Teg 5000 thrombelastograph hemostasis analyzer system

The whole blood samples were collected into heparin-rinsed tubes by cardiac puncture 48 h after CLP. Three hundred and forty µl of each blood sample was added to a disposable heparinase-coated cuvette and analyzed by the TEG^® 5000 Thrombelastograph^® Hemostasis Analyzer System (Haemonetics Corporation, Braintree, MA). The following parameters were evaluated: SP (Split Point, time from sample placement to first divergence of the trace; denotes the initial fibrin formation rate), R (Reaction time, time from sample placement until TEG^® tracing amplitude reaches 2 mm; denotes the initial fibrin formation rate), K (measures the time from clotting factor initiation (R) until clot formation reaches amplitude of 20 mm; represents the time for development of fixed degree of viscoelasticity during clot formation), Angle (angle formed by the slope of the initial TEG^® tracing; reflects speed at which solid clot forms), and MA (Maximum Amplitude, the greatest amplitude of the TEG^® tracing; reflects platelet function and absolute strength of the fibrin clot) (14 (link)).

Whole blood samples were collected into heparin-rinsed tubes by cardiac
puncture 48 h after CLP. Three hundred and forty μl of each sample was
placed in a disposable heparinase-coated cuvette and analyzed by TEG®
5000 Thrombelastograph® Hemostasis Analyzer System (Haemonetics
Corporation, Braintree, MA). The following parameters were evaluated: SP (Split
Point, time from sample placement to first divergence of the trace; denotes the
initial fibrin formation rate), R (Reaction time, time from sample placement
until TEG® tracing amplitude reaches 2 mm; denotes the initial fibrin
formation rate), K (time and Kinetics for fibrin cross-linkage, time from
TEG® tracing amplitude reaches 2 mm until it reaches 20 mm; represents
the time for development of fixed degree of viscoelasticity during clot
formation), Angle (angle formed by the slope of the initial TEG® tracing;
reflects speed at which solid clot forms), and MA (Maximum Amplitude, the
greatest amplitude of the TEG® tracing; reflects platelet function and
absolute strength of the fibrin clot) (Figure
1) ^{28 (link)}.

All the CF-LVAD patients in the study were treated with our standard anticoagulation and antiplatelet regimen. Anticoagulation was initiated with a titrated heparin dose with the goal for partial thromboplastin time of 40–45s once chest drainage was less than 30 mL/h for at least 4 hours. Thereafter the goal was aimed to have an anti-Xa activity level of 0.1–0.15 U/mL. The anticoagulation medication was subsequently converted to warfarin with a targeted international normalized ratio (INR) for the HeartMate II (1.8–2.3), the Jarvik 2000 (2.0–3.0) and the HeartWare HVAD (2.0–3.0). Antiplatelet agents were added to the anticoagulation regimen and the dosage was titrated based on measurements of platelet function using a platelet function analyzer (PFA-100^®, Dade Behring, Inc, Deerfield, IL) and thrombelastogram (TEG) (TEG® 5000 Thrombelastograph® Hemostasis Analyzer System, Haemonetics Corporation, Braintree, MA). All the patients received pentoxifylline to improve red blood cell deformability in the hope of mitigating shear-induced hemolysis. Although individual patient anticoagulation/antiplatelet regimen might vary day-to-day, a standard strategy was followed for all the patients.

Anticoagulation was initiated with a titrated heparin dose with the goal for partial thromboplastin time of 40–45s once chest drainage was less than 30 mL/h for at least 4 hours. Thereafter the goal was aimed to have an anti-Xa activity level of 0.1–0.15 U/mL. The anticoagulation medication was subsequently converted to warfarin with a targeted international normalized ratio (INR) for the HeartMate II (1.8 – 2.3), the Jarvik 2000 (2.0 – 3.0) and the HeartWare HVAD (2.0 – 3.0). Antiplatelet agents were added to the anticoagulation regimen and the dosage was titrated based on measurements of platelet function using a platelet function analyzer (PFA-100^®, Dade Behring, Inc, Deerfield, IL) and thrombelastogram (TEG) (TEG® 5000 Thrombelastograph® Hemostasis Analyzer System, Haemonetics Corporation, Braintree, MA). All the patients received pentoxifylline to improve red blood cell deformability in the hope of mitigating shear-induced hemolysis.

Whole blood samples were collected into heparin-rinsed tubes by cardiac puncture 48 h after CLP. Three hundred and forty µl of each sample was added to a disposable heparinase-coated cuvette and analyzed by the TEG^® 5000 Thrombelastograph^® Hemostasis Analyzer System (Haemonetics Corporation, Braintree, MA). The following parameters were evaluated: SP (Split Point, time from sample placement to first divergence of the trace; represents the initial fibrin formation rate), R (Reaction time, time from sample placement until TEG^® tracing amplitude reaches 2 mm; represents the initial fibrin formation rate), K (measures the time from clotting initiation (R) until clot formation reaches amplitude of 20 mm; denotes the time for development of fixed degree of viscoelasticity during clot formation), Angle (angle formed by the slope of the initial TEG^® tracing; reflects speed at which solid clot forms), and MA (Maximum Amplitude, the greatest amplitude of the TEG^® tracing; reflects platelet function and absolute strength of the fibrin clot).[13 (link)]