Elevated thioredoxin after angioplasty in peripheral arterial disease

Oxidative stress and inflammation in the vessel wall may play important roles in the development of restenosis after angioplasty. Reactive oxygen species have been suggested to mediate the proliferative phenotype in smooth muscle cells. The role of the redox-active proteins, thioredoxin and glutaredoxin, after angioplasty in patients with peripheral arterial disease has never been assessed before. Circulating thioredoxin impairs the chemotactic response to local sites of inflammation and administration of human recombinant Trx has been shown to attenuate ischemic reperfusion injury.

Patients with peripheral arterial disease undergoing angioplasty were included in this observational study. Plasma levels of thioredoxin and glutaredoxin were analysed before and 1, 4 and 24 h, and 1 week after angioplasty. Plasma levels of thioredoxin were significantly elevated 4 h after angioplasty [2.3 ng/ml (0.5-14), p=0.02] and returned to baseline within 24 h [1.1 ng/ml (0.5-3.1), p=0.02]. There may also exist an association between patients with elevated levels of thioredoxin after angioplasty and decreased rate of restenosis at follow-up angiography after 6 months. There were no changes in plasma levels of glutaredoxin after angioplasty.

These findings provide a new insight to the role of thioredoxin in the complex process of vascular injury and restenosis in patients with peripheral arterial disease, suggesting thioredoxin both as a marker of oxidative stress and as a therapeutic agent.