Donate Help Contact The AHA Sign In Home
American Heart Association
Circulation
Search: search_blue_button Advanced Search
Circulation. 1999;99:457-460

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Hultin, M. B.
Right arrow Articles by Bertina, R. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Hultin, M. B.
Right arrow Articles by Bertina, R. M.
Right arrowPubmed/NCBI databases
*Substance via MeSH
*Genetics Home Reference
Medline Plus Health Information
*Heart Attack
Related Collections
Right arrow Genomics
Right arrow Coagulation and fibronolysis

(Circulation. 1999;99:457-460.)
© 1999 American Heart Association, Inc.


Correspondence

Factor V Leiden, Prothrombin 20210 Gene Variant, and Risk of Myocardial Infarction

Mae B. Hultin, MD

Professor of Medicine and Pathology

Roger C. Grimson, PhD

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 {chi}2 test, with an OR of 1.5 and a CI (0.6–3.8) 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 3.0–12.5 and 2.5–4.2, respectively, indicate that smoking increased the risk of . . . [Full Text of this Article]

Carine J.M. Doggen, MSc; Frits R. Rosendaal, MD, Professor; Volker Manger Cats, MD; Rogier M. Bertina, PhD

Department of Clinical Epidemiology, Department of Cardiology, Hemostasis and Thrombosis Research Center, Leiden University Hospital, Leiden, Netherlands