RapidTEG MA Validation (R-TEG MA)
During normal physiological conditions hemostasis (the ability of blood to clot) is kept in homeostatic balance by feedback mechanisms. These mechanisms involve an extremely complex series of steps on both sides of the coagulation cascade including cellular components (i.e. clot formation and breakdown). However, should this homeostatic balance be upset, normal hemostasis is affected resulting in pathological clotting (vessel blockage) or bleeding (hemorrhage). In instances that include acquired or congenital abnormalities of the hemostatic system it is clinically important to diagnose, monitor and manage the patient to optimize therapeutic intervention. Moreover, it is important to regulate the hemostasis system in the post-surgical outpatient who receives oral anticoagulant therapy to maintain the homeostatic balance.
The TEG® analyzer, using a small whole blood sample, documents the interaction of platelets with the protein coagulation cascade from the time of placing the blood in the analyzer until initial fibrin formation, clot rate strengthening and fibrin-platelet bonding via GPIIb/IIIa, through eventual clot lysis. It displays both qualitatively and quantitatively the two distinct parts of hemostasis - the part that produces the clot and the part that causes the breakdown of the clot. It shows the balance or degree of imbalance in the patient's hemostasis system, highlights any areas of deficiency or excess, and offers a precise view of the patient's hemostasis condition. If the system is not in balance, one can see where the imbalance lies. If a patient is bleeding, it is crucial to determine the cause of bleeding as soon as possible in order to start the proper treatment.
By utilizing a kaolin/tissue factor activator (RapidTEG™), the TEG® system can measure the interaction and simultaneous contribution of the intrinsic and extrinsic coagulation pathways which initiate and result in clot formation. This RapidTEG™ reagent can deliver results faster than activating with Kaolin alone. This protocol will specifically assess one algorithm called MA. MA is a direct function of the maximum dynamic properties of fibrin and platelet bonding via GPIIb/IIIa that represents the ultimate strength of the fibrin clot. This represents platelet function.
The objective of the study is to demonstrate the substantial equivalence of MA RapidTEG vs. MA Kaolin.
|Study Design:||Observational Model: Case-Only
Time Perspective: Prospective
|Official Title:||Validation of the RapidTEG™ MA Compared to Kaolin in Trauma and Cardiac Patients.|
- Correelation of Kaolin to RapidTEG [ Time Frame: Concurrent sample tested <2hrs from blood draw ] [ Designated as safety issue: No ]TEG paramaters were to be correlated in samples run concurrently using Kaolin and RapidTEG assays.
|Study Start Date:||July 2011|
|Study Completion Date:||October 2012|
|Primary Completion Date:||October 2012 (Final data collection date for primary outcome measure)|
Samples tested with TEG which are both citrated and non-citrated and are activated using the reagent RapidTEG.
Samples tested with TEG which are both citrated and non-citrated and are activated using the reagent Kaolin.
Please refer to this study by its ClinicalTrials.gov identifier: NCT01428102
|United States, Maryland|
|Sinai Center for Thrombosis Research|
|Baltimore, Maryland, United States, 21215|
|United States, Tennessee|
|Univserity of Tennessee Health Sciences Center|
|Knoxville, Tennessee, United States, 37996-1529|