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      Thiazolidinediones Do Not Reduce Target Vessel Revascularization in Diabetic Patients Undergoing Percutaneous Coronary Intervention

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          Background: Animal studies have suggested that thiazolidinediones (TZDs) have antirestenotic properties. However, human data are lacking. The goal of this single-center study was to assess the target vessel revascularization (TVR) rate following percutaneous coronary intervention (PCI) among diabetic patients according to TZD use. Methods: A total of 325 consecutive diabetic patients who underwent PCI between January 2000 and December 2001 were included in the analysis. Among them, 82 patients were on TZD and 243 patients were on other hypoglycemic regimens. All patients were treated with stents and platelet glycoprotein IIb/IIIa inhibitors at the time of intervention. TVR and death/myocardial infarction/TVR were assessed at 1 year. Results: TZD patients were more likely to be younger, male and have hyperlipidemia. TVR occurred in 36.6% of TZD patients compared with 23.9% of non-TZD patients (p = 0.04). One-year death, myocardial infarction and TVR occurred in 41.1% of TZD patients compared with 30.8% of non-TZD patients (p = 0.04). Conclusion: In this retrospective analysis, TZD therapy did not decrease the need for repeat revascularization following PCI. Prospective randomized studies are warranted.

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          Troglitazone inhibits vascular smooth muscle cell growth and intimal hyperplasia.

          Vascular smooth muscle cell (VSMC) proliferation and migration are responses to arterial injury that are highly important to the processes of restenosis and atherosclerosis. In the arterial balloon injury model in the rat, platelet-derived growth factor (PDGF) and basic fibroblast growth factor (bFGF) are induced in the vessel wall and regulate these VSMC activities. Novel insulin sensitizing agents, thiazolidinediones, have been demonstrated to inhibit insulin and epidermal growth factor-induced growth of VSMCs. We hypothesized that these agents might also inhibit the effect of PDGF and bFGF on cultured VSMCs and intimal hyperplasia in vivo. Troglitazone (1 microM), a member of the thiazolidinedione class, produced a near complete inhibition of both bFGF-induced DNA synthesis as measured by bromodeoxyuridine incorporation (6.5+/-3.9 vs. 17.6+/-4.3% cells labeled, P < 0.05) and c-fos induction. This effect was associated with an inhibition (by 73+/-4%, P < 0.01) by troglitazone of the transactivation of the serum response element, which regulates c-fos expression. Inhibition of c-fos induction by troglitazone appeared to occur via a blockade of the MAP kinase pathway at a point downstream of MAP kinase activation by MAP kinase kinase. At this dose, troglitazone also inhibited PDGF-BB-directed migration of VSMC (by 70+/-6%, P < 0.01). These in vitro effects were operative in vivo. Quantitative image analysis revealed that troglitazone-treated rats had 62% (P < 0.001) less neointima/media area ratio 14 d after balloon injury of the aorta compared with injured rats that received no troglitazone. These results suggest troglitazone is a potent inhibitor of VSMC proliferation and migration and, thus, may be a useful agent to prevent restenosis and possibly atherosclerosis.
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            Effect of rosiglitazone treatment on soluble CD40L in patients with type 2 diabetes and coronary artery disease.

            Interaction of CD40L with its receptor CD40 is critically involved in inflammatory cell activation in atherogenesis. In addition, serum levels of soluble CD40L are elevated in acute coronary syndromes and have been associated with increased cardiovascular risk in healthy subjects, thus making sCD40L an intriguing target to modulate the inflammatory response in the vasculature. PPARgamma-activating thiazolidinediones, novel insulin-sensitizing antidiabetic agents, have recently been shown to exhibit antiinflammatory effects in the vessel wall. To examine whether thiazolidinedione treatment might modulate serum levels of sCD40L in high-risk patients, we performed a randomized, placebo-controlled, single-blinded trial to assess the effect of rosiglitazone on sCD40L levels in patients with type 2 diabetes and coronary artery disease (CAD). Thirty-nine patients with diabetes and angiographically proven CAD were randomized to receive rosiglitazone (4 mg BID) or placebo for 12 weeks. Baseline parameters did not significantly differ between groups. Rosiglitazone treatment, but not placebo, significantly reduced sCD40L serum levels within the first 2 weeks by 8.1% (17.1 to -32.7) (median percentage [interquartile range]; P<0.05 compared with baseline), further decreasing it by 18.4% (-5.0 to -33.1) after 6 weeks (P<0.05 compared with baseline), and by 27.5% (8.2 to -70.5) after 12 weeks (P<0.05 compared with baseline and with 2 weeks of treatment). Treatment with the PPARgamma-activating thiazolidinedione rosiglitazone reduces sCD40L serum levels in patients with type 2 diabetes and CAD. These data support an antiinflammatory and potentially antiatherogenic effect of thiazolidinediones.
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              Inhibitory activity of clinical thiazolidinedione peroxisome proliferator activating receptor-gamma ligands toward internal mammary artery, radial artery, and saphenous vein smooth muscle cell proliferation.

              The proliferation of vascular smooth muscle cells (VSMCs) is a known response to arterial injury that is an important part of the process of restenosis and atherosclerosis. People with diabetes have an increased risk of cardiovascular disease resulting from accelerated coronary atherosclerosis. The newest drugs for Type 2 diabetes are thiazolidinediones, which are insulin-sensitizing peroxisome proliferator activating receptor-gamma (PPARgamma) ligands. We investigated the antiproliferative effects of troglitazone, rosiglitazone, and pioglitazone on VSMCs derived from the three vascular beds used for coronary artery by-pass grafting: the internal mammary and radial artery and saphenous veins. The three vessels yielded proliferating cells of slightly differing morphology. Inhibition of cell proliferation was assessed by cell counting and cell cycle studies by Western blotting for phosphorylated retinoblastoma protein. All three thiazolidinediones showed inhibitory potency toward cell proliferation with a potency troglitazone>rosiglitazone approximately pioglitazone, and this potency profile was maintained toward the growth factor and insulin-stimulated phosphorylation of the retinoblastoma protein, which controls cell cycle progression. The inhibitory potency of clinical thiazolidinediones toward different vascular sources is dependent on the individual thiazolidinedione and very little on the vascular source.

                Author and article information

                S. Karger AG
                August 2005
                24 August 2005
                : 104
                : 2
                : 97-100
                Department of Cardiology, Loyola University Medical Center, Maywood, Ill., USA
                86748 Cardiology 2005;104:97–100
                © 2005 S. Karger AG, Basel

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                Page count
                Figures: 1, Tables: 3, References: 12, Pages: 4
                General Cardiology


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