Gender-specific correlation between plasma myeloperoxidase levels and serum high-density lipoprotein-associated paraoxonase-1 levels in patients with stable and unstable coronary artery disease
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文摘

Objective

Low high-density lipoprotein (HDL) cholesterol is well-established as a negative risk factor for coronary artery disease (CAD) and its anti-oxidant property has been attributed mainly to the HDL-bound enzyme paraoxonase-1 (PON-1). Recently, myeloperoxidase (MPO), a pro-oxidant enzyme released from activated neutrophils, has been shown to alter the atheroprotective function of HDL to a dysfunctional form. This study investigated the relationship between plasma MPO and serum PON-1 levels in patients with stable (SAP) and unstable angina pectoris (UAP).

Methods

Plasma MPO levels and serum PON-1 concentration/activity were measured in patients with SAP (n聽=聽226), UAP (n聽=聽151) and in control subjects (n聽=聽99).

Results

Plasma MPO levels in UAP patients were significantly higher than those in SAP patients or in control subjects (UAP, 21.6[16.7-44.6]; SAP, 19.3[15.7-29.1]; control, 15.9[14.7-18.7]聽ng/mL; P聽<聽0.0001). Serum PON-1 concentrations in UAP and SAP patients were significantly lower than those in control subjects (UAP, 55.6[45.9-69.7]; SAP, 55.0[46.9-64.9]; control, 62.5[51.1-78.8]聽渭g/mL; P聽=聽0.0002). Plasma MPO levels showed a weak inverse correlation with serum PON-1 concentrations in all subjects (R聽=聽鈭?.163, P聽<聽0.0005). Moreover, in women, plasma MPO levels showed a significant inverse correlation with serum PON-1 concentrations and PON-arylesterase activity in SAP (concentration: R聽=聽鈭?.537, P聽<聽0.0001; arylesterase-activity: R聽=聽鈭?.469, P聽<聽0.001) and UAP (concentration: R聽=聽鈭?.340, P聽<聽0.05; arylesterase-activity: R聽=聽鈭?.350, P聽<聽0.05) patients, but not in men.

Conclusion

This study demonstrates that plasma MPO levels have a significant inverse correlation with PON-1 levels, especially in women, in SAP and UAP patients, and suggests that an imbalance between pro-oxidants and anti-oxidants may contribute to the progression of coronary plaque instability.

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