Native and ox-Lp(a) increases after PCI in ACS and stable CAD patients
MedWire News: Percutaneous coronary intervention (PCI) temporarily increases native and oxidized (ox-)lipoprotein (Lp)(a) levels in patients with acute coronary syndromes (ACS) and those with stable coronary artery disease (CAD), a study suggests.
Changes in ox-Lp(a) levels correlated with extent of angiographically documented disease in ACS patients, report Jun-Jun Wang and colleagues from Jinling Hospital in China.
They say their observations support the hypothesis that ox-Lp(a) is present in ruptured or permeable plaques and is released into the circulation by PCI.
The team studied plasma levels of Lp(a) and several ox-Lp(a) markers immediately before and up to 6 months after PCI and stenting in 111 patients with ACS and 68 with stable CAD.
A further 29 control participants underwent diagnostic coronary angiography without PCI.
Immediately after PCI, levels of Lp(a), ox-Lp(a), and Lp(a) immune complexes increased and auto-antibody concentrations decreased in both patients with ACS and those with stable CAD.
Mean levels of Lp(a) in the ACS group rose from 195.59 mg/l before intervention to 274.72 afterwards, those of ox-Lp(a) rose from 8.91 to 15.44 µg/ml, and those of Lp(a) immune complexes rose from 2.72 to 3.60 AU. Levels of ox-Lp(a) autoantibody levels decreased from 0.81 to 0.72 AU.
In the stable CAD group, Lp(a) increased from 184.01 to 244.64 mg/l, ox-Lp(a) from 7.36 to 12.82 µg/ml, and Lp(a) immune complexes from 2.09 to 2.90 AU, while ox-Lp(a) autoantibody levels decreased from 0.78 to 0.68 AU.
Levels of all the lipoproteins returned to baseline in coronary patients within 1 or 2 days. There were no significant changes in the control group after angiography.
The absolute change in ox-Lp(a) levels was significantly and positively related to both the diameter of stenosis and the number of diseased vessels in ACS patients, but not in those with stable CAD.
Reporting in the journal Clinical Biochemistry, the researchers say: "These observations provide impetus to further investigate the clinical value of ox-Lp(a) in atherosclerotic cardiovascular disease and to explore the exact pathogenic role of ox-Lp(a)."
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By Anita Wilkinson