Statin therapy is associated with improved patency of autogenous infrainguinal bypass grafts.

[1]  J. Slattery,et al.  Randomised trial of cholesterol lowering in 4444 patients with coronary heart disease: the Scandinavian Simvastatin Survival Study (4S). 1994. , 1994, Atherosclerosis. Supplements.

[2]  Mark A. Creager,et al.  Cholesterol Reduction With Atorvastatin Improves Walking Distance in Patients With Peripheral Arterial Disease , 2003, Circulation.

[3]  A. Zwinderman,et al.  Regression of carotid and femoral artery intima-media thickness in familial hypercholesterolemia: treatment with simvastatin. , 2003, Archives of internal medicine.

[4]  J. Liao,et al.  Endothelium-Dependent Effects of Statins , 2003 .

[5]  Deepak L. Bhatt,et al.  Relation of Inflammation and Benefit of Statins After Percutaneous Coronary Interventions , 2003, Circulation.

[6]  S. Mondillo,et al.  Effects of simvastatin on walking performance and symptoms of intermittent claudication in hypercholesterolemic patients with peripheral vascular disease. , 2003, The American journal of medicine.

[7]  L. Sharma,et al.  Statin Use and Leg Functioning in Patients With and Without Lower-Extremity Peripheral Arterial Disease , 2003, Circulation.

[8]  N. Turner,et al.  Simvastatin inhibits human saphenous vein neointima formation via inhibition of smooth muscle cell proliferation and migration. , 2002, Journal of vascular surgery.

[9]  J. Isner,et al.  Statin Therapy Accelerates Reendothelialization: A Novel Effect Involving Mobilization and Incorporation of Bone Marrow-Derived Endothelial Progenitor Cells , 2002, Circulation.

[10]  N. Turner,et al.  Simvastatin inhibits human saphenous vein neointima formation via inhibition of smooth muscle cell proliferation and migration , 2002 .

[11]  M. Donaldson,et al.  Monocyte adhesion to human vein grafts: a marker for occult intraoperative injury? , 2001, Journal of vascular surgery.

[12]  J. Isner,et al.  HMG-CoA reductase inhibitor mobilizes bone marrow--derived endothelial progenitor cells. , 2001, The Journal of clinical investigation.

[13]  A M Zeiher,et al.  HMG-CoA reductase inhibitors (statins) increase endothelial progenitor cells via the PI 3-kinase/Akt pathway. , 2001, The Journal of clinical investigation.

[14]  N Rifai,et al.  Effect of statin therapy on C-reactive protein levels: the pravastatin inflammation/CRP evaluation (PRINCE): a randomized trial and cohort study. , 2001, JAMA.

[15]  Paul M. Ridker,et al.  Measurement of C-reactive protein for the targeting of statin therapy in the primary prevention of acute coronary events. , 2001, The New England journal of medicine.

[16]  Joerg Kallen,et al.  Statins selectively inhibit leukocyte function antigen-1 by binding to a novel regulatory integrin site , 2001, Nature Medicine.

[17]  P. Ridker,et al.  Rapid Reduction in C-Reactive Protein With Cerivastatin Among 785 Patients With Primary Hypercholesterolemia , 2001, Circulation.

[18]  M Shiomi,et al.  Statins Alter Smooth Muscle Cell Accumulation and Collagen Content in Established Atheroma of Watanabe Heritable Hyperlipidemic Rabbits , 2001, Circulation.

[19]  J. Christenson Preoperative lipid control with simvastatin reduces the risk for graft failure already 1 year after myocardial revascularization. , 2001, Cardiovascular surgery.

[20]  P. Libby,et al.  An HMG-CoA Reductase Inhibitor, Cerivastatin, Suppresses Growth of Macrophages Expressing Matrix Metalloproteinases and Tissue Factor In Vivo and In Vitro , 2001, Circulation.

[21]  Y. Chao,et al.  Simvastatin Has Anti-Inflammatory and Antiatherosclerotic Activities Independent of Plasma Cholesterol Lowering , 2000, Arteriosclerosis, thrombosis, and vascular biology.

[22]  F. Mach,et al.  Statins as a newly recognized type of immunomodulator , 2000, Nature Medicine.

[23]  J. Danesh,et al.  Low grade inflammation and coronary heart disease: prospective study and updated meta-analyses , 2000, BMJ : British Medical Journal.

[24]  A. Mantovani,et al.  Inhibition of Monocyte Chemotactic Protein-1 Synthesis by Statins , 2000, Laboratory Investigation.

[25]  P. Meraj,et al.  Pravastatin: An Antithrombotic Effect Independent of the Cholesterol-lowering Effect , 2000, Thrombosis and Haemostasis.

[26]  P. Ridker,et al.  C-reactive protein and other markers of inflammation in the prediction of cardiovascular disease in women. , 2000, The New England journal of medicine.

[27]  J. Powell,et al.  Regulation by fibrinogen and its products of intercellular adhesion molecule-1 expression in human saphenous vein endothelial cells. , 2000, Arteriosclerosis, thrombosis, and vascular biology.

[28]  P. Libby,et al.  HMG CoA reductase inhibitors reduce plasminogen activator inhibitor-1 expression by human vascular smooth muscle and endothelial cells. , 2000, Arteriosclerosis, thrombosis, and vascular biology.

[29]  A. Brett Pravastatin therapy and the risk of stroke. , 2000, The New England journal of medicine.

[30]  HOMAS,et al.  The Effect of Pravastatin on Coronary Events after Myocardial Infarction in Patients with Average Cholesterol Levels , 2000 .

[31]  Ames,et al.  PREVENTION OF CORONARY HEART DISEASE WITH PRAVASTATIN IN MEN WITH HYPERCHOLESTEROLEMIA , 2000 .

[32]  U. Laufs,et al.  3-Hydroxy-3-methylglutaryl-CoA Reductase Inhibitors Attenuate Vascular Smooth Muscle Proliferation by Preventing Rho GTPase-induced Down-regulation of p27 Kip1 * , 1999, The Journal of Biological Chemistry.

[33]  M. Pfeffer,et al.  Long-Term Effects of Pravastatin on Plasma Concentration of C-reactive Protein , 1999 .

[34]  U. Ikeda,et al.  Statins and monocytes , 1999, The Lancet.

[35]  R. Rosenson,et al.  Inhibition of proinflammatory cytokine production by pravastatin , 1999, The Lancet.

[36]  B. Davis,et al.  Reduction of stroke incidence after myocardial infarction with pravastatin: the Cholesterol and Recurrent Events (CARE) study. The Care Investigators. , 1999, Circulation.

[37]  A. Döring,et al.  C-Reactive protein, a sensitive marker of inflammation, predicts future risk of coronary heart disease in initially healthy middle-aged men: results from the MONICA (Monitoring Trends and Determinants in Cardiovascular Disease) Augsburg Cohort Study, 1984 to 1992. , 1999, Circulation.

[38]  J. Egido,et al.  HMG-CoA reductase inhibition by atorvastatin reduces neointimal inflammation in a rabbit model of atherosclerosis. , 1998, Journal of the American College of Cardiology.

[39]  R. Collins,et al.  Prevention of cardiovascular events and death with pravastatin in patients with coronary heart disease and a broad range of initial cholesterol levels. , 1998, The New England journal of medicine.

[40]  F. Bernini,et al.  HMG-CoA reductase inhibitors reduce MMP-9 secretion by macrophages. , 1998, Arteriosclerosis, thrombosis, and vascular biology.

[41]  M. Essig,et al.  3-Hydroxy-3-methylglutaryl coenzyme A reductase inhibitors increase fibrinolytic activity in rat aortic endothelial cells. Role of geranylgeranylation and Rho proteins. , 1998, Circulation research.

[42]  U. Laufs,et al.  Post-transcriptional Regulation of Endothelial Nitric Oxide Synthase mRNA Stability by Rho GTPase* , 1998, The Journal of Biological Chemistry.

[43]  A. Ortiz,et al.  3-Hydroxy-3-methylglutaryl coenzyme a reductase and isoprenylation inhibitors induce apoptosis of vascular smooth muscle cells in culture. , 1998, Circulation research.

[44]  M. Moskowitz,et al.  Stroke protection by 3-hydroxy-3-methylglutaryl (HMG)-CoA reductase inhibitors mediated by endothelial nitric oxide synthase. , 1998, Proceedings of the National Academy of Sciences of the United States of America.

[45]  M. Yacoub,et al.  Expression of vascular adhesion molecules in saphenous vein coronary bypass grafts. , 1998, The Annals of thoracic surgery.

[46]  A. Gotto,et al.  Primary prevention of acute coronary events with lovastatin in men and women with average cholesterol levels: results of AFCAPS/TexCAPS. Air Force/Texas Coronary Atherosclerosis Prevention Study. , 1998, JAMA.

[47]  U. Laufs,et al.  Upregulation of endothelial nitric oxide synthase by HMG CoA reductase inhibitors. , 1998, Circulation.

[48]  J. Kjekshus,et al.  Effect of simvastatin on ischemic signs and symptoms in the Scandinavian simvastatin survival study (4S). , 1998, The American journal of cardiology.

[49]  R. Rutherford,et al.  Recommended standards for reports dealing with lower extremity ischemia: revised version. , 1997, Journal of vascular surgery.

[50]  T. Warner,et al.  Monocyte chemotactic protein-1 expression is associated with the development of vein graft intimal hyperplasia. , 1997, Arteriosclerosis, thrombosis, and vascular biology.

[51]  M. Donaldson,et al.  Infrainguinal arterial reconstruction with nonreversed greater saphenous vein. , 1996, Journal of vascular surgery.

[52]  B. Davis,et al.  The effect of pravastatin on coronary events after myocardial infarction in patients with average cholesterol levels. Cholesterol and Recurrent Events Trial investigators. , 1996, The New England journal of medicine.

[53]  P. Macfarlane,et al.  Prevention of coronary heart disease with pravastatin in men with hypercholesterolemia , 1995 .

[54]  B. Chang,et al.  Long‐Term Results of In Situ Saphenous Vein Bypass: Analysis of 2058 Cases , 1995, Annals of surgery.

[55]  M. Donaldson,et al.  The impact of gender on the results of arterial bypass with in situ greater saphenous vein. , 1995, American journal of surgery.

[56]  Scandinavian Simvastatin Survival Study Group Randomised trial of cholesterol lowering in 4444 patients with coronary heart disease: the Scandinavian Simvastatin Survival Study (4S) , 1994, The Lancet.

[57]  J. Hoch,et al.  Vein graft intimal hyperplasia: leukocytes and cytokine gene expression. , 1994, Surgery.

[58]  M. Donaldson,et al.  Femoral-distal bypass with in situ greater saphenous vein. Long-term results using the Mills valvulotome. , 1991, Annals of surgery.

[59]  J. Edwards,et al.  Present status of reversed vein bypass grafting: five-year results of a modern series. , 1990, Journal of vascular surgery.