Is lipoprotein(a) regulating prostaglandin I2-synthesis stimulating plasma factor?

Lipoprotein(a) - Lp(a) is accepted as an independent risk factor for the development of atherosclerosis. The mechanism, however, and how it exerts its pathogenetic role is still unclear. More than a decade ago a deficiency of prostacyclin synthesis stimulating plasma factor (PF) was claimed to be associated with an increased Lp(a).

The aim of this retrospective analysis was to assess whether elevated Lp(a) is associated with a PF-deficiency and whether certain risk factors may exert influence.

In a total of 185 patients (131 men and 54 women), aged 30-85 years, suffering from clinically manifested atherosclerosis risk factor profile, lipids, lipoproteins and PF under drug intake were evaluated.

Patients with absent PF-activity did not differ concerning age, height, weight, body mass index, waist circumference and different lipid and lipoprotein parameters. Mean Lp(a) in patients with absent PF-activity was 18 vs. 94 mg/dl (p < 0.001). Laboratory parameters such as C-reactive protein, fibrinogen, protein 5, protein C, activated protein C resistance and others were not different. In patients with normal (< 30 mg/dl) Lp(a) only 4 males (3.4%) and 3 females (4.8%) had PF-deficiency, while the Lp(a) cut-off of 30 mg/dl the prevalence was 61.1% males and 64.4.% females.

These findings indicate that the association of PF-deficiency with increased Lp(a), at least in part, could contribute to the pathogenesis of atherosclerosis in these patients.