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Relation between PAI-1 Gene Locus Polymorphism and Family History of Coronary Artery Disease
- Ospedale Casa Sollievo della Sofferenza; San Giovanni Rotondo 71013 (FG), Italy Universita di Palermo; Palermo, Italy
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TO THE EDITOR:
In western countries, acute myocardial infarction and ischemic stroke are the most common causes of illness and death. Classic risk factors and lifestyle account only in part for the likelihood of ischemic events [1]. The familial aggregation of coronary heart disease is related largely to the clustering of cardiovascular risk factors. It is well recognized that a history of parental coronary heart disease is associated with increased risk for myocardial ischemia [2]. Low fibrinolytic activity is related to increased plasma levels of plasminogen activator inhibitor-1 (PAI-1) and has been documented in persons who later develop myocardial infarction [3]. Recently, a deletion/insertion polymorphism (4G/5G) within the PAI-1 gene locus was shown to influence the expression of this gene [4]. We have investigated the relation between the PAI-1 4G/5G polymorphism in 1179 healthy persons (514 men and 665 women) and the occurrence of coronary artery disease in their first-degree relatives. All participants (mean age, 37.7 years [range, 22 to 66 years]) and their parents were white and had been living in the same area. A family history of ischemic heart disease was assessed by a modified World Health Organization questionnaire. Polymerase chain reaction and endonuclease digestion were used to evaluate PAI-1 4G/5G polymorphism [5]. The group with a first-degree relative (n = 198) who had a coronary ischemic episode had more homozygotes for the deleted allele (4G/5G) than did the group without such a family history (n = 981) (odds ratio, 1.62 [95% CI, 1.17 to 2.25]; P = 0.005). The frequency of the 4G allele was also abnormally high (odds ratio, 1.29 [CI, 1.04 to 1.60]; P = 0.025). These data support the possibility that the 4G variant of the PAI-1 4G/5G polymorphism is a genetically transmissible coronary risk factor. This polymorphism may explain part of the risk for coronary artery disease related to family history.
Maurizio Margaglione, MD
Elvira Grandone
Ospedale Casa Sollievo della Sofferenza; San Giovanni Rotondo 71013 (FG), Italy
The Editors welcome submissions for possible publication in the Letters section. Authors of letters should:
•Include no more than 300 words of text, three authors, and five references
•Type with double-spacing
•Send three copies of the letter, an authors' form signed by all authors, and a cover letter describing any conflicts of interest related to the contents of the letter.
Letters commenting on an Annals article will be considered if they are received within 6 weeks of the time the article was published. Only some of the letters received can be published. Published letters are edited and may be shortened; tables and figures are included only selectively. Authors will be notified that the letter has been received. If the letter is selected for publication, the author will be notified about 3 weeks before the publication date. Unpublished letters cannot be returned.
Annals welcomes electronically submitted letters.
- Copyright ©2004 by the American College of Physicians
