana Volod is a consultant for Haemonetics. Francisco A. Arabia is a consultant for SynCardia Systems Inc.

Correspondence: Oksana Volod, MD, 8700 Beverly Blvd., Los Angeles, CA 90048. Email: oksana.volod@cshs.org.

Currently, more than five million people in the United States are affected by heart failure and this number continues to increase every year.1,2 Over the past 10 years, mechanical circulatory support devices (MCSDs) have become a viable treatment option for patients with end-state heart failure or as a bridge to heart transplantation. However, the treatment comes with significant side effects.

The implantation of a MCSD creates a prothrombotic environment because of the activation of systemic inflammatory response. Despite this, hemorrhagic complications associated with surgical blood loss, arteriovenous malformation leading to GI bleeding, and acquired von Willebrand syndrome are common adverse events.3,4 The need to manage both ends of the hemostatic spectrum requires a prophylactic antithrombotic therapy that is customized to the patient’s current hemostatic status that results in providing a normocoagulable state in the presence of a prothrombotic environment.

A variety of anticoagulant and antiplatelet strategies exist to treat patients with a MCSD.5–8 These strategies have focused on the adequacy of anticoagulation and protection from thromboembolic (TE) events versus achieving “normocoagulability.” Thus, there is still uncertainty in the experts in the field regarding the optimal treatment regimen for patients and the best way to assess the adequacy of any given treatment regimen.

In 1994, the classic hemostasis cascade model was challenged by the introduction of a cell-based model of hemostasis showing the importance of tissue factor (TF) and the cells expressing it as the initiators of coagulation and the role of platelets in this process.9 The necessity to analyze whole blood to accurately characterize coagulopathies have led to the revival and interest in viscoelastic assays and its utility in a variety of clinical settings. The thrombelastograph (TEG, Haemonetics) is a device that measures the global viscoelastic properties of whole blood clot formation and lysis under low shear stress conditions. Unlike the conventional coagulation screening assays, such as activated partial thromboplastin time (aPTT) and the prothrombin time (PT) with corresponding calculated international normalized ratio (INR), which only measure the adequacy of coagulation factor levels in plasma, TEG utilizes whole blood and assesses how clotting factors, platelets, fibrinolysis, various anticoagulation medications and antiplatelet agents affect the viscoelastic properties of whole blood in the real-time. A modification of the TEG test, the TEG Platelet Mapping (TEG PM) assay, provides a way to assess the effects of antiplatelet agents on platelet function. Together, the TEG and TEG PM provide a valuable tool that can be used to tailor anticoagulant and antithrombotic therapies to define normocoagulability in patients implanted with a MCSD.

The primary objective of this study was to use the TEG and TEG PM parameters to retrospectively characterize and compare the hemostatic status of patients implanted with a MCSD who experienced a TE event during implantation versus patients without a TE event. A second objective was to identify the TEG parameters significant in defining “normocoagulability” during anticoagulation and antithrombotic therapy in MCS patients.

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Methods

A retrospective analysis of the TEG assay results from 98 patients implanted with a MCSD between January 1, 2012 and November 1, 2014 at our institution. Only patients implanted with long-term MCSDs, such as the SynCardia Total Artificial Heart (TAH), Thoratec PVAD biventricular assist device (BiVAD), Thoratec HeartMate II (HMII), and Heart Ware (HW) were included in the study.

All patients received warfarin dosed to a target INR of 2.0–3.0 or 2.5–3.5, based on the type of MCSD received and at least one type of antiplatelet agent such as aspirin or dipyridamole (dosed based on our device protocol) (Table 1).

Table 1

Table 1

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Laboratory Setting and Processing of Specimen

The TEG and TEG PM analysis was performed using whole blood samples. Samples were collected in a 3.2% sodium citrate and lithium heparin tubes; hand carried to the coagulation laboratory and ran within 30 minutes of collection. Blood was analyzed according to manufacturer’s instructions (TEG, Haemonetics Corporation, Braintree, MA) and using manufacturer’s reagents. Citrate anticoagulation was reversed by adding calcium chloride to the TEG cup. Kaolin, an activator was added to initiate coagulation per manufacturer’s instructions. Quality controls were performed on the TEG analyzers every 8 hours per CLIA and CAP guidelines. Thromboelastography and TEG PM tracings were interpreted by the hematopathologist.

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Thromboelastography Overview and Parameter Definitions

Principle of thromboelastography.

Three hundred and forty microliters of citrated blood is placed into the heated cup (37°C) with 20 μl calcium chloride (to overcome the citrate) and kaolin (to activate the intrinsic coagulation pathway). These reagents will produce a maximum clot. Thromboelastography operates by moving a cup in a limited arc (±4°45′ every 10 seconds) filled with blood that engages a pin/wire transduction system as clot formation occurs. As the fibrin clot begins to form between the cup and pin, the transmitted rotations are detected at the pin and a reaction curve is generated, the magnitude of which is directly related to the strength of the clot. As the test proceeds, the fibrinolytic phase begins to break down the clot, reducing the size of the curve. Figure 1 reproduces a typical, normal thrombin generated TEG tracing.

Figure 1

Figure 1

Table 2

Table 2

The inhibition of platelets by platelet inhibitor will not be revealed by the TEG using a kaolin-activated sample. This is due to thrombin generation in the blood sample, which results in maximum activation of platelets that overrides other inhibited platelet receptor sites, demonstrating what the underlying hemostasis would be if the patient was not on any antiplatelet agents.

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Determining effect of antiplatelet agents: platelet mapping (PM).

TEG PM can demonstrate the degree of platelet inhibition produced via the adenosine diphosphate (ADP) and arachidonic acid (AA) receptor sites. Platelet mapping measures the presence of platelet inhibition using heparin to suppress thrombin, activator F, to replace thrombin in converting fibrinogen into fibrin and ADP or AA to determine the amount of inhibition at each receptor site. The TEG PM assay involves four separate assays performed:

  • A baseline cup, where the maximal hemostatic activity is measured by a kaolin-activated whole blood sample treated with citrate (MA-CK).
  • The activator cup, in which heparin suppresses native thrombin activity, and an activator (in place of thrombin) cleaves fibrinogen to fibrin and converts FXIII to FXIIIa. By inactivating platelets, we can examine the contribution of fibrin to the clot (MA-A).
  • The ADP cup includes activator to form the fibrin clot and ADP to activate noninhibited platelets via the GP IIb/IIIa receptor (this allows measuring residual platelet activity, if any, in a patient on antiplatelet drugs (ADP or GP IIb/IIIa receptor inhibitors) maximal amplitude adenosine diphosphate (MA-ADP).
  • The AA cup, includes activator (for fibrin clot) and AA to activate the thromboxane A2 pathway that leads to platelet aggregation and this allows to measure residual platelet activity in a patient on aspirin maximal amplitude arachidonic acid (MA-AA).

The platelet inhibition in response to the agonist is calculated using following equation:

Platelet inhibition is a derived percentage and is computed separately for ADP and TxA2 (AA)-receptor inhibition.

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Thromboelastography/thromboelastography platelet mapping parameters.

The directly measured para meters from TEG/TEG PM included in this study were the split point (SP, minutes), the reaction time (R, minutes) from start of test to 2 mm clot growth and looks at factor function, angle (°) measured from SP to the tangent of the curve and looks at mostly fibrinogen function, (K minutes) looks at the kinetics of the clot from 2 mm of growth to 22 mm of growth, maximal amplitude (MA, mm) and looks at the platelet function (MA-AA, mm) (MA-ADP). G value (G dynes/cm2) and coagulation index (CI) = –0.6516Rc – 0.3772Kc + 0.1224MAc + 0.0759αc −7.7922 are both calculated parameters (versus directly measured) (Figure 1, Table 2).

In our study, to determine adequacy of platelet inhibition, we used MA-AA and MA-ADP values of TEG PM that reflect residual platelet reactivity, instead of percentage of inhibition (Figure 2).

Figure 2

Figure 2

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How Thromboelastography/Thromboelastography Platelet Mapping Differs from Conventional Coagulation Screening Assays

Platelet function analyzer (PFA-100).

The PFA-100 is designed to measure platelet adhesion and aggregation under high shear conditions, mimicking injured endothelium (using collagen coated cartridge). The PFA-100 has replaced bleeding times and is considered to be an assay that assesses primary hemostasis. The PFA test result is dependent on platelet number and function, plasma fibrinogen, von Willebrand Factor level, and hematocrit. The PFA-100 is sensitive to the presence of aspirin but not the adequacy of aspirin.

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Prothrombin time and activated partial thromboplastin.

PT and aPTT determine the adequacy of coagulation factor levels in platelet poor plasma. The INR is a calculation based on results of a PT and is used to monitor individuals who are being treated with warfarin (Coumadin).

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Thromboelastography/Thromboelastography Platelet Mapping Limitations

Von Willebrand disease (defect in the adhesion of platelets to the endothelial surface) cannot be assessed, because there is no endothelial component (collagen) in the current version of the assay.

Thromboelastography PM and INR were performed once a day. Thromboelastography PM duplicate samples were tested and found to be acceptable during validation studies, such that, patient duplicate sampling was not warranted.

This type of assay performance relies significantly on the proper training in operating the TEG PM instrument as well as taking into consideration preanalytical variables and interpretation expertise. We have a team of eight laboratory scientists who are trained by the Manufacturer. An extensive validation process was undertaken within the laboratory before TEG PM usage and special attention was given to preanalytical or blood collection variables. To minimize preanalytical variables, the following guidelines were established: blood drawn and hand carried to the laboratory immediately, underfilled specimens are rejected, blood tested within 30 minutes of collection, and interpretation performed by a pathologist with expertise in coagulation using established guidelines.

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Plan of Analysis

The INR was chosen for the analysis because it is used to monitor individuals who are being treated with warfarin (Coumadin). Thromboelastography parameters and INR were compared between subjects who developed at least one TE event and subjects who did not develop any TE events. For subjects who developed TE events, TEG parameters and INR closest to each TE event date were obtained. Because TEG analysis was not considered as part of the initial protocol for monitoring MCS device patients, the time between TEG monitoring before a TE event and the TE event was a median of 7 days with a mean of 18.2 ± 18.3 (mean ±SD). The time between TEG analysis after a TE event and the TE event date was a median of 1 day and mean of 1.4 ± 1.4 days. For those who did not develop any TE events, TEG parameters and INR were collected when patients were clinically adequately anticoagulated. Numerical data were analyzed using Wilcoxon rank sum test.

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Data Sources

All study data were obtained directly from extraction of electronic medical records. The data collected included types of MCS devices, dates of implant, types of TE and non TE events, and dates of TE and non TE events. INR and TEG parameters closest to the date of event or when patient was clinically and adequately anticoagulated were also obtained.

The Institutional Review Board and the Committee on Human Research reviewed and approved all aspects of the retrospective study including data collection and analysis.

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Results

The study included 98 eligible patients (Figure 3). Subjects that met the inclusion criteria were categorized based on presence of TE event and type of MCS device. Thromboelastography parameters and INR closest to the TE event were analyzed in the TE events group (median of 1 day; mean + SD of 1.42 + 1.44 days), while TEG parameters and INR during adequate anticoagulation were analyzed in the non TE events group. Subjects in the non TEG events group were further classified by type of MCS device.

Figure 3

Figure 3

Figure 4

Figure 4

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Thromboembolic Events

Among all study subjects, 11 (11.2%) subjects developed at least one TE event during the study period and two patients’ experienced two TE events.

In terms of types of MCS devices, among the TE group, 7 (63.6%) patients had TAH, 2 (18.2%) had HM II, 1 (9.1%) had BIVAD, and 1 (9.1%) had HW. Among the non-TE group, 28 (32.2%) had TAH, 23 (26%) had HM II, 6 (6.9%) had BIVAD, and 30 (34.4%) had HW as shown on Table 3.

Table 3

Table 3

In terms of types of events, a total of 100 events were reviewed, including 13 (13%) TE events and 87 (87%) non TE events. Of the 87 non TE events, 28 (32.2%) occurred in patients with TAH, 30 (34.5%) in those with HM II, 23 (26.4%) in those with HW, and 6 (6.9%) in those with BiVAD. Of the 13 TE events, 8 (61.5%) events occurred in patients with TAH, 2 (15.4%) in those with BiVAD, 2 (15.4%) in those with HM II, and 1 (7.7%) in those with HW. The TE events included cerebral vascular accidents (61.5%), transient ischemic accident (7.7%), RVAD thrombosis (23.1%) and acute coronary event (7.7%)

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Thromboelastography and Thromboelastography Platelet Mapping Parameters

The mean of all TEG parameters were either measured (R, α, MA) or calculated (G, CI) and compared between subjects with TE events and without TE events (when adequately anticoagulated) based on the type of MCS device (Table 4). A significantly higher CI was observed in the TE group compared with the non TE group in all four types of MCS devices (TE versus non-TE mean for TAH 3.12 vs. 1.12, HM II 2.79 vs. 1.74, HW 2.79 vs. 1.70 and for BiVAD 2.79 vs. 1.72). The CI value provides an indication of the global hemostatic state of a patient. It is derived and calculated from a linear combination of the kinetic parameters of clot development (R, K, angle) and clot strength (MA) CI = –0.6516Rc – 0.3772Kc + 0.1224MAc + 0.0759αc − 7.7922. Positive values above the range suggest overall hypercoagulability, whereas negative values below the range suggest overall hypocoagulability. The normal range for CI was calculated based on our validation studies for the laboratory. The normal CI range was found to be from −5.3 to 1.5. This range was developed from normal donors. The range of the CI values calculated for patients implanted with the different MCS devices without a TE event are presented in Table 4.

Table 4

Table 4

During TE events, a higher G and α were observed when compared with periods of non-TE events, with significant differences for those with HW, HM II, and BIVAD. A trend toward higher α, MA, G, and MA-ADP were observed in the TE group compared with the non TE group. There were no significant differences seen in MA-AA and INR between the two groups (Table 4).

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Patient’s Outcome

Of the 87 non TE patients

  • 26/87 (30%) were transplanted and 14/87 (16.1%) expired by > 1 year point.
  • 23/87 (26.4%) were transplanted and 13/87 (14.9%) expired by 1 year point.

Of the 11 with TE patients

  • 5/11 (45.5%) were transplanted and 2/11 (18.2%) expired by > 1 year point.
  • 5/11 (45.5%) were transplanted and 1/11 (9.1%) expired by 1 year point
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Discussion

One of the largest TAH study describing anticoagulation protocol with a very low neurologic adverse event rate (0.016 event/patient-month) attributed their success to the single so-called “La Pitie” anticoagulation protocol that was required to be followed by all physicians taking care of device patients.5 According to that protocol, hemostatic status of a patient was analyzed through many coagulation assays that allows for very specific anticoagulation management.

Our hands-on experience with TAH started in 2012, when the first TAH heart was implanted at our Institution, which is quaternary care teaching center with state of art surgery service, postoperative intensive care units, and a specialized coagulation laboratory. Our MCSD team included experienced surgeons, cardiologists, anesthesiologists, hematologist-oncologist, coagulation expert (hematopathologist), pharmacist, physician assistants, and nurses as well as residents and fellows rotating through the service. In our hands TEG PM appeared to be single most useful real time assay of overall hemostasis changes including increased fibrinolysis. But despite continuous and in depth MCSD team training on how to interpret TEG PM, it was very difficult to decide how to adjust anticoagulation and antiplatelet therapy using all the described parameters.

Thrombelastography (TEG, Haemonetics) is a device that measures global viscoelastic properties of whole blood clot formation and lysis in one test. Currently, this technology has been used extensively in hemostasis monitoring during major surgeries, trauma, obstetrical complications, and management of deep vein thrombosis whereas its other assay, TEG PM, is used to monitor antiplatelet agent’s activity.10,11

This type of assay that uses whole blood better mimics the in vivo hemostatic processes that are described in the cell-based model of hemostasis. Interaction of TF expressing cells, platelets, coagulation factors, and inhibitors form the basis of the hemostatic balance. Therefore, we speculate that the TEG with TEG PM can be a more valuable tool in tailoring therapy for MCS D patients who have a high risk of developing major thrombosis or bleeding events.

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Thromboelastography Platelet Mapping-Guided Anticoagulation Protocol

Despite data showing its clinical utility and because of its complexity in interpreting multiple variables, the initially suggested TEG PM-based anticoagulation protocol, was not followed by all who were involved in the MCSD patients care. For some of the patients, TEG PM was performed either sporadically or only immediately after a thrombotic or bleeding event. Even in our center, with specialized coagulation laboratory and a coagulation expert, esoteric coagulation assays are either not performed (thrombomodulin, platelet factor 4) or are available only on scheduled days (platelet aggregometry, antithrombin III).

These limitations have led to this pilot study with the objective of developing an individually-tailored anticoagulation protocol that is cost effective and standardized with a simple and easy to follow set of defined target parameters. The outlined protocol includes only four parameters (CI, INR, MA-AA, and MA-ADP) performed daily with two assays (TEG PM and INR).

The implantation of an MCSD induces a systemic inflammatory response that often leads to daily alterations of normal hemostasis as it is depicted in Figure 4. During the immediate postoperative and recovery period (especially during the first 2 weeks), the TEG PM assay may be a useful tool in preventing TE and or bleeding events in patients with durable MCS devices such as HW, HMII, and TAH. Once the patient is stabilized (Figure 5), TEG PM can be performed once or twice per week until discharge, and only if necessary (in case of bleeding and or clotting event) after the discharge. In our experience, infrequently observed TEG PM with high MA-A value requires another assay to assess aspirin response (platelet aggregometry).

Figure 5

Figure 5

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Assessment of Anticoagulation Therapy Adequacy

The single most statistically significant TEG parameter in our study used to define overall normocoaguability is the CI, which is calculated from the R, K, α, and MA values from a kaolin-activated TEG assay. Our results support what others have found about the utility of the CI parameter for maintaining a patient within the normocoaguable range and free from a TE event.7 The University of Arizona group used nonactivated blood samples for TEG analysis (native TEG) to monitor their MCSD patients. The CI range for normocoagulability for their MCSD patients was calculated to be from 0.29 to +3.66.12 Their range was also shifted from the reference range provided by manufacturer. At our institution Kaolin-activated TEG analysis is performed. The range of CI values determined from normal donors was from −5.3 to 1.5 (mean −1.9 ± 1.7), which is different from manufacturer suggested range from −3 to 3. With the underlying hemostatic abnormality for MCSD patients being hypercoagulable, the range for a normocoagulable state (free from thrombotic events) in our pilot study was 0.19–2.09 for TAH, 0.67–2.76 for BiVAD, 1.27–2.22 for HM II, and 1.23–2.17 for HW groups. Based on our results, patients with HM II and HW devices should be maintained at a CI value ≤1.5, whereas patients on TAH devices should be maintained at a value ≤1.2. Because of the design of devices, patients with HM II and HW are at higher risk of hemorrhagic complications owing to von Willebrand factor multimer loss.3,4 For this reason, their targeted CI value is higher than for patients implanted with TAH. The validity of the proposed values will be evaluated in a larger study.

There was no significant difference observed in INR between the two groups, signifying that aggressive TEG R-targeted titration of anticoagulant therapy is not necessary. Instead, the patient should be kept within device-specific INR goal ranges to achieve adequate Vitamin K-dependent factors inhibition.

At an INR of >3.5, the activity levels of all four factors are usually less than 30%, which is below the hemostatic range.13 Further increase in warfarin dose may cause significant inhibition of Vitamin K-dependent factors (VII, II, IX, and X), but will have no effect on fibrinogen and factor VIII, both of which are acute phase reactants and are usually elevated leading to normal TEG R values despite a prolonged INR. In cases of elevated CI but therapeutic INR, it may be helpful to review other TEG parameters for possible hypercoagulable states such as (infection, inflammation) and should be treated accordingly.

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Assessment of Antiplatelet Therapy Adequacy

Because of the predominant nature of TE events (cerebrovascular accidents), reactive thrombocytosis and platelet hyperactivity, focus should be on stabilization of their reactivity with antiplatelet agents. Because an MA-AA and MA-ADP value of 50 provides the lowest number for the normal range of MA in a thrombin-generated kaolin assay, an MA-AA and MA-ADP benchmark value of less than 50 appears to define normocoagulability in all MCS patients. In our experience, adequacy of the antiplatelet therapy cannot be assessed when MA-A value is elevated above 40 mm, platelet aggregometry may be used instead.

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Assessment of Bleeding

Thromboelastography is a useful real time assay of overall hemostasis, especially in cases of complex coagulopathies. It allows a wider scope of detection to help identify bleeding cause (factors, including fibrinogen, platelets, or their combination) and guide appropriate blood products transfusion intraoperatively.

Fibrinolysis, either primary or secondary (both can be seen in patients on MCSD), presents clinically as bleeding and requires different approaches to manage, but it is not apparent with conventional coagulation assays. Thromboelastography can be used to help in detection of fibrinolysis based on the LY30 parameter, which is the amount of lysis seen 30 minutes after MA.

If the patient develops a GI bleed when MA-AA and MA-ADP are therapeutic and TEG is normocoaguable, acquired von Willebrand disease should be ruled out with appropriate work up, because TEG is not sensitive to detect this defect.

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Study Limitations

There were several limitations of this study including the small sample size (n = 98) and the disproportionate amount of subjects without TE events (n = 87) compared with those with at least 1 TE event (n = 11). With the limited number of patients who developed TE events, the interpretations of our results were only based on a total number of 13 TE events. For this reason, a one-to-one comparison between two groups based on types of MCSD could not be performed; rather the TE events group included all types of MCS devices, while non-TE events group was categorized based on the type of MCSD. Another limitation of our study was that some of the patients with TE events did not have their TEG PM assays collected before or on the day of the TE event. As a result, the TEG PM assay for these patients may not accurately reflect the true nature of their hypercoaguability at the time of the event. A larger study will be conducted at our Institution to evaluate the validity of this established protocol.

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Summary

The healthcare team involved with the management of MCS patients normally comprises doctors of different subspecialties, pharmacists, physician assistants, and nurses. Therefore, a standardized yet individually-tailored anticoagulation protocol is imperative for successful patient outcomes. Laboratory tests that assess anticoagulation adequacy must be simple to interpret, cost effective, and have defined target parameters for normocoaguability. Based on our pilot study results, the CI, MA-AA, and MA-ADP are minimally required. Thromboelastography PM parameters that need to be assessed and correlated with device-specific INR ranges to help individualize a MCS patient’s antiplatelet and anticoagulation therapy.

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Acknowledgment

The authors thank Mike Miller, Manager Haemonetics Hemostasis clinical resources, for his help in describing TEG and TEG PM Parameters.

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Keywords:

thromboelastography platelet mapping; mechanical circulatory support devices; anticoagulation protocol; single institutional; normocoagulability definition

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