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


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.


CONCLUSIONS
Factor V Leiden mutation is not a risk factor for LV thrombus formation in patients with AMI.
Celik
S
S
KTU Faculty of Medicine, Department of Cardiology, Trabzon, Turkey. ercevdet@gul.net.tr
Ovali
E
E
Baykan
M
M
Uçar
F
F
Erdöl
C
C
Durmuş
I
I
Kaplan
S
S
D000704:Analysis of Variance; D016022:Case-Control Studies; D016009:Chi-Square Distribution; D005165:Factor V / Q000235:genetics / Q000502:physiology*; D005260:Female; D006331:Heart Diseases / Q000097:blood / Q000209:etiology* / Q000235:genetics; D006352:Heart Ventricles; D006801:Humans; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D009154:Mutation; D009203:Myocardial Infarction / Q000097:blood / Q000150:complications*; D011446:Prospective Studies; D012307:Risk Factors; D013927:Thrombosis / Q000097:blood / Q000209:etiology* / Q000235:genetics
C095381:factor V Leiden; D005165:Factor V