Beneficial effects of cholesterol-lowering therapy on the coronary endothelium in patients with coronary artery disease.
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W. Weintraub | A. Kosinski | R. Alexander | J. Talley | M. Stillabower | S. Boccuzzi | J. L. Klein | C. Treasure | J. Zhang | J. Cedarholm | Jian Zhang | J. Klein
[1] P. Diggle. Analysis of Longitudinal Data , 1995 .
[2] M-heart investigators. Effect of simvastatin on coronary atheroma: the Multicentre Anti-Atheroma Study (MAAS) , 1994, The Lancet.
[3] M. Sugimachi,et al. Reduction in serum cholesterol with pravastatin improves endothelium-dependent coronary vasomotion in patients with hypercholesterolemia. , 1994, Circulation.
[4] James P. Martucci,et al. Short-term cholesterol lowering decreases size and severity of perfusion abnormalities by positron emission tomography after dipyridamole in patients with coronary artery disease. A potential noninvasive marker of healing coronary endothelium. , 1994, Circulation.
[5] Lloyd D. Fisher,et al. 2. Biostatistics: A Methodology for the Health Sciences , 1994 .
[6] Stanley Azen,et al. Coronary Angiographic Changes with Lovastatin Therapy: The Monitored Atherosclerosis Regression Study (MARS) , 1993, Annals of Internal Medicine.
[7] C. Lau,et al. Beneficial effect of cholesterol-lowering therapy on coronary endothelium-dependent relaxation in hypercholesterolaemic patients , 1993, The Lancet.
[8] D. Harrison,et al. Hypercholesterolemia increases endothelial superoxide anion production. , 1993, The Journal of clinical investigation.
[9] W. Weintraub,et al. Background and methods for the lovastatin restenosis trial after percutaneous transluminal coronary angioplasty. The Lovastatin Restenosis Trial Study Group. , 1992, The American journal of cardiology.
[10] T Sandor,et al. Quantitative angiographic and statistical methods to assess serial changes in coronary luminal diameter and implications for atherosclerosis regression trials. , 1992, The American journal of cardiology.
[11] G. Watts,et al. Effects on coronary artery disease of lipid-lowering diet, or diet plus cholestyramine, in the St Thomas' Atherosclerosis Regression Study (STARS) , 1992, The Lancet.
[12] D. Harrison,et al. Chronic treatment with polyethylene-glycolated superoxide dismutase partially restores endothelium-dependent vascular relaxations in cholesterol-fed rabbits. , 1991, Circulation research.
[13] D. Harrison,et al. Diet-induced atherosclerosis increases the release of nitrogen oxides from rabbit aorta. , 1990, The Journal of clinical investigation.
[14] J J Albers,et al. Regression of coronary artery disease as a result of intensive lipid-lowering therapy in men with high levels of apolipoprotein B. , 1990, The New England journal of medicine.
[15] R. Cohen,et al. Oxidized low density lipoproteins cause contraction and inhibit endothelium-dependent relaxation in the pig coronary artery. , 1990, The Journal of clinical investigation.
[16] A. Yeung,et al. Coronary vasomotor response to acetylcholine relates to risk factors for coronary artery disease. , 1990, Circulation.
[17] A. M. Lefer,et al. Cardiovascular effects of acute hypercholesterolemia in rabbits. Reversal with lovastatin treatment. , 1989, The Journal of clinical investigation.
[18] J. Steinberg. Book ReviewAmbulatory Pediatric Care , 1989 .
[19] D. Harrison,et al. Restoration of endothelium-dependent relaxation by dietary treatment of atherosclerosis. , 1987, The Journal of clinical investigation.
[20] P. Ganz,et al. Paradoxical vasoconstriction induced by acetylcholine in atherosclerotic coronary arteries. , 1986, The New England journal of medicine.
[21] J. J. Gerbrands,et al. Assessment of short-, medium-, and long-term variations in arterial dimensions from computer-assisted quantitation of coronary cineangiograms. , 1985, Circulation.
[22] J L Witztum,et al. Modification of low density lipoprotein by endothelial cells involves lipid peroxidation and degradation of low density lipoprotein phospholipids. , 1984, Proceedings of the National Academy of Sciences of the United States of America.