Factor V Leiden and its relation to left ventricular thrombus in acute myocardial infarction

• Published in: Acta Cardiologica 2001-02, Vol.56 (1), p.1-6
• Main Authors: Çelik, Şükrü, Ovali, Ercüument, Baykan, Merih, UÇar, Fahri, ErdÖl, Cevdet, Durmusş, Ismet, Kaplan, Şahin
• Format: Article
• Language: English
• Subjects: acutemyocardial infarction; Analysis of Variance; Biological and medical sciences; Cardiology. Vascular system; Case-Control Studies; Chi-Square Distribution; Coronary heart disease; Factor V - genetics; Factor V - physiology; factor V Leiden; Female; Heart; Heart Diseases - blood; Heart Diseases - etiology; Heart Diseases - genetics; Heart Ventricles; Humans; left ventricular thrombus; Logistic Models; Male; Medical sciences; Middle Aged; Mutation; Myocardial Infarction - blood; Myocardial Infarction - complications; Prospective Studies; Risk Factors; Thrombosis - blood; Thrombosis - etiology; Thrombosis - genetics
• ISSN: 0001-5385; 1784-973X; 0001-5385
• DOI: 10.2143/AC.56.1.2005587

Objective - The genetic defect of coagulation factor V, known as factor V Leiden, produces a resistance to degradation by activated protein C (APC) and increases the risk of venous thrombosis. However, the role of factor V Leiden in the formation of left ventricular (LV) thrombus has not been studied.We investigated whether factor V Leiden is a risk factor for LV thrombus in patients with acute myocardial infarction (AMI). Methods and results - We have analyzed clinical, echocardiographic and biochemical data in 135 consecutive patients (aged 58 ± 13 years; 31 women) with first anterior AMI. Two-dimensional echocardiographic examination was performed on days I, 3, 7, 15 and 30; LV thrombus was detected in 33 (24.4%) of 135 patients with AMI. The study also included 95 control subjects. Healthy age and sex-matched subjects without a personal or family history of ischaemic heart disease, stroke or thromboembolic disease served as a control group. Blood samples from the patients and controls were analyzed for the factor V Leiden mutation by DNA analysis, using the polymerase chain reaction. In addition, concentrations of fibrinogen, von Willebrand factor (vWF), tissue plasminogen activator (t-PA), plasminogen activator inhibitor-I (PAI-1) and D-dimer were measured in 135 patients. There was no significant difference in the prevalence of factor V Leiden between patients and control subjects. The prevalence of the factor V mutation was 9% (3/33) in patients with thrombus, and 7.7% (8/103) in patients without thrombus. The prevalence of factor V Leiden was 7.3% (7/95) in control subjects. No significant differences in plasma fibrinogen (480 ± 195 vs. 444 ± 179 mg/dl, p = 0.6), D-dimer (471 ± 256 vs. 497 ± 293 ng/dl, p = 0.7), vWF (112 ± 18 vs. 103 ± 15%, p = 0.5), PAI-I (26.7 ± 9.8 vs. 28.1 ± 10.2 ng/dl, p = 0.6), and t-PA (19.8 ± 8.7 vs. 17.2 ± 9.1 ng/dl, p = 0.7), levels are found in patients with LV thrombus when compared with those without LV thrombus. Multivariate analyses showed that peak creatine kinase level (p = 0.002) and LV wall motion score index (p = 0.003) were independent predictors of LV thrombus formation. Conclusion - Factor V Leiden mutation is not a risk factor for LV thrombus formation in patients with AMI. (Acta Cardiol 2001; 56(1 ): 1-6)