Author + information
- Received June 3, 1991
- Revision received July 29, 1991
- Accepted August 23, 1991
- Published online February 1, 1992.
- Yi Shi, MD, PhD,
- Donald Nardone, MD,
- Antonio Hernandez-Martinez, MD,
- Paul Walinsky, MD, FACC,
- Thorir D. Bjornsson, MD, PhD and
- Andrew Zalewski, MD∗
- ↵∗Address for reprints: Andrew Zalewski, MD, Division cf Cardiology, Thomas Jefferson University, Suite 5360 Gibbon Building, 111 South 11th Street Philadelphia, Pennsylvania 19107.
The goal of this study was to assess fibrinolytic activity after vessel wall injury and to correlate changes in fibrinolytic activity with angiographic and histologic findings. Accordingly, in 18 atherosclerotic rabbits, vessel wall injury was produced by means of iliac artery balloon angioplasty (the injury group), whereas 8 atherosclerotic rabbits served as a control group. In all rabbits from the injury group, deep vessel wall injury was documented by either angiography or histologic study. Plasminogen activator inhibitor-1 activity in plasma increased significantly, from 21.79 ± 1.29 arbitrary units/ml (AU/ml) at baseline study to 32.05 ± 1.47 AU/ml at 6 h after vessel wall injury (p < 0.01), whereas activity remained unchanged throughout the 24h period in the control group. Plasma levels of tissue plasminogen activator activity were similar in both groups. Intravascular thrombus was found in five of six additional rabbits 6 h after vessel wall injury, that is, at the time of impaired fibrinolytic activity, whereas no thrombus was found in the control group (p < 0.05).
It is concluded that deep vessel wall injury is associated with reduced fibrinolytic activity. In addition to other procoagulant factors, elevated plasminogen activator inhibitor-1 activity may lead to intravascular thrombosis and impaired resolution of thrombus.
☆ This study was supported in part by Grant HL-45593 and by Biomedical Research Support Grant 2SO7RR05414-29 from the National Institutes of Health, Bethesda, Maryland and was presented in part at the 40th Annual Scientific Session of the American College of Cardiology, Atlanta, Georgia, March, 1991.
- Received June 3, 1991.
- Revision received July 29, 1991.
- Accepted August 23, 1991.