Plasma myeloperoxidase level and peripheral arterial disease

Eur J Clin Invest 2012; 42 (5): 463–469 Abstract Background Myeloperoxidase (MPO) is involved in a multitude of inflammatory processes involving oxidative modification of soluble components and cellular surfaces. Thus, MPO plays a key role in promoting atherosclerosis via oxidative stress by modification of both high‐ and low‐density lipoprotein and production of other bioactive molecules. A polymorphism (MPO 463G>A, rs2333227) results in different expression rates of MPO. We aimed to assess whether MPO could be of clinical use as a risk marker for vascular disease in a high‐risk group. Material and methods Plasma MPO levels of 406 patients suffering from peripheral arterial disease (PAD) were measured on an Abbott Architect i2000sr and grouped into patients with high (>115 ng/mL) and low (< 115 ng/mL) MPO levels. Genotyping of rs2333227 was performed on an ABI TaqMan 7900HT RT‐PCR thermocycler. Results The relative risk of major adverse cardiovascular events (MACE) for patients with high plasma MPO is 1·2 (95%CI: 1·038–1·377, P < 0·05), initial event‐free periods in male patients are significantly longer in patients with MPO <115 ng/mL (mean = 875 days compared with mean = 734 days, P < 0·05) In smokers, an increased hazard ratio was computed for patients with high MPO levels (HR = 3·127, 95%CI: 1·258–7·772, P < 0·05). Effects of MPO [‐463A] allele on initial MACE‐free intervals did not persist after multivariate analysis. Conclusions Hence, we suggest consideration of plasma MPO for risk stratification of MACE in patients with PAD. In contrast, MPO‐463G>A is not an independent risk factor for MACE in patients suffering from PAD.