Editorials |
From the Division of Angiology and Hemostasis, Department of Internal Medicine, University Hospital of Geneva, Geneva, Switzerland.
Correspondence to Dr. H. Bounameaux, Division of Angiology and Hemostasis, Department of Internal Medicine, University Hospital of Geneva, Geneva, Switzerland. E-mail bounamea@cmu.unige.ch and Egbert.Kruithof@hcuge.ch
Key Words: Editorials coronary heart disease myocardial infarction recurrence risk factors inflammation
For a long time, we have known that a decrease in fibrinolytic activity is linked to an increase in risk of myocardial infarction.1 2 3 Paradoxically, the most convincing association between fibrinolysis and cardiovascular risk was an increased level of the profibrinolytic enzyme itself, tissue plasminogen activator (tPA).4 5 This unexpected finding was said to be due to the methods of measurement, which were unable to distinguish free tPA from tPA complexed with various inhibitors, the most important one being plasminogen activator inhibitor 1 (PAI-1), but this explanation had never been proven.
Recently, specific 2-site ELISAs have been developed that
allow independent measurements of complexes of tPA with its
inhibitors PAI-1, C1'-inhibitor, and
antiplasmin.6 In a substudy of the Stockholm Heart
Epidemiology Program (SHEEP), Wiman and
colleagues7 studied these particular components, as well
as the more classic tPA and PAI-1 antigens, and PAI-1 activity in 1212
patients who were enrolled
3 months after a myocardial infarction.
The results of this case-control study are reported in the present
issue of the Journal (p 2020).
The baseline measurements of the variables of interest were
compared with the recurrence rate of myocardial infarction
during a follow-up of 3 years. These parameters were also
compared with other variables that are either known or suspected to
correlate with a recurrence of cardiac events, such as lipids,
fibrinogen, and von Willebrand factor (vWF). Eighty-six
patients of the cohort (7.1%; 95% confidence interval, 5.7% to
8.7%) experienced reinfarction. When compared with matched patients
from the cohort and also with matched
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