Fibrinogen and silent atherosclerosis in subjects with cardiovascular risk factors.

Fibrinogen may play an active role in the development and progression of atherosclerotic plaques. We assessed the association between fibrinogen levels and atherosclerotic plaques over three different arterial sites in an asymptomatic never-treated male population with increased cardiovascular risk. We included 652 men aged 40 to 60 years old with at least one of the following cardiovascular risk factors: cholesterol > 6.2 mmol/L and/or systolic blood pressure > or = 160 mm Hg and/or diastolic blood pressure > or = 95 mm Hg, and/or because they smoked. Carotid and femoral arteries and the abdominal aorta were assessed by using ultrasonographic methods for the presence of plaque, and subjects were categorized according to the presence (or absence) and extent (one versus two or three sites) of plaque. Plasma fibrinogen was measured according to the thrombin-time method of Clauss. While the presence of atherosclerosis was significantly related to age, current smoking, systolic pressure, LDL cholesterol, and fibrinogen levels, the extent of atherosclerosis was related to age and triglyceride and fibrinogen levels. Multiple regression analysis indicated independent associations between fibrinogen and the presence and extent of atherosclerosis. Plaque prevalence was significantly more pronounced with increasing tertile of fibrinogen levels. The odds ratio of the upper to lower fibrinogen tertiles for the presence of plaque was 1.6 (95% confidence interval, 1.4 to 1.8) and 1.4 (95% confidence interval, 1.2 to 1.7) for its extent. Adjustment for other risk factors slightly reduced the association between fibrinogen and atherosclerosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Increasing erythrocyte aggregability with the progressive grades of chronic venous insufficiency: importance and mechanisms.

Erythrocyte aggregation (EA) has appeared as the most interesting parameter among rheological measurements in chronic venous insufficiency (CVI). We therefore conducted two different kinds of studies to provide further information about the distribution and mechanisms of EA in CVI. We first analysed EA values in 67 patients, classified according to 3 evolutive groups: 27 patients suffering only from subjective symptoms of venous disease (grade 1), 19 patients with varicosis and sapheno-femoral incompetence (grade 2), 21 patients with varicosis and trophic skin changes (grade 3). EA values were also measured in 22 healthy controls. Analysis of EA was performed for equal concentrations of fibrinogen and adjusted for age. EA was significantly higher in CVI. The aggregation index, related to the kinetics of aggregates formation, rose significantly even from grade 1 while compared to controls and rose further with the evolutive grades. The same trend was found with the partial dissociation threshold (i.e. red cells aggregates cohesion). As the measurements were performed at standardized hematocrit and the results expressed after fibrinogen levels adjustment, this suggests the involvement of other factors. We subsequently investigated whether red cells from CVI patients aggregate more than those of controls when suspended in the same medium. The results showed that a cellular factor is unlikely to be involved, and that an interaction between red cells and plasma proteins other than fibrinogen could also explain the increased EA in CVI.

Improvement of microcirculation abnormalities in sickle cell patients upon buflomedil treatment.

The efficacy of the vasoactive compound buflomedil on previously described microcirculation abnormalities observed in sickle cell disease (SCD) was investigated using bulbar conjunctival angioscopy (BCA) and laser doppler flux metering. Eleven sickle cell disease patients at steady state were studied in a double-blind randomized parallel-versus-placebo study (5 patients were given placebo and 6 patients received 600 mg buflomedil per day for 21 days after a washout period of 15 days). The blood flux score measured by BCA improved, indicating reduced entrapment of sickle red blood cells. There was a striking improvement of reactive alterations of vasomotion in the buflomedil group, particularly in postocclusive reactive hyperemia; the half return time was also significantly reduced. These results encourage further studies with buflomedil to investigate long-term effects of this compound in SCD, potential prevention of acute vaso-occlusive events, and degenerative complications.

Hypercholesterolaemia alters arterial and blood factors related to atherosclerosis in hypertension.

To evaluate the influence of hypercholesterolaemia on arterial and blood factors related to cardiovascular disease in hypertension, 20 normocholesterolaemic and 31 hypercholesterolaemic hypertensive patients underwent determinations of whole blood filterability (WBF), plasma fibrinogen concentration (PF) and aortic pulse wave velocity (PWV). Both of the groups had similar age, body mass index, cumulative smoking dose and blood pressure. Hypercholesterolaemics had lower WBF (P less than 0.02), higher PF (P less than 0.02) and higher PWV (P less than 0.01) than normocholesterolaemics. In the whole population WBF correlated with age (P less than 0.005), mean blood pressure (P less than 0.01), total cholesterol (P less than 0.05) and plasma fibrinogen (P less than 0.01). However, in a multivariate analysis where age and pressure were controlled as variables, only the association between WBF and PF remained significant (P less than 0.001). Thus, the higher fibrinogen affects whole blood filterability in hypercholesterolaemic hypertensive patients. In the whole population PWV correlated positively with HDL cholesterol (P less than 0.01) and age (P less than 0.001) and the association with HDL cholesterol remained significant in a multivariate analysis (P less than 0.001) where age was controlled. The effect of ageing on arterial rigidity seems to be similar in both hypertensive groups as deduced from the identical regression slopes relating pulse wave velocity to age. So in hypertension with high cholesterol, arterial rigidity was increased without changes in arterial stiffening with age.