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Tissue-type plasminogen activator -7,351C/T enhancer polymorphism is associated with a first myocardial infarction.

Artikel i vetenskaplig tidskrift
Författare Per Ladenvall
Lars Johansson
Jan-Håkan Jansson
Sverker Jern
Torbjörn K Nilsson
Anna Tjärnlund
Christina Jern
Kurt Boman
Publicerad i Thrombosis and haemostasis
Volym 87
Nummer/häfte 1
Sidor 105-9
ISSN 0340-6245
Publiceringsår 2002
Publicerad vid Hjärt-kärlinstitutionen
Institutionen för klinisk neurovetenskap
Sidor 105-9
Språk en
Länkar www.ncbi.nlm.nih.gov/entrez/query.f...
Ämnesord Apolipoprotein A-I, analysis, Binding Sites, Cardiovascular Diseases, epidemiology, Case-Control Studies, Enhancer Elements (Genetics), genetics, Female, Genetic Predisposition to Disease, Health Surveys, Humans, Hypertension, epidemiology, Intervention Studies, Male, Middle Aged, Multivariate Analysis, Myocardial Infarction, epidemiology, genetics, Obesity, epidemiology, Odds Ratio, Plasminogen Activator Inhibitor 1, analysis, Polymorphism, Genetic, Prognosis, Prospective Studies, Risk, Risk Factors, Sp1 Transcription Factor, metabolism, Sweden, epidemiology, Tissue Plasminogen Activator, genetics, secretion
Ämneskategorier Fysiologi, Medicinsk genetik

Sammanfattning

We recently identified a polymorphic Sp1 binding site in an enhancer at the tissue-type plasminogen activator (tPA) locus (tPA -7,351C/T), which was associated with vascular tPA release. Subjects homozygous for the -7,351C allele had twice the tPA release rate compared to subjects carrying the -7,351T allele. In this study we tested the hypothesis that the tPA -7,351C/T polymorphism is associated with myocardial infarction (MI). In a population-based prospective nested case-control study within northern Sweden, genotypes were determined among 61 MI cases and 120 controls. In a multivariate model, the tPA -7,351C/T polymorphism (OR 2.68 for T allele carriers; 95% CI 1.31-5.50), tPA antigen (OR 1.16; 95% CI 1.07-1.25) and apo A-I (OR, 0.997; 95% CI 0.995-0.999) were independently associated with a first MI. These findings suggest that genetic markers of local tPA release and circulating steady-state tPA levels carry independent prognostic information.

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