Thromb Haemost 2000; 84(01): 78-82
DOI: 10.1055/s-0037-1613971
Commentary
Schattauer GmbH

Plasminogen Activator Inhibitor-1 (PAI-1) 4G/5G Polymorphism, Coronary Thrombosis, and Myocardial Infarction in Middle-aged Finnish Men who Died Suddenly

Authors

  • Jussi Mikkelsson

    1   From the Medical School, University of Tampere and Tampere University Hospital, Tampere, Finland
  • Markus Perola

    2   Department of Human Molecular Genetics, National Public Health Institute, Helsinki, Finland
  • Ulla Wartiovaara

    3   Department of Clinical Chemistry and Biomedicine, Helsinki University Central Hospital, Helsinki, Finland
  • Leena Peltonen

    2   Department of Human Molecular Genetics, National Public Health Institute, Helsinki, Finland
  • Aarno Palotie

    3   Department of Clinical Chemistry and Biomedicine, Helsinki University Central Hospital, Helsinki, Finland
  • Antti Penttilä

    4   Department of Forensic Medicine, University of Helsinki, Finland
  • Pekka J. Karhunen

    1   From the Medical School, University of Tampere and Tampere University Hospital, Tampere, Finland
    5   Department of Clinical Pathology and Forensic Medicine, University of Kuopio, Finland
Further Information

Publication History

Received 22 December 1999

Accepted after resubmission 23 February 2000

Publication Date:
10 December 2017 (online)

Summary

High plasminogen activator inhibitor-1 (PAI-1) plasma levels increase future risk of myocardial infarction (MI). The 4G allele of the 4G/5G polymorphism of the PAI-1 gene has been associated with increased plasma levels of PAI-1. The association of the PAI-1 polymorphism with coronary narrowings, coronary thrombosis and myocardial infarction (MI) was studied in a prospective autopsy series of 300 middle-aged Caucasian Finnish men (33 to 69 yrs) suffering sudden out-of-hospital death (Helsinki Sudden Death Study). The 4G allele was found in 76.8% of men with sudden cardiac death (SCD) compared to 67.5% in men who died accidentally and 63.2% in men who died of other diseases (p = 0.08 and p = 0.055, respectively). Men possessing the 4G allele had more often acute MI (OR 3.5; p <0.05) and coronary thrombosis (OR 5.5; p = 0.01) compared to 5G homozygotes. 5G homozygotes, comprising one third of the men in our study, seem to be at a decreased risk of thrombosis, whereas carriers of the common 4G allele have an increased risk of thrombosis, AMI and possibly SCD compared to 5G homozygotes.