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Background: It is known that resistance to activated protein C (APCR), often associated with a single point mutation (Arg506-->Gln) in the coagulation factor V gene (factor V Leiden), is the most frequent inherited abnormality of blood coagulation. It plays a key role as pathogenetic factor of venous thromboembolism, but its association with an increased risk of arterial thrombosis is uncertain. Aim of the present study was to evaluate the prevalence of APCR in men, who suffered myocardial infarction more than 6 months earlier and without cardiovascular risk factors (hypercholesterolemia, smoking, diabetes, obesity and hypertension)., Methods: The study was carried on 20 men aged <65 years who have suffered myocardial infarction. Twenty healthy subjetcs matched for sex and age were recruited as controls. We determined: PTT, PTT-PCA (Activated Protein C), PTT-PCA/PTT, AntiThrombin III, Protein C, Protein S, Fibrinogen, Glucose, Triglycerides, Cholesterol, HDL-C, LDL-C, APO A1, APO B100, Lp(a), oxizided LDL antibody and some components of the complement system (C3c, C4)., Results: In the group of patients there were six subjects (30%) with APCR, while there were no subjects in the control group (0%) with APCR. Patients were subdivided into two groups: with and without APCR. Patients with APCR displayed significantly higher levels of fibrinogen (367.5+/-48.4 vs 268.3+/-37.7), LDL-C (147.0 +/-20.7 vs 125.8+/-25,6), APO B100 (133.8+/-29.8 vs 121.8+/-31.5), oxizide LDL antibody (596.8+/-357 vs 315.3+/-179.6) and C4 (45.6+/-10 vs 37.85+/-11,3). Significant positive correlations (p<0.05) were observed between PTT-PCA/PTT ratio and fibrinogen (r=0.68) and between PTT-PCA/PTT ratio and oxidized LDL antibody (r=0.61)., Conclusions: In conclusion, the high prevalence of APCR (30%) in our patients seems to be important in order to carry out a primary prevention of arterial thrombosis and a secondary prevention of new thromboembolic complications.

Objectives: The aim of the present study was to evaluate the effects of pravastatin treatment on lipid, inflammation, and coagulation parameters in patients suffering from myocardial infarction with or without carotid atherosclerotic lesions (groups 1 and 2, respectively)., Methods: In the first phase of the study, a cross-sectional comparison of lipid, inflammation, and coagulation parameters was performed between the patients and the control group (group 3). Highly significant differences in these parameters were observed, especially in group 1. In the second phase of the study, we assessed the effects of a persistent reduction in cholesterol synthesis induced by increasing doses of pravastatin (20 mg daily for 8 weeks and 40 mg daily for a further 8 weeks). In addition to the well-established lipid-lowering effect, significant changes in inflammation and coagulation parameters were observed. In particular, pravastatin at a dosage of 20 mg/ day significantly reduced only fibrinogen levels, while at a dosage of 40 mg/day significantly reduced factor VII, fibrinogen, prothrombin fragments 1 and 2, thrombin-antithrombin complexes, tissue plasminogen activator antigen (tPA:Ag) before venous occlusion (b.o.), inhibitor of plasminogen activator activity (PAI) b.o., PAI activity after occlusion (a.o.), the human autoantibodies against oxidized low-density lipoprotein (LDL), and the c fraction of the third component system levels, and significantly increased tPA:Ag a.o. levels., Results: Our results show that in patients suffering from myocardial infarction the risk of thrombotic complications can be decreased with pravastatin, especially by larger doses. However, the relationship must be further investigated because the observed reductions in the hemostatic system and inflammatory response seemed to be dose dependent, while the effects of pravastatin treatment were not significantly correlated with total and LDL cholesterol changes.

The aim of the present study was to evaluate metabolic, coagulation and fibrinolytic parameters in 45 patients [31 men, 14 women, aged 56.5 +/- 3.5 years (mean +/- SD)] who had suffered myocardial infarction more than 6 months earlier, with or without carotid atherosclerotic lesions. After the extracranial carotid arteries had been evaluated using a B-mode Duplex scanning system, patients were subdivided into two groups: group 1 (n = 20) with carotid plaques or measurable intima-media thickness; and group 2 (n = 25) without carotid plaques or measurable intima-media thickness. Twenty-two age- and sex-matched subjects were recruited as controls (group 3). Groups 1 and 2 displayed significantly higher levels of total cholesterol, apolipoprotein B, human autoantibodies against oxidised low-density lipoprotein and the c fraction of the third component system, and significantly lower levels of high-density lipoprotein cholesterol and apolipoprotein A1 than group 3. However, serum levels of triglyceride and lipoprotein (a) were significantly higher in group 1 than in the control group. Moreover, groups 1 and 2 displayed significantly higher levels of factor VII, fibrinogen, fragment 1+2, thrombin-antithrombin complex and plasminogen activator inhibitor after venous occlusion, and significantly lower levels of tissue-type plasminogen activator after venous occlusion than group 3. Significantly higher levels of tissue-type plasminogen activator and plasminogen activator inhibitor before venous occlusion were observed in groups 1 and 2 and significantly lower levels of antithrombin III, protein C and protein S were observed in group 1 compared with the controls. Patients were also analysed according to levels of lipoprotein (a). The lowest levels of tissue-type plasminogen activator after venous occlusion and the highest levels fragment 1 + 2, the c fraction of the third component system, and plasminogen activator inhibitor after venous occlusion were observed in patients with the highest levels of lipoprotein (a). Our data demonstrate an activation of coagulation and deficient fibrinolysis in survivors of myocardial infarction, particularly in those with associated carotid atherosclerotic lesions. We speculate that this thrombophilic state may play a key role in the pathogenesis of atherosclerotic vascular disease and thromboembolic complications.

The aim of the present study was to evaluate some metabolic, coagulation and fibrinolytic parameters in 35 patients (24 males and 11 females, mean age 57 +/- 4 years) suffering from myocardial infarction more than 6 months before with or without carotid atherosclerotic lesions. After evaluation by B-mode duplex scanning system of extracranial carotid arteries, the patients were subdivided into two groups: Group 1 (n = 16, with carotid plaques or intima-media thickening) and Group 2 (n = 19, without carotid plaques or intima-media thickening). Eighteen age- and sex-matched subjects were recruited as controls (Group 3). Groups 1 and 2 displayed significantly higher levels of total cholesterol and apolipoprotein B and significantly lower levels of HDL-cholesterol and apolipoprotein A1 than Group 3, while serum triglyceride and lipoprotein (a)-Lp (a) levels were significantly higher in Group 1 as compared to the control group. Moreover, Group 1 and 2 displayed significantly higher levels of factor VII, fibrinogen, F1+2, thrombin-antithrombin complex and plasminogen activator inhibitor (PAI) post venous occlusion and significantly lower levels of tissue plasminogen activator (t-PA) post venous occlusion than Group 3. Significantly higher levels of t-PA and PAI pre venous occlusion and significantly lower levels of antithrombin III, C-protein and S-protein were observed in Group 1 as compared to controls. In patients with highest Lp(a) level, the lowest t-PA level post venous occlusion and the highest PAI level post venous occlusion were observed. Our data show an activation of coagulation and a deficient fibrinolysis in survivors of myocardial infarction, particularly in those with associated carotid atherosclerotic lesions. We speculate that this thrombophilic state may play a key role in the pathogenesis of atherosclerotic vascular disease and thromboembolic complications.