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Articles by W. Virgil Brown
Total Records ( 27 ) for W. Virgil Brown
  W. Virgil Brown , Luther Clark , James M. Falko , John R. Guyton , Tomas J. Rees , Gustav Schonfeld and Maria F. Lopes-Virella
  Patients with diabetes or metabolic syndrome frequently have higher triglycerides, lower high-density lipoprotein (HDL) cholesterol, and more particles containing apolipoprotein B (ApoB); this combination contributes significantly to their cardiovascular risk. Optimal management of dyslipidemia and increased atherosclerotic risk requires a fundamental understanding of diabetic dyslipidemia, the clinical evidence for different interventional strategies, and the potential benefit of achieving therapeutic targets. For this review, we considered guidelines, recent reviews, and clinical trial results. The features of dyslipidemia in type 2 diabetes and the metabolic syndrome are linked metabolically and are related to central adiposity and insulin resistance. Levels of ApoB and HDL cholesterol are particularly important markers of risk. Guidelines broadly agree that low-density lipoprotein (LDL) cholesterol should be reduced below population average levels. Additional or secondary strategies in patients with diabetes or the metabolic syndrome are to decrease non-HDL cholesterol, ApoB and/or LDL particle concentration, to increase HDL cholesterol, and to reduce triglycerides. Lifestyle changes and statins are the bedrock of treatment, although second-line treatment using fibrates or niacin will likely benefit many patients with residual risk. Ezetimibe, too, has a favorable effect on lipid profile and inflammatory biomarkers of risk. Dyslipidemia in type 2 diabetes and metabolic syndrome has a distinct profile, suggesting the need for a tailored therapy that targets the key features of lowered HDL cholesterol and raised triglycerides, in addition to the primary antiatherogenic strategy of lowering ApoB-containing lipoproteins, such as LDL. With the prominent failure of some recent intervention trials, new therapeutic strategies-particularly safe and effective means to raise HDL-are needed to manage dyslipidemia in this high-risk population.
  W. Virgil Brown , Anne C. Goldberg , John R. Guyton and Robert H. Knopp
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  W. Virgil Brown , Alan S. Brown , Paolo Raggi and Laurence S. Sperling
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  W. Virgil Brown , Gerald F. Fletcher and Peter W. Wilson
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  W. Virgil Brown , H. Bryan Brewer , Daniel J. Rader and Ernst J. Schaefer
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  W. Virgil Brown , Nanette Wenger , Vera Bittner and Eliot Brinton
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  W. Virgil Brown , Don P. Wilson , Michael Freemark and Peter O. Kwiterovich
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  W. Virgil Brown , Ronald B. Goldberg , Maria Lopes-Virella and Peter Reaven
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  W. Virgil Brown , Harold Bays , Michael Davidson and Anne Goldberg
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  W. Virgil Brown , George Bakris , Edgar Lerma and Glenn Chertow
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  Michael H. Davidson , Christie M. Ballantyne , Terry A. Jacobson , Vera A. Bittner , Lynne T. Braun , Alan S. Brown , W. Virgil Brown , William C. Cromwell , Ronald B. Goldberg , James M. McKenney , Alan T. Remaley , Allan D. Sniderman , Peter P. Toth , Sotirios Tsimikas , Paul E. Ziajka , Kevin C. Maki and Mary R. Dicklin
  The National Cholesterol Education Program Adult Treatment Panel guidelines have established low-density lipoprotein cholesterol (LDL-C) treatment goals, and secondary non-high-density lipoprotein (HDL)-C treatment goals for persons with hypertriglyceridemia. The use of lipid-lowering therapies, particularly statins, to achieve these goals has reduced cardiovascular disease (CVD) morbidity and mortality; however, significant residual risk for events remains. This, combined with the rising prevalence of obesity, which has shifted the risk profile of the population toward patients in whom LDL-C is less predictive of CVD events (metabolic syndrome, low HDL-C, elevated triglycerides), has increased interest in the clinical use of inflammatory and lipid biomarker assessments. Furthermore, the cost effectiveness of pharmacological intervention for both the initiation of therapy and the intensification of therapy has been enhanced by the availability of a variety of generic statins. This report describes the consensus view of an expert panel convened by the National Lipid Association to evaluate the use of selected biomarkers [C-reactive protein, lipoprotein-associated phospholipase A2, apolipoprotein B, LDL particle concentration, lipoprotein(a), and LDL and HDL subfractions] to improve risk assessment, or to adjust therapy. These panel recommendations are intended to provide practical advice to clinicians who wrestle with the challenges of identifying the patients who are most likely to benefit from therapy, or intensification of therapy, to provide the optimum protection from CV risk.
  W. Virgil Brown , Harold Bays , William Harris and Michael Miller
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  W. Virgil Brown , Robert Brook , Linda C. Hemphill and Patrick M. Moriarty
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  W. Virgil Brown , Jan Breslow and Christie Ballantyne
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  W. Virgil Brown , John D. Brunzell , Robert H. Eckel and Neil J. Stone
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  W. Virgil Brown , Harold E. Bays , Kevin C. Maki and Robert A. Wild
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  W. Virgil Brown , Terry A. Jacobson and Lynne T. Braun
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  Harold E. Bays , Peter P. Toth , Penny M. Kris-Etherton , Nicola Abate , Louis J. Aronne , W. Virgil Brown , J. Michael Gonzalez-Campoy , Steven R. Jones , Rekha Kumar , Ralph La Forge and Varman T. Samuel
  The term “fat” may refer to lipids as well as the cells and tissue that store lipid (ie, adipocytes and adipose tissue). “Lipid” is derived from “lipos,” which refers to animal fat or vegetable oil. Adiposity refers to body fat and is derived from “adipo,” referring to fat. Adipocytes and adipose tissue store the greatest amount of body lipids, including triglycerides and free cholesterol. Adipocytes and adipose tissue are active from an endocrine and immune standpoint. Adipocyte hypertrophy and excessive adipose tissue accumulation can promote pathogenic adipocyte and adipose tissue effects (adiposopathy), resulting in abnormal levels of circulating lipids, with dyslipidemia being a major atherosclerotic coronary heart disease risk factor. It is therefore incumbent upon lipidologists to be among the most knowledgeable in the understanding of the relationship between excessive body fat and dyslipidemia. On September 16, 2012, the National Lipid Association held a Consensus Conference with the goal of better defining the effect of adiposity on lipoproteins, how the pathos of excessive body fat (adiposopathy) contributes to dyslipidemia, and how therapies such as appropriate nutrition, increased physical activity, weight-management drugs, and bariatric surgery might be expected to impact dyslipidemia. It is hoped that the information derived from these proceedings will promote a greater appreciation among clinicians of the impact of excess adiposity and its treatment on dyslipidemia and prompt more research on the effects of interventions for improving dyslipidemia and reducing cardiovascular disease risk in overweight and obese patients.
  W. Virgil Brown , Catherine J. McNeal and Samuel S. Gidding
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  W. Virgil Brown , Daniel J. Rader and John Kane
  The diagnosis of familial hypercholesterolemia is usually straightforward. The severely elevated low-density lipoprotein cholesterol and the occurrence of high concentrations of low-density lipoprotein cholesterol in the parents provide the diagnosis. The presence of tendon xanthomata is confirmation but not necessary. However, this relatively simple picture becomes much more complicated when one attempts to define the genetic variants that actually produced this clinical syndrome. In this Roundtable discussion, I am joined by two experts in the identification of genetic abnormalities discovered in those with phenotypic familial hypercholesterolemia. Dr. John Kane from the University of California, San Francisco, and Dr. Daniel Rader from the University of Pennsylvania share their knowledge in and experience with this topic.
  W. Virgil Brown , Daniel J. Rader and Anne C. Goldberg
  Clinical lipidologists are often asked to manage patients with severely elevated low-density lipoprotein cholesterol (LDL-C) and other apolipoprotein B-containing lipoproteins. Statins at maximum doses and in combination with other drugs may not achieve adequate reductions in LDL-C in such patients. The most dramatic elevations are usually in patients with genetic abnormalities in the LDL receptor gene on both chromosome pairs. LDL-C values well in excess of 400 mg/dL are not fully responsive to current treatments. In the past few months, the Food and Drug Administration has approved 2 new drugs for special use in such patients; these are mipomersen and lomitapide. During the National Lipid Association's Scientific Sessions, 2 highly experienced clinician scientists who have completed research studies with these agents agreed to answer questions pertinent to the prescription use of these agents. These scientists are Dr Anne Goldberg from Washington University in St. Louis and Dr Daniel Rader from the University of Pennsylvania.
  W. Virgil Brown , Alan S. Brown , Karen E. Aspry and Matthew K. Ito
  One of the most serious challenges to all physicians is the maintenance of therapy for those chronic disorders that at present cannot be cured. Elevations of low-density lipoprotein and very low-density lipoprotein are among the most common of those disorders. We are now in an era in which 2 fundamental developments of modern technology have come together. These are the supply of effective and safe lipid-lowering drugs as well as the ability to closely monitor pertinent measures in our patients. The rapid conversion of our health care systems into large teams of professionals with direct support from third-party payers has made it possible to coordinate chronic care through electronic medical records and electronic communication. As a result, with effective planning and organization, we can guide our patients toward better adherence to successful medical regimens. These issues are evolving rapidly and have been presented in some detail in the December 2013 issue of the Journal. I was joined in this Roundtable discussion by 3 health professionals who have had extensive experience with the application of health information technology. They are Dr. Karen Aspry and Dr. Alan Brown, both clinical cardiologists, and Dr. Matthew Ito, a Doctor of Pharmacy.
  Gerald F. Watts , Samuel Gidding , Anthony S. Wierzbicki , Peter P. Toth , Rodrigo Alonso , W. Virgil Brown , Eric Bruckert , Joep Defesche , Khoo Kah Lin , Michael Livingston , Pedro Mata , Klaus G. Parhofer , Frederick J. Raal , Raul D. Santos , Eric J.G. Sijbrands , William G. Simpson , David R. Sullivan , Andrey V. Susekov , Brian Tomlinson , Albert Wiegman , Shizuya Yamashita and John J.P. Kastelein
  Familial hypercholesterolemia (FH) is a dominantly inherited disorder present from birth that markedly elevates plasma low-density lipoprotein cholesterol and causes premature coronary heart disease. There are at least 20 million people with FH worldwide, but the majority remains undetected, and current treatment is often suboptimal. To address this major gap in coronary prevention we present, from an international perspective, consensus-based guidance on the care of FH. The guidance was generated from seminars and workshops held at an international symposium. The recommendations focus on the detection, diagnosis, assessment, and management of FH in adults and children and set guidelines for clinical purposes. They also refer to best practice for cascade screening and risk notifying and testing families for FH, including use of genetic testing. Guidance on treatment is based on risk stratification, management of noncholesterol risk factors, and the safe and effective use of low-density lipoprotein-lowering therapies. Recommendations are given on lipoprotein apheresis. The use of emerging therapies for FH is also foreshadowed. This international guidance acknowledges evidence gaps but aims to make the best use of contemporary practice and technology to achieve the best outcomes for the care of FH. It should accordingly be used to inform clinical judgment and be adjusted for country-specific and local healthcare needs and resources.
  W. Virgil Brown , Harold Bays and George A. Bray
  Our topic is the evaluation and treatment of obesity in the practice of medicine. I am joined by Dr. Harold Bays who has carried out many studies of dietary and medical interventions in patients with obesity. I am also honored to have Dr. George Bray who is known for his many years of research into causes of obesity and its therapy. Our goal is bring this clinical and research experience to bear on the office practice of medicine.
  W. Virgil Brown , Benjamin J. Ansell , Rachel H. Mackey and Peter P. Toth
  One of the most difficult and confusing issues for clinical lipidologists and physicians in general has been the management of low concentrations of high-density lipoprotein cholesterol. We know this to be a very powerful predictor of risk in scores of community-based and clinical trial cohorts. Raising this number in many patients would seem to provide a great therapeutic opportunity, but so far this concept has been very difficult to prove. I have been joined for this discussion by a cardiovascular epidemiologist, Dr. Rachel Mackey, from the University of Pittsburgh and two clinical lipidologists who have studied and written in depth about this problem. These are Dr. Benjamin Ansell from the University of California in Los Angeles and Dr. Peter Toth from Johns Hopkins University School of Medicine. Our objective in this discussion is to give primary care clinicians our thoughts about the recent research findings and the implications of these data on the best clinical practice.
  W. Virgil Brown , Robert J. Desnick and Gregory A. Grabowski
  There are several inherited disorders that involve abnormal storage of lipids in tissues leading to severe compromise of organs. Sadly, these are often accompanied by lifelong morbidity and early mortality. Disorders such as Gaucher, Fabry, and lysosomal acid lipase deficiencies (Wolman and cholesteryl ester storage diseases) have been known for many years, and provide a difficult and frustrating set of problems for patients, their families, and their physicians. With recombinant methods of protein synthesis, it is now possible to literally replace the defective enzymes that underlie the basic pathophysiology of many such disorders. The delivery of these enzymes into the affected cells is possible because of their location in the lysosomes where the natural degradation of their lipid substrates occurs. I have asked 2 well-known investigators to join us for this Roundtable. These are professors who have been involved with the research that has made this type of therapy possible and who have participated in the clinical trials that demonstrated the value of enzyme replacement therapy. They are Dr. Robert Desnick, dean of Genetic and Genomic Medicine and professor and chairman emeritus of the Department of Genetics and Genomic Sciences at the Icahn School of Medicine at Mount Sinai in New York City, and Dr. Gregory Grabowski, professor of Microbiology, Biochemistry, and Pediatrics, at the University of Cincinnati College of Medicine. Dr. Grabowski recently retired from that school to become the chief science officer of Synageva, a company involved in producing enzymes for this type of therapy.
  Terry A. Jacobson , Matthew K. Ito , Kevin C. Maki , Carl E. Orringer , Harold E. Bays , Peter H. Jones , James M. McKenney , Scott M. Grundy , Edward A. Gill , Robert A. Wild , Don P. Wilson and W. Virgil Brown
  Various organizations and agencies have issued recommendations for the management of dyslipidemia. Although many commonalities exist among them, material differences are present as well. The leadership of the National Lipid Association (NLA) convened an Expert Panel to develop a consensus set of recommendations for patient-centered management of dyslipidemia in clinical medicine. The current Executive Summary highlights the major conclusions in Part 1 of the recommendations report of the NLA Expert Panel and includes: (1) background and conceptual framework for formulation of the NLA Expert Panel recommendations; (2) screening and classification of lipoprotein lipid levels in adults; (3) targets for intervention in dyslipidemia management; (4) atherosclerotic cardiovascular disease risk assessment and treatment goals based on risk category; (5) atherogenic cholesterol-non-high-density lipoprotein cholesterol and low-density lipoprotein cholesterol-as the primary targets of therapy; and (6) lifestyle and drug therapies intended to reduce morbidity and mortality associated with dyslipidemia.
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