Thrombin Generation in Acute Ischaemic Stroke

Introduction. Stroke remains a global leading cause of death and disability. Traditional description of plasma biology in the aftermath of acute ischaemic stroke favours development of hypercoagulability, resulting from complex interplay between plasma and endothelial factors. However, no single ass...

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Main Authors: Ibrahim O. Balogun, Lara N. Roberts, Raj Patel, Rohan Pathansali, Lalit Kalra, Roopen Arya
Format: Article
Language:English
Published: Wiley 2016-01-01
Series:Stroke Research and Treatment
Online Access:http://dx.doi.org/10.1155/2016/7940680
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author Ibrahim O. Balogun
Lara N. Roberts
Raj Patel
Rohan Pathansali
Lalit Kalra
Roopen Arya
author_facet Ibrahim O. Balogun
Lara N. Roberts
Raj Patel
Rohan Pathansali
Lalit Kalra
Roopen Arya
author_sort Ibrahim O. Balogun
collection DOAJ
description Introduction. Stroke remains a global leading cause of death and disability. Traditional description of plasma biology in the aftermath of acute ischaemic stroke favours development of hypercoagulability, resulting from complex interplay between plasma and endothelial factors. However, no single assay measures the overall global coagulation process. We postulate that thrombin generation would assist in identifying coagulation abnormalities after acute stroke. Aim. To investigate the coagulation abnormalities after acute ischaemic stroke using thrombin generation. Methods. We evaluated thrombin generation, measured with calibrated automated thrombography in stroke of different aetiological types (n=170) within 48 hours of symptoms onset (baseline) and in the second week (time 2) and in normal healthy volunteers (n=71). Results. Two-point thrombin generation assays showed prolonged lag time and time to peak at baseline (3.3 (2.9, 4.0) versus 3.6 (3.2, 4.7); p=0.005) and (3.3 (2.9, 4.0) versus 3.6 (3.2, 4.7); p=0.002), respectively, and at time 2 (3.5 (2.9, 4.2) versus 4.0 (3.1, 4.9); p=0.004) and (5.9 (5.3, 6.6) versus 6.8 (5.8, 7.7) p=0.05), respectively, in cardioembolic stroke (n=39), when compared to noncardioembolic stroke (n=117). The result was reproduced in multiple comparisons between acute ischaemic stroke subgroups and normal healthy volunteers. Endogenous thrombin potential and peak thrombin did not indicate hypercoagulability after acute ischaemic stroke, and thrombolytic therapy did not affect thrombin generation assays. Conclusion. Our findings suggest that thrombin generation in platelet poor plasma is not useful in defining hypercoagulability in acute ischaemic stroke. This is similar to observed trend in coronary artery disease and contrary to other hypercoagulable states.
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spelling doaj-art-ae31a9c93ca84ac193801345906bae512025-02-03T05:52:40ZengWileyStroke Research and Treatment2090-81052042-00562016-01-01201610.1155/2016/79406807940680Thrombin Generation in Acute Ischaemic StrokeIbrahim O. Balogun0Lara N. Roberts1Raj Patel2Rohan Pathansali3Lalit Kalra4Roopen Arya5King’s Thrombosis Centre, Department of Haematological Medicine, King’s College Hospital NHS Foundation Trust, London, UKKing’s Thrombosis Centre, Department of Haematological Medicine, King’s College Hospital NHS Foundation Trust, London, UKKing’s Thrombosis Centre, Department of Haematological Medicine, King’s College Hospital NHS Foundation Trust, London, UKDepartment of Stroke Medicine, King’s College Hospital NHS Foundation Trust, London, UKClinical Neuroscience Department, Academic Neuroscience Centre, King’s College London, London, UKKing’s Thrombosis Centre, Department of Haematological Medicine, King’s College Hospital NHS Foundation Trust, London, UKIntroduction. Stroke remains a global leading cause of death and disability. Traditional description of plasma biology in the aftermath of acute ischaemic stroke favours development of hypercoagulability, resulting from complex interplay between plasma and endothelial factors. However, no single assay measures the overall global coagulation process. We postulate that thrombin generation would assist in identifying coagulation abnormalities after acute stroke. Aim. To investigate the coagulation abnormalities after acute ischaemic stroke using thrombin generation. Methods. We evaluated thrombin generation, measured with calibrated automated thrombography in stroke of different aetiological types (n=170) within 48 hours of symptoms onset (baseline) and in the second week (time 2) and in normal healthy volunteers (n=71). Results. Two-point thrombin generation assays showed prolonged lag time and time to peak at baseline (3.3 (2.9, 4.0) versus 3.6 (3.2, 4.7); p=0.005) and (3.3 (2.9, 4.0) versus 3.6 (3.2, 4.7); p=0.002), respectively, and at time 2 (3.5 (2.9, 4.2) versus 4.0 (3.1, 4.9); p=0.004) and (5.9 (5.3, 6.6) versus 6.8 (5.8, 7.7) p=0.05), respectively, in cardioembolic stroke (n=39), when compared to noncardioembolic stroke (n=117). The result was reproduced in multiple comparisons between acute ischaemic stroke subgroups and normal healthy volunteers. Endogenous thrombin potential and peak thrombin did not indicate hypercoagulability after acute ischaemic stroke, and thrombolytic therapy did not affect thrombin generation assays. Conclusion. Our findings suggest that thrombin generation in platelet poor plasma is not useful in defining hypercoagulability in acute ischaemic stroke. This is similar to observed trend in coronary artery disease and contrary to other hypercoagulable states.http://dx.doi.org/10.1155/2016/7940680
spellingShingle Ibrahim O. Balogun
Lara N. Roberts
Raj Patel
Rohan Pathansali
Lalit Kalra
Roopen Arya
Thrombin Generation in Acute Ischaemic Stroke
Stroke Research and Treatment
title Thrombin Generation in Acute Ischaemic Stroke
title_full Thrombin Generation in Acute Ischaemic Stroke
title_fullStr Thrombin Generation in Acute Ischaemic Stroke
title_full_unstemmed Thrombin Generation in Acute Ischaemic Stroke
title_short Thrombin Generation in Acute Ischaemic Stroke
title_sort thrombin generation in acute ischaemic stroke
url http://dx.doi.org/10.1155/2016/7940680
work_keys_str_mv AT ibrahimobalogun thrombingenerationinacuteischaemicstroke
AT laranroberts thrombingenerationinacuteischaemicstroke
AT rajpatel thrombingenerationinacuteischaemicstroke
AT rohanpathansali thrombingenerationinacuteischaemicstroke
AT lalitkalra thrombingenerationinacuteischaemicstroke
AT roopenarya thrombingenerationinacuteischaemicstroke