S
Scott M. Grundy
Researcher at University of Texas Southwestern Medical Center
Publications - 849
Citations - 246629
Scott M. Grundy is an academic researcher from University of Texas Southwestern Medical Center. The author has contributed to research in topics: Cholesterol & Lipoprotein. The author has an hindex of 187, co-authored 841 publications receiving 231821 citations. Previous affiliations of Scott M. Grundy include University of California, San Francisco & University of California, Davis.
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Journal ArticleDOI
Lipid-Altering Efficacy and Safety of Ezetimibe/Simvastatin Versus Atorvastatin in Patients With Hypercholesterolemia and the Metabolic Syndrome (from the VYMET Study)
Jennifer G. Robinson,Christie M. Ballantyne,Scott M. Grundy,Willa A. Hsueh,Hans-Henrik Parving,Jeffrey B. Rosen,Adeniyi J. Adewale,Adam B. Polis,Joanne E. Tomassini,Andrew M. Tershakovec +9 more
TL;DR: Ezetimibe/simVastatin was more likely to result in lipid treatment end points than atorvastatin and was generally well tolerated at the doses compared in patients.
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Responsiveness of plasma lipids and lipoproteins to plant stanol esters.
TL;DR: Study 3 found that plant stanols provide additional lowering of LDL cholesterol when added to ongoing statin therapy, which makes plant stanol an attractive dietary component to help to achieve the goals of LDL- Lowering therapy in patients requiring an LDL-lowering drug.
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Intestinal absorption of stearic acid after consumption of high fat meals in humans
Andrea Bonanome,Scott M. Grundy +1 more
TL;DR: The data suggest that intestinal absorbability of stearic acid is similar to that of palmitic acid, and both saturated fatty acids appear to be absorbed almost as well as oleic acid.
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Consensus statement : role of therapy with statins in patients with hypertriglyceridemia
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Low density lipoprotein metabolism in hypertriglyceridemic and normolipidemic patients with coronary heart disease.
TL;DR: Hypertriglyceridemic patients with CHD and a portion of normolipidemic doctors' patients withCHD were characterized by increases in both transport and fractional catabolic rate of LDL-apoB; these abnormalities in LDL metabolism may have contributed to their coronary heart disease.