The rs11573156C variant in PLA2G2A (encoding sPLA<sub>2</sub>-IIA) had the strongest effect on sPLA<sub>2</sub>-II: median (25th-75th percentile, ng/mL) for CC and GG genotypes: 2.79 (1.97-4.01) and 7.38 (5.38-10.19), respectively; and had nonsignificant trend for higher CVD risk (hazard ratio, 1.11; 95% CI, 0.89-1.38; P=0.34).
Prospective cohort of 1735 children (45% females) who had serum sPLA2 enzyme activity levels and other cardiovascular disease risk factors measured in 1980 that were followed-up in 2001.
Our data indicate that increased expression of sPLA(2) might represent a novel causative risk factor contributing to the increased cardiovascular disease morbidity and mortality in ESRD.
We speculate that an elevated PLA(2)enzyme activity in pre-eclamptic decidual tissue could be of importance in the pathogenesis of 'acute atherosis', comparable to the atherogenesis in cardiovascular diseases.
The association of PLA2 status with overall cardiovascular disease in the general population is significant but weak; higher risk has been identified in less heterogeneous subgroups as in the younger cohorts and in the restenosis subset with stents.
In blood plasma, PLA(2) can modify the circulating lipoproteins and so induce formation of small dense LDL particles, which are associated with increased risk for cardiovascular disease.