Prevalence of resistance against activated protein C resulting from factor V Leiden is significantly increased in myocardial infarction: investigation of 507 patients with myocardial infarction |
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Authors: | Middendorf Katharina Göhring Peter Huehns Tanya Y Seidel Dietrich Steinbeck Gerhard Nikol Sigrid |
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Affiliation: | a Medical Clinic I, Klinikum Großhadern, Ludwig Maximilian University, Munich, Germany b Institute of Clinical Chemistry, Klinikum Großhadern, Ludwig Maximilian University, Munich, Germany c British Heart Foundation, Cardiovascular Medicine, Imperial College School of Technology and Medicine, Hammersmith Hospital, London, Great Britain, UK d Department of Cardiology and Angiology, University of Münster, Münster, Germany |
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Abstract: | BackgroundA point mutation in the gene encoding coagulation factor V is a cause of resistance against activated protein C. The presence of factor V Leiden is linked to 50% of congenital defects causing venous thrombosis. Its relationship to arterial thrombosis, particularly to myocardial infarction, has not been defined. Therefore, we performed a study on the role of factor V Leiden in patients with myocardial infarction. The study was carried out in Bavarians of German origin, a relatively homogeneous population.Methods and resultsThe study group consisted of 507 patients with documented myocardial infarction (77.5% (393/507) men, 22.5% (114/507) women), with a mean age of 56.1 (range 18--86) years. Strict criteria for patient selection and highly sensitive and specific functional tests for factor V Leiden were used. In addition, all patients with pathological test results were genotyped. The prevalence of factor V Leiden in patients with myocardial infarction was 8.7% (44/507), a significant increase in the prevalence of this mutation compared with the control group (3.7%, P = .0025). The odds ratio was 2.46 (95% CI 1.35-4.50).ConclusionsA significantly increased prevalence of factor V Leiden in patients with documented myocardial infarction was seen. Patients with this mutation appear to have a predisposition for myocardial infarction. |
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