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(Circulation. 1999;99:457-460.)
© 1999 American Heart Association, Inc.
Correspondence |
Professor of Medicine and Pathology
Associate Professor of Preventive Medicine University Medical Center, State University of New York, Stony Brook, NY
To The Editor:
Doggen et al1 reported a case-control study
assessing the effect of factor V Leiden and the prothrombin 20210 gene
variant on the risk of myocardial infarction in men. The authors stated
in their conclusions that "the 20210 G
A variant of prothrombin is
associated with an increased risk of myocardial infarction" and that
"the combined presence of major cardiovascular risk
factors and carriership of a coagulation defect increases the risk
considerably." A review of their data in Tables 1 through 4 leads us
to conclude that neither claim is supported by statistical
significance. In Table 2, the prevalence of the prothrombin variant in
cases (1.8%) is not significantly different from the prevalence in
controls (1.2%) by the
2 test, with an OR of
1.5 and a CI (0.63.8) that includes unity. A larger study would be
required to prove that an OR of 1.5 is truly increased. The likelihood
that this OR of 1.5 is not significantly different from 1.0 is also
suggested by the fact that it is based on the unexpected finding of a
lower prevalence of the variant in the controls (1.2%) than in the
general population(2%) rather than a higher prevalence in the
cases.
The second conclusion, that a coagulation defect added to the effect of
a metabolic defect, also does not stand up to scrutiny of
the data. In Table 3, the ORs of 6.1 and 3.3, with their overlapping
CIs of 3.012.5 and 2.54.2, respectively, indicate that smoking
increased the risk of
Department of Clinical Epidemiology, Department of Cardiology, Hemostasis and Thrombosis Research Center, Leiden University Hospital, Leiden, Netherlands
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