Aim: To investigate the possible mechanisms and association of increased complexes of β(2)-glycoprotein I with lipoprotein(a) [β(2)-GPI-Lp(a)] levels with the presence and extent of coronary artery disease (CAD).
Methods: β(2)-GPI-Lp(a) levels were measured in 116 patients with acute coronary syndromes (ACS), 72 patients with stable CAD and 100 control subjects.
Results: Compared to the control, β(2)-GPI-Lp(a) levels (expressed after logarithmically transformation: ACS, 0.22±0.45 U/mL; stable CAD, 0.05±0.55 U/mL; control, -0.31±0.61 U/mL) significantly increased in both patients with ACS (p <0.001) and stable CAD (p <0.001). Univariate logistic regression analysis of risk factors revealed that the presence of β(2)-GPI-Lp(a), ox-Lp(a) or Lp(a) was a strong risk factor for stable CAD [β(2)GPI-Lp(a), OR 3.17, 95% CI 1.65, 6.07; ox-Lp(a), OR 2.54, 95% CI 1.33, 4.85; Lp(a), OR 3.00, 95% CI 1.56, 5.75; respectively], and especially for ACS [β(2)-GPI-Lp(a), OR 5.38, 95% CI 2.97, 9.74; ox-Lp(a), OR 7.55, 95% CI 4.12, 13.84; Lp(a), OR 4.33, 95% CI 2.40, 7.80; respectively]. In multivariate analysis, adjusting for age, sex and plasma lipid levels, the presence of β(2)-GPI-Lp(a) or Lp(a) was a risk factor for both stable CAD and ACS. Ox-Lp(a) was a risk factor only for ACS, while not for stable CAD. β(2)-GPI-Lp(a) levels were found to be positively associated with Lp(a), ox-Lp(a), maximal stenosis and a number of vessel diseases in patients with ACS or stable CAD, respectively. Multiple linear regression analysis found that ox-Lp(a) and maximal stenosis accounted for 46.2% of the variation in β(2)-GPI-Lp(a) levels.
Conclusions: Elevated levels of β(2)-GPI-Lp(a) are associated with the presence and severity of CAD, and may be a strong risk factor for atherosclerosis.