Thromb Haemost 2003; 90(04): 717-723
DOI: 10.1160/TH03-03-0159
Vascular Development and Vessel Remodelling
Schattauer GmbH

Plasminogen activator inhibitor-1 and outcome after femoropopliteal angioplasty: analysis of genotype and plasma levels

Wolfgang Mlekusch
1   Department of Angiology Chemical Laboratory Diagnostics, University of Vienna, Medical School, Vienna, Austria
,
Martin Schillinger
1   Department of Angiology Chemical Laboratory Diagnostics, University of Vienna, Medical School, Vienna, Austria
,
Markus Exner
2   Department of Medical and Chemical Laboratory Diagnostics, University of Vienna, Medical School, Vienna, Austria
,
Schila Sabeti
1   Department of Angiology Chemical Laboratory Diagnostics, University of Vienna, Medical School, Vienna, Austria
,
Christine Mannhalter
2   Department of Medical and Chemical Laboratory Diagnostics, University of Vienna, Medical School, Vienna, Austria
,
Erich Minar
1   Department of Angiology Chemical Laboratory Diagnostics, University of Vienna, Medical School, Vienna, Austria
,
Oswald Wagner
2   Department of Medical and Chemical Laboratory Diagnostics, University of Vienna, Medical School, Vienna, Austria
› Author Affiliations
Financial support: The study was supported by grant P15231 of the “Fonds zur Förderung der Wissenschaftlichen Forschung” (to M.E. and M.S.).
Further Information

Publication History

Received 19 March 2003

Accepted after resubmission 24 June 2003

Publication Date:
05 December 2017 (online)

Summary

Plasminogen activator inhibitor-1 (PAI-1) is suggested to be involved in the pathophysiology of early thrombosis and late restenosis after percutaneous transluminal angioplasty (PTA). The role of the PAI-1 promoter genotype in this context is indeterminate. We investigated the association of the (4G/5G) polymorphism at nucleotide position (–675) in the PAI-1 gene promoter, PAI-1 plasma levels, and postangioplasty outcome after femoropopliteal PTA.

We studied 251 consecutive patients who underwent femoropopliteal PTA. In a subgroup of 86 patients PAI-1 plasma levels at baseline,8,24 and 48 hours postintervention were measured and correlated to the genotype. Patients were followed for early thrombosis and the late restenosis (≥50%) within 12 months. Multivariate Cox proportional hazards analysis was performed to assess the association between the PAI-1 genotype and PTA failure.

Results show that the PAI-1 genotype was neither associated with PAI-1 plasma levels (p=0.40) nor the change of PAI-1 from baseline to 8 (p=0.39), 24 (p=0.86) and 48 hours (p=0.89). Three out of 35 homozygous (4G/4G) patients (9%) had early thrombotic reocclusions, compared to two out of 153 heterozygous (4G/5G) patients (1%) and none of the 63 homozygous (5G/5G) patients (p=0.007). Restenosis after median 5 months (interquartile range 3 to 9) was found in 117 patients (42%), without significant association between the PAI-1 genotype and late postangioplasty failure (Log Rank p=0.95).

We can conclude that carriers of the 4G allele exhibited a higher frequency of early thrombotic reocclusions after percutaneous angioplasty. However, the PAI-1 gene promoter polymorphism (4G/5G) was not associated with PAI-1 plasma levels or late postangioplasty restenosis.

 
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