The complex link between oxidised low-density lipoprotein and unstable angina.J Cardiovasc Med (Hagerstown) 2007; 8(5):387-91JC
The role of oxidised low-density lipoprotein (ox-LDL) in plaque destabilisation is controversial; therefore we aimed at comparing plaque and plasma ox-LDL content in stable and unstable ischaemic syndromes. We also assessed the correlation between plaque or plasma ox-LDL and angiographic complex stenosis morphology.
Ten consecutive patients with chronic stable angina (SA) and 10 consecutive patients with unstable angina (UA) were studied. Plaque sections obtained by directional coronary atherectomy were immunostained with the monoclonal antibody mAb-4E6, which recognises several oxidation epitopes on LDL (mAb-4E6 ox-LDL), and with the monoclonal antibody mAb-1H11 (mAb-1H11 ox-LDL), which recognises malondialdehyde-modified LDL. An mAb-4E6-based competition ELISA was used for quantification of ox-LDL in plasma. C-reactive protein serum levels were measured by a high-sensitivity nephelometric assay. An angiographic analysis was performed to assess severity and extent of coronary atherosclerotic disease and stenosis morphology.
Percent plaque area occupied by mAb-4E6 ox-LDL or mAb-1H11 ox-LDL was similar in patients with SA or UA (22.4 +/- 13.1 vs. 21.1 +/- 19.7%, P = 0.8 and 19.3 +/- 10.4 vs. 16.8 +/- 16.9%, P = 0.6, respectively), whereas ox-LDL plasma levels were significantly higher in patients with UA than in patients with SA (2.4 +/- 1.1 vs. 0.9 +/- 0.6 mg/dl; P = 0.03). Furthermore, a significant correlation was found between plasma levels of ox-LDL and the number of angiographically complex lesions (P = 0.03) or C-reactive protein serum levels (P = 0.04).
Neither plaque mAb-4E6 ox-LDL nor plaque mAb-1H11 ox-LDL seem to be a major trigger of coronary plaque instability. However, circulating ox-LDL might be involved in plaque vulnerability and coronary artery disease activity.