Thromb Haemost 1999; 82(01): 100-103
DOI: 10.1055/s-0037-1614636
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Schattauer GmbH

Plasmin-α2-antiplasmin Complex in Patients with Atrial Fibrillation

William M. Feinberg
1   From the Department of Neurology, The University of Arizona, Tucson, Arizona
,
Elizabeth Macy
2   From the Laboratory for Clinical Biochemistry Research, Department of Pathology, University of Vermont, Burlington, Vermont
,
Elaine S. Cornell
2   From the Laboratory for Clinical Biochemistry Research, Department of Pathology, University of Vermont, Burlington, Vermont
,
Sarah D. Nightingale
2   From the Laboratory for Clinical Biochemistry Research, Department of Pathology, University of Vermont, Burlington, Vermont
,
Lesly A. Pearce
3   From the Statistical Consultant, Minot, North Dakota, USA
,
Russell P. Tracy
2   From the Laboratory for Clinical Biochemistry Research, Department of Pathology, University of Vermont, Burlington, Vermont
,
Edwin G. Bovill
2   From the Laboratory for Clinical Biochemistry Research, Department of Pathology, University of Vermont, Burlington, Vermont
,
for the Stroke Prevention in Atrial Fibrillation Investigators › Author Affiliations
This study was supported by grant R01-NS-24224 from the Division of Stroke and Trauma, National Institute of Neurological Disorders and Stroke, Bethesda, MD. The authors note the valuable contribution of the SPAF Study Coordinators at the participating institutions who collected the samples for analysis.
Further Information

Publication History

Received 17 October 1997

Accepted after revision 19 March 1999

Publication Date:
11 December 2017 (online)

Summary

Plasmin-α2-antiplasmin complex (PAP) is an index of recent fibrinolytic activity. We examined PAP levels in patients with atrial fibrillation (AF) to determine whether these levels are correlated with clinical characteristics associated with stroke risk. We obtained blood for measurement of PAP in a non-random sample of 586 patients with AF on entering the Stroke Prevention in Atrial Fibrillation III Study. PAP levels were measured with an ELISA assay. PAP values were transformed with a natural logarithm (PAPln) prior to all analyses. Older age, female gender, recent congestive heart failure, decreasing fractional shortening, recent onset of AF, and coronary artery disease were each univariately associated with higher levels of PAP (all p <0.05, two-sample t-test, simple linear regression). Older age, recent congestive heart failure, decreasing fractional shortening, and recent onset of AF were independently associated with higher PAP levels by multivariate analysis (linear regression). Among patients receiving warfarin, PAP levels were not correlated with INR levels (linear regression, p = 0.60). Patients classified as high-risk for thromboembolism by our risk stratification criteria (systolic blood pressure >160 mm Hg, prior thromboembolism, recent congestive heart failure, poor left ventricular function, and women over age 75) had higher PAP levels than low-risk patients (antilog mean PAPln 5.6 vs 4.9, p <0.001, two-sample t-test). PAP levels in patients with AF are associated with clinical characteristics predictive of thromboembolism. Elevated PAP levels are particularly associated with poor left ventricular function and are not affected by anticoagulation. PAP levels may be a marker of stroke risk in patients with AF.

Presented in part at the American Heart Association 22nd annual Joint Conference on Stroke and the Cerebral Circulation, Anaheim, CA, February, 1997.

 
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