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PLoS One. 2013 Jun 24;8(6):e66977. doi: 10.1371/journal.pone.0066977. Print 2013.

Thrombin generation in the Glasgow Myocardial Infarction Study.

Author information

1
Laboratory of Clinical Thrombosis and Haemostasis, Department of Internal Medicine, Cardiovascular Research Institute Maastricht, Maastricht University, Maastricht, The Netherlands.

Abstract

BACKGROUND:

Thrombin is a key protease in coagulation also implicated in complex pathology including atherosclerosis. To address the role of thrombin in relation to myocardial infarction (MI) we explored thrombin generation analysis in plasma from patients and controls that had participated in the Glasgow MI Study (GLAMIS).

METHODS:

Thrombin generation at 1 and 2 pM TF and with and without thrombomodulin (TM) was performed on plasmas from 356 subjects (171 cases, 185 age and sex matched controls) from GLAMIS collected between 3 and 9 months after the MI event.

RESULTS:

Although thrombin generation was slightly delayed in cases (lag time increased from 3.3 to 3.6 min) at the highest trigger, the overall potential to generate thrombin was increased by 7% for the ETP and by 15% for the peak height (both at the 1 pM TF trigger) in cases. Addition of TM did not reveal differences. Furthermore, an increased thrombin generation was associated with MI [normalized ETP: adjusted OR for the highest percentile = 2.4 (95% CI 1.3-4.5) and normalized peak height: adjusted OR = 2.6 (1.3-5.0)] at the lowest trigger; normalized ETP and peak height being 2.1 (1.1-3.8) and 2.0 (1.0-4.1) at the higher 2 pM trigger.

CONCLUSION:

In GLAMIS, patients with a previous MI had an increased thrombin generation compared to controls. The absence of a clear difference in TM reduction suggests an unaltered anticoagulant activity in these patients. Further research is needed in order to unravel the underlying mechanisms of enhanced thrombin generation after MI.

PMID:
23826181
PMCID:
PMC3691168
DOI:
10.1371/journal.pone.0066977
[Indexed for MEDLINE]
Free PMC Article

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