Hyperalphalipoproteinemia and prostaglandin I2 stability.

PGI2 is a powerful regulator of thromboresistance modulating the local platelet/vessel wall interaction. Beside the amount synthesised the availability of the biologically active compound depends on its half-life at the site of action. Plasmatic half-life of PGI2 is extremely shortened during severe infections, but also in acute myocardial infarction with extremely lowered levels of HDL-c and apoAI, the latter being described as a potential PGI2-stabilising factor. These conditions are characterised by an enhanced thrombophilic risk. This study investigated for the first time whether high levels of HDL-c (mean: 95 +/- 13 mg/dl) and apoAI (mean: 179 +/- 13 mg/dl) which have been shown epidemiologically to protect against coronary heart disease in turn might be associated with an increase in PGI2 half-life. Results were obtained from 31 healthy subjects with hyperalpha-LP as compared with 10 controls. The biological half-life of PGI2 (hyperalpha-LP: mean: 915 +/- 118 sec vs. controls: 714 +/- 70 sec; p = 0.001) was positively related to HDL-c (r = 0.8795, p < 0.001) and apoAI levels (r = 0.8025, p < 0.001). The partial correlation coefficient correcting for the association between HDL-c and apoAI levels was also significant (PGI2 to HDL-c: r = 0.6000, p < 0.001). These results suggest that the antiatherosclerotic properties of HDL might be at least partly due to an increase in PGI2 half-life.