Lipoprotein(a) complexes with beta2-glycoprotein I in patients with coronary artery disease.

AIM: To investigate the possible mechanisms and association of increased complexes of ß(2)-glycoprotein I with lipoprotein(a) [ß(2)-GPI-Lp(a)] levels with the presence and extent of coronary artery disease (CAD). METHODS: ß(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, ß(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 ß(2)-GPI-Lp(a), ox-Lp(a) or Lp(a) was a strong risk factor for stable CAD [ß(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 [ß(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 ß(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. ß(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 ß(2)-GPI-Lp(a) levels. CONCLUSIONS: Elevated levels of ß(2)-GPI-Lp(a) are associated with the presence and severity of CAD, and may be a strong risk factor for atherosclerosis.

Percutaneous coronary intervention results in acute increases in native and oxidized lipoprotein(a) in patients with acute coronary syndrome and stable coronary artery disease.

OBJECTIVE: To investigate possible changes of native and oxidized lipoprotein(a) [ox-Lp(a)] levels after percutaneous coronary intervention (PCI). DESIGN AND METHODS: Lp(a), ox-Lp(a), and Lp(a) immune complexes (IC) and autoantibody levels were studied in 111 patients with acute coronary syndrome (ACS) and 68 patients with stable coronary artery disease (CAD) before and after PCI. RESULTS: Compared with pre-PCI, Lp(a), ox-Lp(a), and Lp(a)-IC levels acutely increased, while the autoantibody decreased in both the ACS and stable CAD patients. They all returned toward baseline by 1 to 2 days. The absolute change of ox-Lp(a) was found positively related with both the diameter of stenosis (R=0.273, P=0.004) and the number of vessel disease (R=0.312, P=0.001) in the ACS patients, while not in the stable CAD patients. CONCLUSION: PCI results in acute plasma increases of ox-Lp(a) and Lp(a). Ox-Lp(a) may be present in ruptured or permeable plaques and be released into the circulation by PCI.

Measurement of oxidized lipoprotein (a) in patients with acute coronary syndromes and stable coronary artery disease by 2 ELISAs: using different capture antibody against oxidized lipoprotein (a) or oxidized LDL.

OBJECTIVE: To evaluate clinical value of oxidized lipoprotein(a) [ox-Lp(a)] levels. DESIGN AND METHODS: Ox-Lp(a) were measured by 2 ELISAs using antibodies against ox-Lp(a) [ox-Lp(a)1] or oxidized low-density lipoprotein [ox-Lp(a)2], and studied in 161 acute coronary syndromes (ACS) patients, 114 stable coronary artery disease (CAD) and 100 control subjects. RESULTS: Ox-Lp(a)1 was found related with ox-Lp(a)2 (r=0.864, P=0.000). Controlling for plasma lipids, Lp(a) and clinical characteristics, odds ratios of ox-Lp(a)1 on ACS and stable CAD were 5.06 (95% confidence interval 1.82-14.04) and 2.20 (0.78-6.22); those of ox-Lp(a)2 were 3.37 (1.07-10.63) and 1.35 (0.41-4.48), respectively. Receiver-operating characteristic curve analysis confirmed that performances of ox-Lp(a)1 were significantly superior to those for ox-Lp(a)2 in ACS (area: 0.803 vs. 0.723, P<0.001) and stable CAD (area: 0.670 vs. 0.607, P<0.01). CONCLUSION: Ox-Lp(a) levels using antibodies against ox-Lp(a) may represent a better risk marker than those using antibodies against oxidized low-density lipoprotein for ACS and stable CAD.

Elevated concentrations of oxidized lipoprotein(a) are associated with the presence and severity of acute coronary syndromes.

OBJECTIVE: To investigate possible mechanisms and association of increased oxidized Lp(a) [ox-Lp(a)] levels with presence and extent of acute coronary syndromes (ACS). METHODS: Ox-Lp(a) levels were studied in 96 patients with ACS, 89 patients with stable coronary artery disease (CAD), and 100 control subjects. RESULTS: Compared to control, ox-Lp(a) levels increased in stable CAD patients (P<0.001), and especially in ACS (P<0.001) (ACS, 16.29+/-13.80 microg/ml; stable CAD, 10.04+/-10.32 microg/ml; control, 7.10+/-9.16 microg/ml). The ratio of ox-Lp(a) to Lp(a) was higher in the ACS than those in the stable CAD (P<0.05) and control (P<0.001). Ox-Lp(a) levels were found associated with a graded increase in extent of angiographically documented CAD in the ACS (R=0.275, P=0.007), while not in the stable CAD (R=0.090, P=0.402). Multiple linear regression analysis found ox-Lp(a) (beta=0.271, P=0.019), age (beta=0.244, P=0.038) and TG (beta=0.213, P=0.070) accounted for 11.1% of the variation in the extent of angiographically documented CAD in ACS patients; Lp(a) (beta=0.415, P=0.000) and extent of CAD (beta=0.193, P=0.071) accounted for 21.5% of that in ox-Lp(a) levels. CONCLUSION: Elevated ox-Lp(a) levels are associated with presence and severity of ACS, and may be useful for identification of patients with ACS.