Disease relevance of Coronary Restenosis

• Potential role of human cytomegalovirus and p53 interaction in coronary restenosis [1].
• Lovastatin, an HMG-CoA reductase inhibitor, has been shown to reduce myointimal hyperplasia in animal models of restenosis and in one clinical coronary restenosis trial [2].
• CONCLUSION: Hyperhomocysteinemia is probably a weak risk factor for coronary restenosis after angioplasty, although it is still difficult to ascertain whether homocysteine plays a causative role in restenosis [3].

High impact information on Coronary Restenosis

• Decreased rate of coronary restenosis after lowering of plasma homocysteine levels [4].
• Using both cultured human CASMCs and coronary atherectomy tissues, we studied the roles of osteopontin (OPN) and one of its receptors, alphavbeta3 integrin, in the pathogenesis of coronary restenosis [5].
• Because mithramycin has been shown to be well tolerated by humans and to effectively inhibit transcription of c-myc in proliferating human cells, this agent may be useful in the prevention of coronary restenosis [6].
• The results also suggest a potential role of antisense strategies designed to inhibit c-myc expression for the prevention of coronary restenosis [7].
• Plasminogen activator inhibitor-1 plasma levels and coronary restenosis [8].

Chemical compound and disease context of Coronary Restenosis

• In contrast, late coronary restenosis developed in only 7 (11%) of 65 vessels and in 5 (14%) of 37 patients with a nonischemic thallium-201 scintigram on day 1 (p less than 0.005) [9].
• In a recent clinical study, tranilast, an anti-allergic agent, was shown to reduce the rate of coronary restenosis after percutaneous transluminal coronary angioplasty, although the mechanism of this effect is unclear [10].
• The powerful antioxidant probucol has been shown to prevent coronary restenosis after balloon angioplasty in the MultiVitamins and Probucol (MVP) trial and other clinical studies [11].
• Catheter-based intracoronary radiation therapy using iridium-192 (Ir-192) has been shown to be effective in reducing recurrent coronary restenosis after initial percutaneous treatment of in-stent restenosis [12].
• Costs of coronary restenosis (Lovastatin Restenosis Trial) [13].

Biological context of Coronary Restenosis

• The IE2 gene of human cytomegalovirus has been implicated in the development of coronary restenosis, and the gene product appears to inhibit p53-dependent transactivation [14].
• These data indicate that increased smooth muscle cell proliferation contributes to coronary restenosis in humans and support the concept that the extracellular matrix synthesis of adult smooth muscle cells is important to lesion formation [15].
• RESULTS: In 14 patients without coronary restenosis, the time constant of VO(2) kinetics was significantly shortened from (mean +/- SD) 57.4 +/- 12.6 before PTCA to 48.2 +/- 9.5 s after PTCA (p = 0. 0035), indicating improved kinetics of the VO(2) response [16].

Anatomical context of Coronary Restenosis

• Monocyte integrin expression and monocyte-platelet complex formation in humans with coronary restenosis [17].
• Increased leukocyte CD15 expression during the intervention may contribute to coronary restenosis [18].

Gene context of Coronary Restenosis

• Plasma urokinase antigen and plasminogen activator inhibitor-1 antigen levels predict angiographic coronary restenosis [19].
• Furthermore, the incidence of coronary restenosis during six-month follow-up was not related to TnT status (3% vs. 4.5%; p = 0.49); however, it was significantly related to CRP status (7% vs. 2.3%; p = 0.03) [20].
• Inhibition of coronary restenosis by antithrombin III in atherosclerotic swine [21].
• CONCLUSIONS: These findings indicate that combined treatment with statin and ARB after stenting is a useful strategy for the prevention of coronary restenosis [22].

Analytical, diagnostic and therapeutic context of Coronary Restenosis

• A decrease in plasminogen activator inhibitor-1 activity after successful percutaneous transluminal coronary angioplasty is associated with a significantly reduced risk for coronary restenosis [23].
• Advanced c-myc antisense (AVI-4126)-eluting phosphorylcholine-coated stent implantation is associated with complete vascular healing and reduced neointimal formation in the porcine coronary restenosis model [24].
• METHODS: In patients with previous coronary restenosis, balloon dilatation and/or coronary stenting was undertaken and then patients were randomly assigned to receive either Iridium-192 or placebo [25].

References