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CLINICAL STUDIES

Antithrombin activity during the period of percutaneous coronary revascularization

Relation to heparin use, thrombotic complications and restenosis

William H. Matthai, Jr., MD, FACC^*, Peter B. Kurnik, MD, FACC, William C. Groh, MD, FACC^*, William J. Untereker, MD, FACC^* and Jamie E. Siegel, MD

^* Department of Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA
Department of Medicine, UMDNJ/Robert Wood Johnson Medical School at Camden, Camden, New Jersey, USA
Department of Medicine, UMDNJ/Robert Wood Johnson Medical School, New Brunswick, New Jersey, USA

Manuscript received August 12, 1998; revised manuscript received November 6, 1998, accepted December 23, 1998.

Reprint requests and correspondence: Dr. William H. Matthai, Jr., Cardiology Division, Presbyterian Medical Center, 39th and Market Streets, Philadelphia, Pennsylvania 19104
william_matthai{at}uphs.upenn.edu

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.

Abbreviations and Acronyms   ACT = activated clotting time   AT = antithrombin   PTCR = percutaneous transluminal coronary revascularization

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