Coronary stenting in diabetic patients: Results from the ROSETTA registry.

OBJECTIVE Diabetes mellitus is associated with high rates of restenosis and adverse outcomes after percutaneous transluminal coronary angioplasty (PTCA). It is unclear whether coronary stenting reduces adverse events in diabetic patients after PTCA. Our purpose was to determine whether coronary stenting improves clinical event rates in diabetic patients after PTCA. METHODS The Routine Versus Selective Exercise Treadmill Testing After Angioplasty (ROSETTA) registry was a prospective multicenter observational study examining functional testing and adverse outcomes after successful PTCA. RESULTS Among the 791 patients enrolled, 180 were diabetic. A total of 90 diabetics received stents while the remaining 90 patients did not. Baseline clinical characteristics were similar between the 2 groups of patients. However, patients with stents were more likely to have complex lesions, whereas those without stents were more likely to undergo atherectomy and have greater residual coronary stenosis. At 6-month follow-up, the composite end point defined as cardiac death, unstable angina, myocardial infarction, need for repeat PTCA, or coronary artery bypass graft surgery (CABG) occurred in 25.0% of stented and 22.2% of nonstented diabetic patients (P not significant [NS]). A multivariate logistic regression analysis showed that coronary stenting was not associated with a reduced incidence of the composite end point among diabetic patients (odds ratio 0.97, 95% CI 0.46-2.05, P NS). CONCLUSION Coronary stenting does not improve clinical event rates in diabetic patients after PTCA.

[1]  Deepak L. Bhatt,et al.  Abciximab reduces mortality in diabetics following percutaneous coronary intervention. , 2000, Journal of the American College of Cardiology.

[2]  Deepak L. Bhatt,et al.  Optimizing the percutaneous interventional outcomes for patients with diabetes mellitus: results of the EPISTENT (Evaluation of platelet IIb/IIIa inhibitor for stenting trial) diabetic substudy. , 1999, Circulation.

[3]  E. Topol,et al.  Diabetes mellitus: biological determinants of atherosclerosis and restenosis. , 1999, Seminars in interventional cardiology : SIIC.

[4]  M. Hadamitzky,et al.  Diabetes mellitus and the clinical and angiographic outcome after coronary stent placement. , 1998, Journal of the American College of Cardiology.

[5]  M. Leon,et al.  The influence of diabetes mellitus on acute and late clinical outcomes following coronary stent implantation. , 1998, Journal of the American College of Cardiology.

[6]  P. Amouyel,et al.  Predictors of restenosis after coronary stent implantation. , 1998, Journal of the American College of Cardiology.

[7]  M. Hadamitzky,et al.  Predictive factors of restenosis after coronary stent placement. , 1997, Journal of the American College of Cardiology.

[8]  C. Bauters,et al.  Restenosis rates in diabetic patients: a comparison of coronary stenting and balloon angioplasty in native coronary vessels. , 1997, Circulation.

[9]  M. Leon,et al.  Increased restenosis in diabetes mellitus after coronary interventions is due to exaggerated intimal hyperplasia. A serial intravascular ultrasound study. , 1997, Circulation.

[10]  D. Faxon,et al.  Coronary angioplasty in diabetic patients. The National Heart, Lung, and Blood Institute Percutaneous Transluminal Coronary Angioplasty Registry. , 1996, Circulation.

[11]  J. Hirshfeld,et al.  Three-year clinical follow-up after Palmaz-Schatz stenting. , 1996, Journal of the American College of Cardiology.

[12]  Z. Bloomgarden,et al.  Potential mechanisms promoting restenosis in diabetic patients. , 1996, Journal of the American College of Cardiology.

[13]  C. White,et al.  Unstable angina. A comparison of angioscopic findings between diabetic and nondiabetic patients. , 1995, Circulation.

[14]  A. Piccoli,et al.  Insulin stimulates endothelin-1 secretion from human endothelial cells and modulates its circulating levels in vivo. , 1995, The Journal of clinical endocrinology and metabolism.

[15]  W. Weintraub,et al.  Influence of diabetes mellitus on early and late outcome after percutaneous transluminal coronary angioplasty. , 1995, Circulation.

[16]  P. Teirstein,et al.  A randomized comparison of coronary-stent placement and balloon angioplasty in the treatment of coronary artery disease. Stent Restenosis Study Investigators. , 1994, The New England journal of medicine.

[17]  W Rutsch,et al.  A comparison of balloon-expandable-stent implantation with balloon angioplasty in patients with coronary artery disease. Benestent Study Group. , 1994, The New England journal of medicine.

[18]  C. Simpfendorfer,et al.  Risk stratification for long-term outcome after elective coronary angioplasty: a multivariate analysis of 5,000 patients. , 1994, Journal of the American College of Cardiology.

[19]  P. Serruys,et al.  Recoil following Wiktor stent implantation for restenotic lesions of coronary arteries. , 1994, Catheterization and cardiovascular diagnosis.

[20]  F. Dai,et al.  Endothelial dysfunction in mesenteric resistance arteries of diabetic rats: role of free radicals. , 1994, The American journal of physiology.

[21]  P. Winocour,et al.  Continued platelet interaction with de-endothelialized aortae associated with slower re-endothelialization and more extensive intimal hyperplasia in spontaneously diabetic BB Wistar rats. , 1993, International journal of experimental pathology.

[22]  P. Winocour.  Platelet Abnormalities in Diabetes Mellitus , 1992, Diabetes.

[23]  A. Paterson,et al.  Glucose and glucosamine regulate growth factor gene expression in vascular smooth muscle cells. , 1992, Proceedings of the National Academy of Sciences of the United States of America.

[24]  R. Bucala,et al.  Advanced glycosylation endproducts block the antiproliferative effect of nitric oxide. Role in the vascular and renal complications of diabetes mellitus. , 1992, The Journal of clinical investigation.

[25]  R. Cohen,et al.  Free radicals mediate endothelial cell dysfunction caused by elevated glucose. , 1992, The American journal of physiology.

[26]  M. Loeken,et al.  Stimulation of endothelin-1 gene expression by insulin in endothelial cells. , 1991, The Journal of biological chemistry.

[27]  K. Tracey,et al.  Advanced glycosylation products quench nitric oxide and mediate defective endothelium-dependent vasodilatation in experimental diabetes. , 1991, The Journal of clinical investigation.

[28]  Julio C. Palmaz,et al.  Clinical Experience With the Palmaz‐Schatz Coronary Stent: Initial Results of a Multicenter Study , 1991, Circulation.

[29]  S. Chakrabarti,et al.  Insulin Regulation of IGF-I Expression in Rat Aorta , 1990, Diabetes.

[30]  G. King,et al.  Insulin, insulin-like growth factor I and platelet-derived growth factor interact additively in the induction of the protooncogene c-myc and cellular proliferation in cultured bovine aortic smooth muscle cells. , 1989, Molecular endocrinology.

[31]  F Joffre,et al.  Intravascular stents to prevent occlusion and restenosis after transluminal angioplasty. , 1987, The New England journal of medicine.

[32]  R E Vlietstra,et al.  Restenosis after percutaneous transluminal coronary angioplasty (PTCA): a report from the PTCA Registry of the National Heart, Lung, and Blood Institute. , 1984, The American journal of cardiology.

[33]  J. N. Upshur.  The Medical College of Virginia. , 1889 .

[34]  Charles L. Brown,et al.  Can restenosis after coronary angioplasty be predicted from clinical variables? , 1993, Journal of the American College of Cardiology.

[35]  R. Erbel,et al.  Quantitative analysis of elastic recoil after balloon angioplasty and after intracoronary implantation of balloon-expandable Palmaz-Schatz stents. , 1993, Journal of the American College of Cardiology.

[36]  M. Kern,et al.  Predictors of long-term cardiac survival in patients with multivessel coronary artery disease undergoing percutaneous transluminal coronary angioplasty. , 1991, The American journal of cardiology.