Background Thromboelastography (TEG) measures the dynamics of coagulation. There are limited data about TEG in acute ischemic stroke other than a single study from 1974 suggesting that acute ischemic stroke patients are hypercoagulable. There have been no studies of TEG in the thrombolytic era despite its potential usefulness as a measure of clot lysis. This study was designed to provide initial TEG data in stroke patients before and after tissue plasminogen activator (tPA) therapy, and to provide the necessary preliminary data for further study of TEG’s ability to identify clot subtype and predict response to tPA therapy. Methods All acute ischemic stroke patients presenting between 11/2009 and 2/2011 eligible for tPA therapy were screened and 56 enrolled. Blood was drawn before (52 patients) and 10 minutes after tPA bolus (30 patients). Demographics, vitals, labs, 24hr National Institutes of Health Stroke Scale (NIHSS) and computed tomography (CT) scan results were collected. Patients were compared to normal controls. Results Acute ischemic stroke patients had shorter R (4.8±1.5 vs 6.0 ±1.7 min, p =0.0004), greater a-Angle (65.0±7.6 vs 61.5 ± 5.9°, p =0.01), and shorter K (1.7 ±0.7 vs 2.1 ±0.7 min, p =0.002) indicating faster clotting. Additionally, a subset formed clots with stronger platelet-fibrin matrices. Treatment with tPA resulted in reduction in all indices of clot strength (LY30=0(0–0.4) vs 94.4 (15.2–95.3) p<0.0001), however there was considerable variability in response. Conclusions TEG demonstrates that many acute ischemic stroke patients are hypercoaguable. TEG values reflect variable clot subtype and response to tPA. Further study based on these data will determine if TEG is useful for measuring the dynamic aspects of clot formation and monitoring lytic therapy.
Background and Purpose Iodinated contrast agents used for computed tomography angiography (CTA) may alter fibrin fiber characteristics and decrease fibrinolysis by tissue plasminogen activator (tPA). Thromboelastography (TEG™) measures the dynamics of coagulation and correlates with thrombolysis in acute ischemic stroke (AIS) patients. We hypothesized that receiving CTA prior to tPA will not impair thrombolysis as measured by TEG™. Methods AIS patients receiving 0.9 mg/kg tPA within 4.5 hours of symptom onset were prospectively enrolled. For CTA, 350 mg/dL of iohexol or 320 mg/dL of iodixanol at a dose of 2.2 ml/kg was administered. TEG™ was measured prior to tPA and 10-minutes after tPA bolus. CTA timing was left to the discretion of the treating physician. Results Of 136 AIS patients who received tPA, 47 had CTA prior to tPA bolus, and 42 had either CTA following tPA and post-tPA TEG™ draw or no CTA (non-contrast group). The median change in clot lysis (LY30) following tPA was 95.3% in the contrast group vs. 95.0% in the non-contrast group (p = 0.74). Thus, tPA-induced thrombolysis did not differ between contrast and non-contrast groups. Additionally, there was no effect of contrast on any pre-tPA TEG™ value. Conclusions Our data do not support an effect of iodinated contrast agents on clot formation or tPA activity.
Introduction: Modern treatment of acute ischemic stroke (AIS) has increasingly incorporated multimodal CT imaging. Data illustrating that radiographic contrast agents alter fibrin fiber characteristics and decrease fibrinolysis by thrombolytic agents are potentially concerning. Thromboelastography (TEG) provides an integrated, dynamic view of coagulation and has recently been correlated with thrombolysis in AIS patients. This is the first study to examine the effects of contrast agents on tPA-induced clot lysis using TEG. We hypothesized that receiving computed tomography angiography (CTA) prior to tPA will impair thrombolysis as measured by TEG. Methods: AIS patients receiving 0.9 mg/kg tPA within 4.5 hours of symptom onset were enrolled. For CTA, iohexol dose was calculated using Medrad’s P3T software. Blood was drawn for TEG prior to CTA or tPA treatment and again 10-minutes after tPA bolus. TEG values, time of TEG draw and tPA administration, and CTA times were recorded. TEG values in patients having CTA prior to tPA were compared with patients in whom a CTA was performed either after tPA or not at all. Results were analyzed using Mann-Whitney U Test. Results: 100 AIS patients received tPA. Of these, 17 patients had CTA prior to TEG blood draws and tPA bolus. 57 patients had either CTA following tPA or no CTA. The median change in clot lysis (LY30) following tPA was 94.8% in the contrast group vs. 94.5% in controls (p = 0.84). The median reduction in clot strength (G) was -8.8 dyn/cm 2 in the contrast group vs. -8.6 dyn/cm 2 in controls (p = 0.51). Pre-tPA G appeared to be attenuated by contrast (7.7 vs. 5.9 dyn/cm 2 ) when corrected for platelet activity; however, this difference was not significant (p = 0.14). There was no effect of contrast on any other pre-tPA TEG value. Conclusion: The current data do not support any impairment of tPA-induced clot lysis by contrast agents. Baseline TEG also appears to be unaffected by contrast, but more patients are needed to better examine a possible interaction between clot strength and contrast agents.
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