Print Email Facebook Twitter Tissue plasminogen activator and risk of myocardial infarction: The Rotterdam study Title Tissue plasminogen activator and risk of myocardial infarction: The Rotterdam study Author van der Bom, J.G. de Knijff, P. Haverkate, F. Bots, M.L. Meijer, P. de Jong, P.T.V.M. Hofman, A. Kluft, C. Grobbee, D.E. Gaubius Instituut TNO Publication year 1997 Abstract Background: Impaired fibrinolytic capacity, as assessed by euglobulin clot lysis time or plasma concentration of fibrinolytic parameters, has been associated with an increased risk of myocardial infarction (MI). We studied the association of a polymorphism in the gene for TPA and of plasma concentrations of TPA (antigen and activity) with the prevalence of MI. Methods and Results: A case-control study was performed. Subjects with a history of MI (n= 121) and controls (n=250) were drawn from the Rotterdam Study, a population based cohort study of 7983 subjects ≤ 55 years old. We determined TPA antigen and activity in plasma and genotyped all subjects for the Alu repeat insertion/deletion polymorphism in intron h in the TPA gene. Homozygosity for the insertion was associated with twice as many cases of MI as was homozygosity for the deletion (odds ratio. 2.24; 95% CI, 1.11-4.50). TPA antigen was positively associated with the risk of MI; compared with that in the lowest quartile, the relative risks (odds ratio) in the second, third, and upper quartiles were 1.7 (CI.0.9-3.3), 2.3 (1.2-4.4), and 2.0 (1.03.8), respectively. When adjusted for body mass index, HDL and total cholesterol, systolic and diastolic blood pressures, and current smoking, the risk associated with TPA antigen concentration was attenuated. Increased concentrations of TPA activity tended to be associated with an increased risk of MI. Conclusions: This study provides evidence for an independent association of the insertion allele of the insertion/deletion polymorphism in the TPA gene with nonfatal MI. Increased TPA antigen is associated with an increased risk of MI; however, this association was not independent of cardiovascular disease risk factors. Subject BiologyCardiovascular diseasesFibrinolysisThrombolysisAdultAlleleCoronary riskDiastolic blood pressureGene insertionGenotypeHeart infarctionMajor clinical studySurvival rateAgedCase-Control StudiesCohort StudiesCross-Sectional StudiesDNA Transposable ElementsFemaleGene DeletionHumansImmunologic TechniquesMaleMiddle AgedMyocardial InfarctionPolymorphism, GeneticProspective StudiesRisk FactorsTissue Plasminogen Activator To reference this document use: http://resolver.tudelft.nl/uuid:1a63b8d5-18c2-4eb4-8f54-65b881774563 TNO identifier 233956 ISSN 0009-7322 Source Circulation, 95 (12), 2623-2627 Document type article Files To receive the publication files, please send an e-mail request to TNO Library.