Immunosuppressive therapy for the prevention of restenosis after coronary artery stent implantation (IMPRESS study)

Versaci, Francesco; Gaspardone, Achille; Tomai, Fabrizio; Ribichini, Flavio; Russo, Paolo; Proietti, Igino; Ghini, Anna S.; Ferrero, Valeria; Chiariello, Luigi; Gioffrè, Pier Agostino; Romeo, Francesco; Crea, Filippo

doi:10.1016/s0735-1097(02)02562-7

Cited by 196 publications

(84 citation statements)

References 28 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…25,26 It is well-known that other parameters, such as C-reactive protein (CRP), are predictive of restenosis. In fact, recently the IMPRESS Study 27 showed that high CRP levels 72 hours after successful coronary stenting is predictive of a worse prognosis at 12 months, probably suggesting an additional activation of the inflammatory process within the plaque itself and as a response to injury during coronary stenting. Moreover, CRP level at 48 hours after stent implantation in the carotid arteries was associated with a significantly higher 6-month restenosis.…”

Section: Influence Of Increased Leptin Levels On Restenosis After Cormentioning

confidence: 99%

Association of insulin resistance, hyperleptinemia, and impaired nitric oxide release with in-stent restenosis in patients undergoing coronary stenting

Piatti¹,

Mario²,

Monti³

2004

ACC Current Journal Review

View full text Add to dashboard Cite

Background-Previously undiagnosed diabetes, impaired glucose tolerance, and insulin resistance are common in patients with acute myocardial infarction and coronary heart disease (CHD) and might be involved in early restenosis after stent implantation. To evaluate whether markers of insulin resistance syndrome, including leptin, and endothelial dysfunction are related to increased rate of early restenosis, we studied nondiabetic patients with CHD after successful coronary stenting. Methods and Results-Both patients with CHD undergoing coronary stenting (120 patients) and control subjects (58 patients) were submitted to an oral glucose tolerance test (OGTT). Fasting leptin levels and fasting and postglucose load insulin sensitivity were assessed. Endothelial function was measured by nitrite and nitrate release (NOx) during OGTT. More than 50% of patients treated with stent implantation presented impaired glucose tolerance or type 2 diabetes, which was previously undiagnosed. These patients also had higher glucose, insulin, and leptin levels than control subjects. Among the stented patients, insulin and leptin levels were higher in patients with restenosis than in patients without restenosis. A significant increase in NOx levels was found during OGTT both in patients without restenosis and in control subjects. On the contrary, NOx profiles were blunted in patients with restenosis. At multiple regression analysis, only ⌬AUC-NOx areas and insulin sensitivity index showed an independent correlation with the minimal lumen diameter at follow-up. Conclusions-We demonstrated that insulin resistance and endothelial dysfunction are independent predictors of early restenosis after coronary stenting.

show abstract

Section: Influence Of Increased Leptin Levels On Restenosis After Cormentioning

confidence: 99%

Association of insulin resistance, hyperleptinemia, and impaired nitric oxide release with in-stent restenosis in patients undergoing coronary stenting

Piatti¹,

Mario²,

Monti³

2004

ACC Current Journal Review

View full text Add to dashboard Cite

show abstract

“…Although initial studies with glucocorticoids failed to show reduction in postballoon restenosis, 24,25 prolonged immunosuppressive therapy with prednisone was found to reduce in-stent restenosis in high-risk high-Creactive protein patients (IMPRESS study). 26 Thus, systemic immunomodulation effectively suppresses the reparation that leads to neointimal formation in a high-risk "inflammatory" subset of patients. Glucocorticoids suppress both innate and adaptive immunity, with a possible acute stimulatory affect on innate immunity.…”

Section: Danenberg Et Al Liposomal Alendronate Inhibits In-stent Restmentioning

confidence: 99%

Liposomal Alendronate Inhibits Systemic Innate Immunity and Reduces In-Stent Neointimal Hyperplasia in Rabbits

et al. 2003

View full text Add to dashboard Cite

Background-Innate immunity is of major importance in vascular repair. The present study evaluated whether systemic and transient depletion of monocytes and macrophages with liposome-encapsulated bisphosphonates inhibits experimental in-stent neointimal formation. Methods and Results-Rabbits fed on a hypercholesterolemic diet underwent bilateral iliac artery balloon denudation and stent deployment. Liposomal alendronate (3 or 6 mg/kg) was given concurrently with stenting. Monocyte counts were reduced by Ͼ90% 24 to 48 hours after a single injection of liposomal alendronate, returning to basal levels at 6 days. This treatment significantly reduced intimal area at 28 days, from 3.88Ϯ0.93 to 2.08Ϯ0.58 and 2.16Ϯ0.62 mm 2 . Lumen area was increased from 2.87Ϯ0.44 to 3.57Ϯ0.65 and 3.45Ϯ0.58 mm 2 , and arterial stenosis was reduced from 58Ϯ11% to 37Ϯ8% and 38Ϯ7% in controls, rabbits treated with 3 mg/kg, and rabbits treated with 6 mg/kg, respectively (meanϮSD, nϭ8 rabbits/group, PϽ0.01 for all 3 parameters). No drug-related adverse effects were observed. Reduction in neointimal formation was associated with reduced arterial macrophage infiltration and proliferation at 6 days and with an equal reduction in intimal macrophage and smooth muscle cell content at 28 days after injury. Conversely, drug regimens ineffective in reducing monocyte levels did not inhibit neointimal formation. Conclusions-Systemic

show abstract

“…The confluence of clinical and basic evidence suggests that CRP should predict outcome after vascular intervention. Indeed, several reports have demonstrated a worsened outcome, including high rates of angiographic restenosis, in patients with high pre-procedural CRP levels [6][7][8]. Others however, found no correlation between CRP and restenosis [9][10][11].…”

Section: Introductionmentioning

confidence: 99%

Neointimal formation is reduced after arterial injury in human crp transgenic mice

et al. 2008

View full text Add to dashboard Cite

Objectives/Methods-Elevated CRP levels predict increased incidence of cardiovascular events and poor outcomes following interventions. There is the suggestion that CRP is also a mediator of vascular injury. Transgenic mice carrying the human CRP gene (CRPtg) are predisposed to arterial thrombosis post-injury. We examined whether CRP similarly modulates the proliferative and hyperplastic phases of vascular repair in CRPtg when thrombosis is controlled with daily aspirin and heparin at the time of trans-femoral arterial wire-injury.Results-Complete thrombotic arterial occlusion at 28 days was comparable for wild-type and CRPtg mice (14 and 19%, respectively). Neointimal area at 28d was 2.5 fold lower in CRPtg (4190 ± 3134 μm 2 , n = 12) compared to wild-types (10,157 ± 8890 μm 2 , n = 11, p < 0.05). Likewise, neointimal/media area ratio was 1.10 ± 0.87 in wild-types and 0.45 ± 0.24 in CRPtg (p < 0.05). Seven days post-injury, cellular proliferation and apoptotic cell number in the intima were both less pronounced in CRPtg than wild-type. No differences were seen in leukocyte infiltration or endothelial coverage. CRPtg mice had significantly reduced p38 MAPK signaling pathway activation following injury.Conclusions-The pro-thrombotic phenotype of CRPtg mice was suppressed by aspirin/ heparin, revealing CRP's influence on neointimal growth after trans-femoral arterial wire-injury. Signaling pathway activation, cellular proliferation, and neointimal formation were all reduced in CRPtg following vascular injury. Increasingly we are aware of CRP multipotent effects. Once considered only a risk factor, and recently a harmful agent, CRP is a far more complex regulator of vascular biology.

show abstract

Immunosuppressive therapy for the prevention of restenosis after coronary artery stent implantation (IMPRESS study)

Abstract: In patients with persistently high CRP levels after successful coronary artery stent implantation, oral immunosuppressive therapy with prednisone results in a striking reduction of clinical events and angiographic restenosis rate.

Cited by 196 publications

References 28 publications

Association of insulin resistance, hyperleptinemia, and impaired nitric oxide release with in-stent restenosis in patients undergoing coronary stenting

Association of insulin resistance, hyperleptinemia, and impaired nitric oxide release with in-stent restenosis in patients undergoing coronary stenting

Liposomal Alendronate Inhibits Systemic Innate Immunity and Reduces In-Stent Neointimal Hyperplasia in Rabbits

Neointimal formation is reduced after arterial injury in human crp transgenic mice

Contact Info

Product

Resources

About