Lipoprotein-associated phospholipase A2, hormone use, and the risk of ischemic stroke in postmenopausal women.
Few studies have investigated the role of elevated lipoprotein-associated
phospholipase A2 (Lp-PLA(2)) with stroke risk, and those that have are based on
small numbers of strokes. No study has evaluated the effect of hormone therapy
use on the association of Lp-PLA(2) and stroke. We assessed the relationship
between Lp-PLA(2) and the risk of incident ischemic stroke in 929 stroke patients
and 935 control subjects in the Hormones and Biomarkers Predicting Stroke Study,
a nested case-control study from the Women's Health Initiative Observational
Study. Mean (SD) levels of Lp-PLA(2) were significantly higher among case
subjects (309.0 [97.1]) than control subjects (296.3 [87.3]; P<0.01). Odds ratio
for ischemic stroke for the highest quartile of Lp-PLA(2), compared with lowest,
controlling for multiple covariates, was 1.08 (95% CI: 0.75 to 1.55). However,
among 1137 nonusers of hormone therapy at baseline, the corresponding odds ratio
was 1.55 (95% CI: 1.05 to 2.28),whereas there was no significant association
among 737 hormone users (odds ratio: 0.70; 95% CI: 0.42 to 1.17; P for
interaction=0.055). Moreover, among nonhormone users, women with high C-reactive
protein and high Lp-PLA2 had more than twice the risk of stroke (odds ratio:
2.26; 95% CI: 1.55 to 3.35) compared with women low levels in both biomarkers.
Furthermore, different stroke cases were identified as high risk by Lp-PLA(2)
rather than by C-reactive protein. Lp-PLA(2) was associated with incident
ischemic stroke independently of C-reactive protein and traditional
cardiovascular risk factors among nonusers of hormone therapy with highest risk
in those who had both high C-reactive protein and high Lp-PLA(2).