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 1, 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-1 (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-1 (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.
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 1, 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-1 (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-1 (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.