Effect of rosiglitazone on restenosis after coronary stenting in patients with type 2 diabetes

Osman, Abdulfatah; Otero, Javier; Brizolara, Alberto; Waxman, Sergio; Stouffer, George A.; Fitzgerald, Peter J.; Uretsky, Barry F.

doi:10.1016/j.ahj.2003.12.006

Cited by 58 publications

(31 citation statements)

References 31 publications

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“…It was previously reported that TZDs reduce neointimal tissue proliferation after coronary intervention (17)(18)(19) and that troglitazone reduces in-stent restenosis in a relatively small number of patients with type 2 diabetes (18). However, these were studies with small patient numbers, and some reports (19,31) demonstrated that TZDs did not reduce the in-stent restenosis despite reducing neointimal proliferation. Although we did not perform an intravascular ultrasound, which can greatly aid the characterization of the neointimal accumulation that cannot be studied with QCA, the present study is the first to our knowledge to demonstrate that the administration of rosiglitazone was quite effective in reducing the in-stent restenosis rate in type 2 diabetic patients.…”

Section: Angiographic Datamentioning

confidence: 81%

Preventative Effects of Rosiglitazone on Restenosis After Coronary Stent Implantation in Patients With Type 2 Diabetes

et al. 2004

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OBJECTIVE -Despite the popularity of coronary stenting in coronary artery disease (CAD), restenosis remains a challenging clinical problem. This study evaluated the efficacy of rosiglitazone for preventing in-stent restenosis in type 2 diabetic patients.RESEARCH DESIGN AND METHODS -We conducted a prospective, randomized, case-controlled trial involving 95 diabetic patients with CAD who were randomly assigned to either the control or rosiglitazone group (48 and 47 patients, respectively). Quantitative coronary angiography (QCA) was performed at study entry and again at 6-month follow-up. The primary end point was the restenosis rate, which was determined by QCA.RESULTS -Eighty-three patients (45 patients with 55 lesions in the control group and 38 patients with 51 lesions in the rosiglitazone group) completed follow-up angiography. Rosiglitazone treatment for 6 months reduced fasting insulin concentration. The high-sensitivity C-reactive protein concentration was significantly reduced in the rosiglitazone group compared with that in the control group (from 2.92 Ϯ 1.98 to 0.62 Ϯ 0.44 mg/l, P Ͻ 0.001 vs. from 2.01 Ϯ 1.33 to 1.79 Ϯ 1.22 mg/l, P ϭ NS). However, the baseline and follow-up glucose and lipid concentrations were not different between two groups. The rate of in-stent restenosis was significantly reduced in the rosiglitazone group compared with the control group (for stent lesions: 17.6 vs. 38.2%, P ϭ 0.030). The rosiglitazone group had a significantly lower degree of diameter stenosis (23.0 Ϯ 23.4% vs. 40.9 Ϯ 31.9%, P ϭ 0.004) compared with the control group. CONCLUSIONS -We demonstrated that treatment with rosiglitazone significantly reduces in-stent restenosis in diabetic patients with CAD who underwent coronary stent implantation.

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Section: Angiographic Datamentioning

confidence: 81%

Preventative Effects of Rosiglitazone on Restenosis After Coronary Stent Implantation in Patients With Type 2 Diabetes

et al. 2004

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“…73 Additional evidence for PPARγ activators' vasoprotective potential comes from restenosis studies in CAD patients: preliminary clinical data suggest that TZDs may limit restenosis after angioplasty in patients with type 2 diabetes. 74,75 Taken together, these data suggest that PPARγ activators, in addition to their metabolic action, may have direct protective effects in the vessel wall and modulate the inflammatory process in atherogenesis.…”

Section: 62mentioning

confidence: 95%

Insulin resistance and cardiovascular disease: the role of PPARγ activators beyond their anti-diabetic action

Walcher

2004

Diabetes and Vascular Disease Research

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O ver the past few years it has been recognised that insulin resistance (IR) is an independent risk factor for major cardiovascular events. In addition, IR is associated with other factors such as hypertension, dyslipidaemia and endothelial dysfunction, and this cluster of metabolic disorders contributes to the cardiovascular risk of patients with IR. Given the increasing number of patients with IR, the modulation of their cardiovascular risk is a major task in diabetology and vascular medicine. This review will focus on the role of IR as a cardiovascular risk factor and on the potential of activators of the nuclear transcription factor peroxisome proliferator-activated receptor gamma (PPARγ) to modulate these risk factors associated with IR. 2004;2:76-81 Diabetes Vasc Dis Res

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“…10,11 Recently, several studies demonstrated that rosiglitazone prevented neointimal hyperplasia after vessel injury in diabetic animals or after coronary stenting in diabetic patients. [12][13][14][15] However, the mechanism of rosiglitazone to reduce neointimal hyperplasia has not been clarified. …”

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confidence: 99%

New Mechanism of Rosiglitazone to Reduce Neointimal Hyperplasia

Lee

Kwon

Yang

et al. 2009

ATVB

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Objective-Mechanism of neointimal hyperplasia after vascular injury includes activation of signaling pathways and matrix metalloproteinases (MMPs) that are involved in cell proliferation and migration. Rosiglitazone, a synthetic peroxisome proliferator-activated receptor-␥ (PPAR-␥) agonist, was reported to inhibit neointimal hyperplasia in diabetic animals and humans. But the underlying mechanism has not been clarified. In this study, we examined how rosiglitazone inhibited neointimal hyperplasia. Methods and Results-The proliferation and survival of cultured rat VSMCs were reduced by rosiglitazone, which was mediated by inhibition of ERK and activation GSK-3␤, without change of Akt. The antiproliferative effect of rosiglitazone was reversed by GSK-3␤ inactivation. The migration of VSMCs was also suppressed by rosiglitazone that inhibited the expression and activity MMP-9 through GSK-3␤ activation. Thus migration of MMP-9(Ϫ/Ϫ) VSMCs from MMP-9 knockout mice was not affected by rosiglitazone. The underlying mechanism of MMP-9 suppression by rosiglitazone was that it inhibited NF-B DNA binding activity, which was also dependent on GSK-3␤. In rat carotid artery, balloon injury significantly inactivated GSK-3␤ with induction of MMP-9, which was effectively prevented by rosiglitazone. Thus, rosiglitazone significantly decreased the ratio of intima to media by reducing proliferation and inducing apoptosis of VSMCs at neointima, which was reversed by inactivation of GSK-3␤ with adenoviral transfer of catalytically-inactive GSK-KM gene. Key Words: restenosis Ⅲ rosiglitazone Ⅲ GSK-3␤ Ⅲ MMP-9 Ⅲ VSMCs A fter vascular injury such as balloon angioplasty, there are diverse mechanisms of VSMC proliferation and neointimal hyperplasia. There have been many studies showing that inhibition of these mechanisms can reduce neointimal hyperplasia. Among these mechanisms, the MAPK signaling pathway was reported to be activated by vascular injury and the inhibition of activated ERK pathway by drugs or gene therapy can reduce neointimal hyperplasia. 1-3 Akt/GSK pathway was also involved, as we and others showed that modulation of Akt or GSK pathway results in reduction of proliferation of VSMCs and neointimal formation. 4 -6 Rosiglitazone is a synthetic peroxisome proliferator-activated receptor-␥ (PPAR-␥) agonist, initially developed as an antidiabetic drug. Previous studies have revealed that rosiglitazone regulates gene expression of key proteins involved in lipid metabolism, vascular inflammation, and proliferation, [7][8][9] resulting in not only improved insulin sensitivity in patients with type 2 diabetes but also protection against development of atherosclerosis. 10,11 Recently, several studies demonstrated that rosiglitazone prevented neointimal hyperplasia after vessel injury in diabetic animals or after coronary stenting in diabetic patients. [12][13][14][15] However, the mechanism of rosiglitazone to reduce neointimal hyperplasia has not been clarified. Conclusions-RosiglitazoneAs a possible mechanism, we are interested in ...

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Effect of rosiglitazone on restenosis after coronary stenting in patients with type 2 diabetes

Cited by 58 publications

References 31 publications

Preventative Effects of Rosiglitazone on Restenosis After Coronary Stent Implantation in Patients With Type 2 Diabetes

Preventative Effects of Rosiglitazone on Restenosis After Coronary Stent Implantation in Patients With Type 2 Diabetes

Insulin resistance and cardiovascular disease: the role of PPARγ activators beyond their anti-diabetic action

New Mechanism of Rosiglitazone to Reduce Neointimal Hyperplasia

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