This study was conducted to test the hypothesis that plasma markers of oxidized low-density
lipoprotein (OxLDL) reflect acute coronary syndromes (ACS).
Oxidized LDL contributes to the pathogenesis of atherosclerosis, but its role in ACS
is not established.
Serial plasma samples were prospectively obtained from patients with an acute myocardial
infarction (MI) (n = 8), unstable angina (UA) (n = 15), stable coronary artery disease
(CAD) (n = 17), angiographically normal coronary arteries (n = 8), and from healthy
subjects (n = 18), at entry into the study, hospital discharge (MI group only), and
at 30, 120, and 210 days. Chemiluminescent enzyme-linked immunosorbent assay was used
to quantitate plasma levels of: 1) immunoglobulin (Ig)M and IgG OxLDL autoantibody
titers (presented as a mean OxLDL autoantibody titer by averaging the results of four
distinct epitopes); 2) LDL-autoantibody immune complexes (LDL-IC); and 3) minimally
OxLDL measured by antibody E06 (OxLDL-E06), as determined by the content of oxidized
phospholipids (OxPL) per apolipoprotein B-100.
Baseline OxLDL IgG autoantibody levels were higher in the MI group (p < 0.0001). At
30-day follow-up, the mean IgM OxLDL titers increased by 48% (p < 0.001) and 20% (p
< 0.001), and IgM LDL-IC increased by 60% (p < 0.01) and 26% (p < 0.01) in the MI
and UA groups, respectively. The OxLDL-E06 levels increased by 54% (p < 0.01) in the
MI group at hospital discharge and by 36% at 30 days. No significant changes in any
OxLDL markers were noted in the other groups. The OxLDL-E06 levels strongly paralleled
the acute rise in lipoprotein(a), or Lp(a), in the MI group, suggesting that toxic
OxPL are preferentially bound to Lp(a). Oxidized LDL-E06 also correlated extremely
well with Lp(a) in the entire cohort of patients (r = 0.91, p < 0.0001).
Circulating OxLDL-specific markers strongly reflect the presence of ACS, implying
immune awareness to newly exposed oxidation-specific epitopes and possible release
of OxLDL in the circulation. The OxLDL-E06 measurements provide novel insights into
plaque rupture and the potential atherogenicity of Lp(a).