Restenosis after PCI

Is homocysteine involved in the pathogenesis of restenosis An association between homocysteine and restenosis is not unlikely, given the fact that homocysteine appears to induce inflammation, impair endothelial function, and stimulate smooth muscle proliferation all these mechanisms are potentially implicated in the development of restenosis. However, the data regarding tHcy levels and the risk of restenosis after coronary angioplasty are conflicting. Some investigators found an increased risk of restenosis after PCI in patients with high plasma levels of homocysteine, especially in patients not treated with stents (70-72), whereas others did not find any increased risk either in patients with (73-75) or without stents (76). 

Restenosis after PCI is not well understood, although it is widely accepted that it is a maladaptive response to angioplasty-induced trauma, resulting in inflammation, while thrombosis, cellular proliferation (peaks at about 7 days) and extracellular matrix production (formation from 1 week onwards) [28]. 

We have recently prepared an open-label phase 1/lla clinical trial (the INDOR study a phase I/Ha open-label multicenter study to assess the inhibitory effects of NF-kB decoy ODN on restenosis after stenting in coronary artery) to evaluate the safety and efficacy of NF-kB decoy ODN. Seventeen patients were treated with NF-kB decoy ODN after percutaneous coronary intervention (PCI) using bare metal stents. As a result, the stenosis improved to 1.4 5.9% after the intervention. Serum monocyte chemotactic protein-1 (MCP-1) levels were significantly suppressed in NF-kB decoy ODN-treated patients on day 3 after the PCI. Significant restenosis was found in (Mily one of the 17 patients after 6 months, and the average restenosis rate was 39.6 22.3%. No in-stent thrombosis was found and no... 

There is no unequivocal answer to whether optimal glucometabolic control influences clinical ontcome after coronary revascularization of diabetic patients with stable and unstable coronary syndromes. Observational studies have reported poor glycaemic regulation to be associated with an increased need for additional target lesion revascularization and restenosis [53,54]. Coronary revascularization results in normalized epicardial flow, which however, not necessarily is followed by improved myocardial perfusion and cardiac fnnction. The angiographic no-flow phenomenon denotes a post-PCI condition of impaired microcirculation despite non-stenotic coronary arteries. There is some evidence that hyperglycaemia predisposes to the no-flow condition in MI patients, more often in diabetic than non-diabetic patients [55,56]. 

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