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Published on: October 12, 2012
Antithrombin activity during the period of percutaneous coronary revascularization: relation to heparin use,
W H Matthai1, P B Kurnik, W C Groh
1Department of Medicine, University of Pennsylvania School of Medicine, Philadelphia, USA. william_matthai@uphs.upenn.edu
Insights
Low antithrombin (AT) activity after percutaneous transluminal coronary revascularization (PTCR) is linked to thrombotic events. Heparin use impacts AT levels, potentially increasing thrombosis risk post-procedure.
Area of Science:
- Cardiovascular Medicine
- Hematology
- Interventional Cardiology
Background:
- Unfractionated heparin is crucial for preventing thrombosis during PTCR.
- Heparin's role as an antithrombin (AT) cofactor can lead to decreased AT activity.
- AT activity below 70% is a known risk factor for thrombosis.
Purpose of the Study:
- To evaluate changes in AT activity during and after PTCR.
- To determine the impact of these AT activity changes on major thrombotic complications.
- To explore the relationship between heparin use and AT activity levels.
Main Methods:
- 250 patients undergoing PTCR were monitored for AT activity.
- AT activity was sampled at PTCR start/end and subsequent mornings.
- Major thrombotic events were recorded and analyzed using discriminant analysis.
Main Results:
- A significant association was found between AT activity <70% and major thrombotic events (p = 0.006).
- AT activity decreased post-PTCR, with 21% of patients showing <70% activity the following morning.
- AT activity normalized over 20 hours after heparin discontinuation; pre-procedure heparin use correlated with lower AT activity.
Conclusions:
- Reduced AT activity may be a contributing factor to major thrombotic complications following PTCR.
- The timing and duration of heparin administration significantly influence the development of low AT activity.
Objectives:
This study evaluated changes in antithrombin (AT) activity around the time of percutaneous transluminal coronary revascularization (PTCR) with unfractionated heparin anticoagulation and the effects these changes had on major thrombotic complications of PTCR.
Background:
Heparin is used during PTCR to prevent thrombosis. However, heparin, a cofactor for AT, causes AT activity to fall. AT activity <70% is associated with thrombosis. There is a prothrombotic state after heparin discontinuation that has not been well explained.
Methods:
Antithrombin activity was sampled at the start and end of PTCR and the next two mornings in 250 consecutive patients. We recorded occurrence of major thrombotic events, defined as 1) major thrombotic complications of PTCR; 2) major in-lab thrombus formation; or 3) subacute occlusion. Discriminant analysis was employed to evaluate the relationship of AT activity to these events. Change in AT activity and its relationship to heparin was evaluated. Evidence of restenosis at six months was obtained.
Results:
There were 14 major thrombotic events. Antithrombin activity <70% was strongly (p = 0.006) associated with these events. The AT activity fell significantly through the morning after PTCR when 21% of patients had AT activity <70%; AT activity did not normalize until >20 h after heparin discontinuation. Pre-PTCR use of heparin led to lower AT activity in proportion to duration of heparin use. There was no relationship between AT activity and restenosis.
Conclusions:
Low AT activity may contribute to major thrombotic complications of PTCR. The way heparin is used before and after PTCR is important to development of low AT activity.
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