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<rdf:RDF xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns="http://purl.org/rss/1.0/"><channel rdf:about="http://www.lipidjournal.com/?rss=yes"><title>Journal of Clinical Lipidology</title><description>Journal of Clinical Lipidology RSS feed: Current Issue. The  Journal of Clinical Lipidology  is published to support the diverse array of medical professionals who work to reduce 
the incidence of morbidity and mortality from dyslipidemia and associated disorders of lipid metabolism. The Journal's readership encompasses 
a broad cross-section of the medical community, including cardiologists, endocrinologists, and primary care physicians, as well as those 
involved in the treatment of such disorders as diabetes, hypertension, and obesity. The  Journal  also addresses allied health 
professionals who treat the patient base described above, such as pharmacists, nurse practitioners and dietitians.  
 
Because the scope 
of clinical lipidology is broad, the topics addressed by the Journal are equally diverse. Typical articles explore lipidology as it is 
practiced in the treatment setting, recent developments in pharmacological research, reports of treatment and trials, case studies, the 
impact of lifestyle modification, and similar academic material of interest to the practitioner. While preference is given to material 
of immediate practical concern, the science that underpins lipidology is forwarded by expert contributors so that evidence-based approaches 
to reducing cardiovascular and coronary heart disease can be made immediately available to our readers. Sections of the  Journal  will 
address pioneering studies and the clinicians who conduct them, case studies, ethical standards and conduct, professional guidance such 
as ATP and NCEP, editorial commentary, letters from readers, National Lipid Association (NLA) news and upcoming event information, as 
well as abstracts from the NLA annual scientific sessions and the scientific forums held by its chapters, when appropriate.</description><link>http://www.lipidjournal.com/?rss=yes</link><dc:publisher>Elsevier Inc.</dc:publisher><dc:language>en</dc:language><dc:rights> © 2010 Published by Elsevier Inc. All rights reserved. </dc:rights><prism:publicationName>Journal of Clinical Lipidology</prism:publicationName><prism:issn>1933-2874</prism:issn><prism:volume>4</prism:volume><prism:number>3</prism:number><prism:publicationDate>May 2010</prism:publicationDate><prism:copyright> © 2010 Published by Elsevier Inc. 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rdf:resource="http://www.lipidjournal.com/article/PIIS1933287410001728/abstract?rss=yes"/></rdf:Seq></items></channel><item rdf:about="http://www.lipidjournal.com/article/PIIS1933287410001790/abstract?rss=yes"><title>Editorial Board</title><link>http://www.lipidjournal.com/article/PIIS1933287410001790/abstract?rss=yes</link><description></description><dc:title>Editorial Board</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S1933-2874(10)00179-0</dc:identifier><dc:source>Journal of Clinical Lipidology 4, 3 (2010)</dc:source><dc:date>2010-05-01</dc:date><prism:publicationName>Journal of Clinical Lipidology</prism:publicationName><prism:publicationDate>2010-05-01</prism:publicationDate><prism:volume>4</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1933-2874(10)X0004-6</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>iii</prism:startingPage><prism:endingPage>iv</prism:endingPage></item><item rdf:about="http://www.lipidjournal.com/article/PIIS1933287410001820/abstract?rss=yes"><title>Table of Contents</title><link>http://www.lipidjournal.com/article/PIIS1933287410001820/abstract?rss=yes</link><description></description><dc:title>Table of Contents</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S1933-2874(10)00182-0</dc:identifier><dc:source>Journal of Clinical Lipidology 4, 3 (2010)</dc:source><dc:date>2010-05-01</dc:date><prism:publicationName>Journal of Clinical Lipidology</prism:publicationName><prism:publicationDate>2010-05-01</prism:publicationDate><prism:volume>4</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1933-2874(10)X0004-6</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>vii</prism:startingPage><prism:endingPage>viii</prism:endingPage></item><item rdf:about="http://www.lipidjournal.com/article/PIIS193328741000173X/abstract?rss=yes"><title>From the Editor-in-Chief</title><link>http://www.lipidjournal.com/article/PIIS193328741000173X/abstract?rss=yes</link><description>The medical community is awaiting significant modifications of our current guidelines for estimating risk and setting targets for treatment in the national effort to reduce cardiovascular diseases. This will involve incorporating the experience during the past three decades of attempting to modify blood pressure and more than two decades of guiding the reduction of increased lipoprotein levels in the population. The work of the Joint National Commission on High Blood Pressure (JNC) and the National Cholesterol Education Program (NCEP) have given us several iterations of guidelines over the years that have dramatically changed medical practice, making the primary care physician a true vascular disease preventionist for the first time and reducing death and disability in patients from vascular events by approximately 50%. Interwoven with this has been changing targets for improved glucose and hemoglobin A1c concentrations in our diabetic patients. The American Diabetes Association and the American Heart Association have been instigators and a driving force in this very successful effort.</description><dc:title>From the Editor-in-Chief</dc:title><dc:creator>W. Virgil Brown</dc:creator><dc:identifier>10.1016/j.jacl.2010.03.074</dc:identifier><dc:source>Journal of Clinical Lipidology 4, 3 (2010)</dc:source><dc:date>2010-04-02</dc:date><prism:publicationName>Journal of Clinical Lipidology</prism:publicationName><prism:publicationDate>2010-04-02</prism:publicationDate><prism:volume>4</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1933-2874(10)X0004-6</prism:issueIdentifier><prism:section>Foreword</prism:section><prism:startingPage>139</prism:startingPage><prism:endingPage>141</prism:endingPage></item><item rdf:about="http://www.lipidjournal.com/article/PIIS1933287410001054/abstract?rss=yes"><title>News from the NLA</title><link>http://www.lipidjournal.com/article/PIIS1933287410001054/abstract?rss=yes</link><description>This year, the NLA will attempt to gather more practice survey data than ever before. With your help, we're going to canvass the entire membership to gain a better understanding of your practice, your goals, and your educational needs and preferences. Check your e-mail for an invitation to participate, and then take a few minutes to complete the brief questionnaire. Your prompt response will help spare us the expense of additional letter mailings and phone campaigns. We'll use your preferences in designing upcoming meetings and courses tailored closely to the specific needs of you, the membership of the NLA.</description><dc:title>News from the NLA</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/j.jacl.2010.03.006</dc:identifier><dc:source>Journal of Clinical Lipidology 4, 3 (2010)</dc:source><dc:date>2010-03-22</dc:date><prism:publicationName>Journal of Clinical Lipidology</prism:publicationName><prism:publicationDate>2010-03-22</prism:publicationDate><prism:volume>4</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1933-2874(10)X0004-6</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>142</prism:startingPage><prism:endingPage>143</prism:endingPage></item><item rdf:about="http://www.lipidjournal.com/article/PIIS1933287410001030/abstract?rss=yes"><title>Should we use apoB for risk assessment and as a target for treatment?†</title><link>http://www.lipidjournal.com/article/PIIS1933287410001030/abstract?rss=yes</link><description>W. Virgil Brown, MD: Today we have three experts on hand to discuss the assessment of lipoproteins for clinical purposes. During the last few years, the use of cholesterol itself (and certainly lipoprotein cholesterol) has been brought into question as being the best way of assessing lipoprotein-related risk. An issue that has come up in both the laboratory and in clinical surveys has been the measurement of the protein component of lipoproteins. This is possible now, it's clinically available, and the question arises as to whether we are using the appropriate component of lipoproteins for optimally judging risk. I've asked three experts to give us a feeling for the current status of using a protein component, apolipoprotein B (apoB), as a measure of risk, as opposed to the cholesterol component of low-density lipoprotein (LDL), and maybe other lipoproteins as well. So we have with us today Dr. Evan Stein, Dr. Allan Sniderman, and Dr. Gary Myers.</description><dc:title>Should we use apoB for risk assessment and as a target for treatment?†</dc:title><dc:creator>W. Virgil Brown, Gary L. Myers, Allan D. Sniderman, Evan Stein</dc:creator><dc:identifier>10.1016/j.jacl.2010.03.004</dc:identifier><dc:source>Journal of Clinical Lipidology 4, 3 (2010)</dc:source><dc:date>2010-03-17</dc:date><prism:publicationName>Journal of Clinical Lipidology</prism:publicationName><prism:publicationDate>2010-03-17</prism:publicationDate><prism:volume>4</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1933-2874(10)X0004-6</prism:issueIdentifier><prism:section>Clinical Lipidology Roundtable Discussion</prism:section><prism:startingPage>144</prism:startingPage><prism:endingPage>151</prism:endingPage></item><item rdf:about="http://www.lipidjournal.com/article/PIIS1933287410001042/abstract?rss=yes"><title>Why is non−high-density lipoprotein cholesterol a better marker of the risk of vascular disease than low-density lipoprotein cholesterol?</title><link>http://www.lipidjournal.com/article/PIIS1933287410001042/abstract?rss=yes</link><description>Abstract: Low-density lipoprotein cholesterol (LDL-C) has been the focus of managing lipoprotein disorders for decades. It is now time to consider a change. Both apolipoprotein B (apoB) and non-high-density lipoprotein cholesterol (HDL-C) have been shown to be more accurate markers of cardiovascular risk than LDL-C. ApoB measures total atherogenic particle number, of which 90% are LDL particles. Therefore, LDL particle number determines plasma apoB in most patients. Non-HDL-C is widely assumed to be superior to LDL-C when triglyceride concentrations are elevated (even modestly) because it includes the cholesterol in very-low-density lipoprotein. However, evidence does not support this concept. Rather, non-HDL-C appears to be an indirect way of estimating apoB. We argue that we should integrate the information from non-HDL-C and apoB for better risk assessment and a better target of therapy.</description><dc:title>Why is non−high-density lipoprotein cholesterol a better marker of the risk of vascular disease than low-density lipoprotein cholesterol?</dc:title><dc:creator>Allan Sniderman, Matt McQueen, John Contois, Ken Williams, Curt D. Furberg</dc:creator><dc:identifier>10.1016/j.jacl.2010.03.005</dc:identifier><dc:source>Journal of Clinical Lipidology 4, 3 (2010)</dc:source><dc:date>2010-03-22</dc:date><prism:publicationName>Journal of Clinical Lipidology</prism:publicationName><prism:publicationDate>2010-03-22</prism:publicationDate><prism:volume>4</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1933-2874(10)X0004-6</prism:issueIdentifier><prism:section>Review Articles</prism:section><prism:startingPage>152</prism:startingPage><prism:endingPage>155</prism:endingPage></item><item rdf:about="http://www.lipidjournal.com/article/PIIS1933287410001029/abstract?rss=yes"><title>Cholesterol crystals piercing the arterial plaque and intima trigger local and systemic inflammation</title><link>http://www.lipidjournal.com/article/PIIS1933287410001029/abstract?rss=yes</link><description>Abstract: The response to arterial wall injury is an inflammatory process, which over time becomes integral to the development of atherosclerosis and subsequent plaque instability. However, the underlying injurious agent, critical to this process, has not received much attention. In this review, a model of plaque rupture is hypothesized with two stages of inflammatory activity. In stage I (cholesterol crystal-induced cell injury and apoptosis), intracellular cholesterol crystals induce foam cell apoptosis, setting up a vicious cycle by signaling more macrophages, resulting in accumulation of extra cellular lipids. This local inflammation eventually leads to the formation of a semi-liquid, lipid-rich necrotic core of a vulnerable plaque. In stage II (cholesterol crystal-induced arterial wall injury), the saturated lipid core is now primed for crystallization, which can manifest as a clinical syndrome with a systemic inflammation response. Cholesterol crystallization is the trigger that causes core expansion, leading to intimal injury. We recently demonstrated that when cholesterol crystallizes from a liquid to a solid state, it undergoes volume expansion, which can tear the plaque cap. This observation of cholesterol crystals perforating the cap and intimal surface was made in the plaques of patients who died with acute coronary syndrome. We have also demonstrated that several agents (ie, statins, aspirin, and ethanol) can dissolve cholesterol crystals and may be exerting their immediate benefits by this direct mechanism. Also, because recent studies have demonstrated that high-sensitivity C-reactive protein may be a reliable marker in selecting patients for statin therapy, it could reflect the presence of intimal injury by cholesterol crystals. This was demonstrated in an atherosclerotic rabbit model. Therefore, we propose that cholesterol crystallization could help explain in part both local and systemic inflammation associated with atherosclerosis.</description><dc:title>Cholesterol crystals piercing the arterial plaque and intima trigger local and systemic inflammation</dc:title><dc:creator>George S. Abela</dc:creator><dc:identifier>10.1016/j.jacl.2010.03.003</dc:identifier><dc:source>Journal of Clinical Lipidology 4, 3 (2010)</dc:source><dc:date>2010-03-17</dc:date><prism:publicationName>Journal of Clinical Lipidology</prism:publicationName><prism:publicationDate>2010-03-17</prism:publicationDate><prism:volume>4</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1933-2874(10)X0004-6</prism:issueIdentifier><prism:section>Review Articles</prism:section><prism:startingPage>156</prism:startingPage><prism:endingPage>164</prism:endingPage></item><item rdf:about="http://www.lipidjournal.com/article/PIIS1933287410000474/abstract?rss=yes"><title>Cost-effectiveness of lower targets for blood pressure and low-density lipoprotein cholesterol in diabetes: The Stop Atherosclerosis in Native Diabetics Study (SANDS)</title><link>http://www.lipidjournal.com/article/PIIS1933287410000474/abstract?rss=yes</link><description>Background: The Stop Atherosclerosis in Native Diabetics Study (SANDS) reported cardiovascular benefit of aggressive versus standard treatment targets for both low-density lipoprotein cholesterol (LDL-C) and blood pressure (BP) in diabetic individuals.Objective: In this analysis, we examined within trial cost-effectiveness of aggressive targets of LDL-C ≤70 mg/dL and systolic BP ≤115 mmHg versus standard targets of LDL-C ≤100 mg/dL and systolic BP ≤130 mmHg.Design: Randomized, open label blinded-to-endpoint 3-year trial.Data Sources: SANDS clinical trial database, Quality of Wellbeing survey, Centers for Medicare and Medicaid Services, Wholesale Drug Prices.Target Population: American Indians ≥age 40 years with type 2 diabetes and no previous cardiovascular events.Time Horizon: April 2003 to July 2007.Perspective: Health payer.Interventions: Participants were randomized to aggressive versus standard groups with treatment algorithms defined for both.Outcome Measures: Incremental cost-effectiveness.Results of Base-Case Analysis: Compared with the standard group, the aggressive group had slightly lower costs of medical services (−$116) but a 54% greater cost for BP medication ($1,242) and a 116% greater cost for lipid-lowering medication ($2,863), resulting in an increased cost of $3,988 over 3 years. Those in the aggressively treated group gained 0.0480 quality-adjusted life-years (QALY) over the standard group. When a 3% discount rate for costs and outcomes was used, the resulting cost per QALY was $82,589.Results of Sensitivity Analysis: The use of a 25%, 50%, and 75% reduction in drug costs resulted in a cost per QALY of $61,329, $40,070, and $18,810, respectively.Limitations: This study was limited by use of a single ethnic group and by its 3-year duration.Conclusions: Within this 3-year study, treatment to lower BP and LDL-C below standard targets was not cost-effective because of the cost of the additional medications required to meet the lower targets. With the anticipated availability of generic versions of the BP and lipid-lowering drugs used in SANDS, the cost-effectiveness of this intervention should improve.</description><dc:title>Cost-effectiveness of lower targets for blood pressure and low-density lipoprotein cholesterol in diabetes: The Stop Atherosclerosis in Native Diabetics Study (SANDS)</dc:title><dc:creator>Charlton Wilson, Chun-Chih Huang, Nawar Shara, Barbara V. Howard, Jerome L. Fleg, Jeffrey A. Henderson, Wm. James Howard, Heather Huentelman, Elisa T. Lee, Mihriye Mete, Marie Russell, James M. Galloway, Angela Silverman, Mario Stylianou, Jason Umans, Matthew R. Weir, Fawn Yeh, Robert E. Ratner</dc:creator><dc:identifier>10.1016/j.jacl.2010.01.008</dc:identifier><dc:source>Journal of Clinical Lipidology 4, 3 (2010)</dc:source><dc:date>2010-02-08</dc:date><prism:publicationName>Journal of Clinical Lipidology</prism:publicationName><prism:publicationDate>2010-02-08</prism:publicationDate><prism:volume>4</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1933-2874(10)X0004-6</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>165</prism:startingPage><prism:endingPage>172</prism:endingPage></item><item rdf:about="http://www.lipidjournal.com/article/PIIS1933287410001017/abstract?rss=yes"><title>Attainment of low-density lipoprotein cholesterol goals in coronary artery disease</title><link>http://www.lipidjournal.com/article/PIIS1933287410001017/abstract?rss=yes</link><description>Background: The National Cholesterol Education Program Guidelines offer an optional low-density lipoprotein cholesterol (LDL-C) goal of less than 70 mg/dL for very high-risk patients with coronary artery disease (CAD). This study evaluated the extent to which this recommendation can be attained by the use of currently available lipid-lowering therapies.Methods: A retrospective, cross-sectional study of patients in the Kaiser Permanente Colorado healthcare system 18 years of age or older with CAD and a predetermined LDL-C goal less than 70 mg/dL. The LDL-C most proximal, but within 1 year before April 1, 2008, was deemed the qualifying LDL-C and used to determine LDL-C goal attainment. Lipid-lowering medication(s) for those attaining goal and factors associated with failure to attain LDL-C goal also were identified.Results: A total of 7427 patients were included in the study. A total of 3226 patients attained a LDL-C less than 70 mg/dL. The majority (92.4%) attaining goal were receiving statin monotherapy or in combination compared with 81.3% not at goal (P &lt; .001). More than one-half attained goal on statin monotherapy with 70.7% at moderate- to high-potency doses and 87.4% on generically available statin. Nearly one-third attaining goal received statin in combination. Ezetimibe (70.6%) was most frequently used with statin. Factors independently associated with failure to attain a LDL-C less than 70 mg/dL were age younger than 65 years, patients not receiving statin, a history of creatine kinase elevation, and female sex.Conclusion: This study reports the greatest rate of LDL-C less than 70 mg/dL goal attainment in a very high-risk population with CAD to date. However, despite a system dedicated to aggressively treat to a LDL-C goal of less than 70 mg/dL, success in the majority is a challenge with the currently available therapies.</description><dc:title>Attainment of low-density lipoprotein cholesterol goals in coronary artery disease</dc:title><dc:creator>Amy B. Kauffman, Kari L. Olson, Morgan L. Youngblood, Emily B. Zadvorny, Thomas Delate, John A. Merenich, Clinical Pharmacy Cardiac Risk Service Study Group</dc:creator><dc:identifier>10.1016/j.jacl.2010.03.002</dc:identifier><dc:source>Journal of Clinical Lipidology 4, 3 (2010)</dc:source><dc:date>2010-03-17</dc:date><prism:publicationName>Journal of Clinical Lipidology</prism:publicationName><prism:publicationDate>2010-03-17</prism:publicationDate><prism:volume>4</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1933-2874(10)X0004-6</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>173</prism:startingPage><prism:endingPage>180</prism:endingPage></item><item rdf:about="http://www.lipidjournal.com/article/PIIS1933287410000565/abstract?rss=yes"><title>New mutations in APOB100 involved in familial hypobetalipoproteinemia</title><link>http://www.lipidjournal.com/article/PIIS1933287410000565/abstract?rss=yes</link><description>Abstract: Familial hypolipoproteinemia (FHBL) is characterized by an inherited low plasma level of apolipoprotein B containing lipoproteins. FHBL may be caused by mutations of APOB. Individuals with FHBL typically have intestinal malabsorption and frequently suffer from a deficiency of fat-soluble vitamins. Most mutations that cause FHBL are APOB truncating mutations. Here we describe a patient with FHBL caused by a novel truncating mutation together with a novel missense mutation.</description><dc:title>New mutations in APOB100 involved in familial hypobetalipoproteinemia</dc:title><dc:creator>Klaus Brusgaard, Lars Kjaersgaard, Anne-Birthe Bo Hansen, Steffen Husby</dc:creator><dc:identifier>10.1016/j.jacl.2010.02.009</dc:identifier><dc:source>Journal of Clinical Lipidology 4, 3 (2010)</dc:source><dc:date>2010-03-03</dc:date><prism:publicationName>Journal of Clinical Lipidology</prism:publicationName><prism:publicationDate>2010-03-03</prism:publicationDate><prism:volume>4</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1933-2874(10)X0004-6</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>181</prism:startingPage><prism:endingPage>184</prism:endingPage></item><item rdf:about="http://www.lipidjournal.com/article/PIIS1933287410001066/abstract?rss=yes"><title>Prevalence of metabolic syndrome and insulin resistance among Egyptian adolescents 10 to 18 years of age</title><link>http://www.lipidjournal.com/article/PIIS1933287410001066/abstract?rss=yes</link><description>Background: The prevalence and magnitude of childhood obesity are increasing dramatically.Objectives: To examine the effect of varying social, demographic, dietary, and activity factors on the prevalence of metabolic syndrome and its relation to insulin resistance, C-reactive protein, and homocysteine levels in a large, representative sample of Egyptian adolescents.Methods: Our survey included 4250 adolescents (from 10 to 18 years of age; male subjects comprised 42.5% of participants) from 7 governorates representing Egypt. Baseline measurements included blood pressure, fasting blood glucose, plasma lipids, C-reactive protein, and homocysteine levels. Because the body mass index varies according to age, we standardized the value for age and sex with the use of conversion to percentiles.Results: The overall prevalence of the metabolic syndrome was 7.4% with no sex or area of residence predilection. Results showed that adolescents with the full criteria of metabolic syndrome (ie, three criterion or more) constituted nearly one fourth of those exhibiting high values of different components, except for systolic blood pressure, where they were 42%, and TG, where they were 31%. Family history of obesity and diabetes mellitus increase the odds for metabolic syndrome significantly (1.68 and 1.3, respectively) as well as inactivity. A high level of C-reactive protein was reported among affected adolescents. Homocysteine level did not have an influence.Conclusions: The prevalence of the metabolic syndrome is considerable among obese adolescents. Proinflammatory markers associated with an increased risk of adverse cardiovascular outcomes are already present in these youth.</description><dc:title>Prevalence of metabolic syndrome and insulin resistance among Egyptian adolescents 10 to 18 years of age</dc:title><dc:creator>Nebal A. Aboul Ella, Dina I. Shehab, Mervat A. Ismail, Awatif A. Maksoud</dc:creator><dc:identifier>10.1016/j.jacl.2010.03.007</dc:identifier><dc:source>Journal of Clinical Lipidology 4, 3 (2010)</dc:source><dc:date>2010-03-22</dc:date><prism:publicationName>Journal of Clinical Lipidology</prism:publicationName><prism:publicationDate>2010-03-22</prism:publicationDate><prism:volume>4</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1933-2874(10)X0004-6</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>185</prism:startingPage><prism:endingPage>195</prism:endingPage></item><item rdf:about="http://www.lipidjournal.com/article/PIIS1933287410000577/abstract?rss=yes"><title>Letter to the Editor</title><link>http://www.lipidjournal.com/article/PIIS1933287410000577/abstract?rss=yes</link><description>Nash et al presented a thorough and balanced report on lipoprotein metabolism and the association with Alzheimer's disease and related disorders (ADRD). This subject remains controversial for several reasons. It is now clear that AB 1-42 production is affected by metabolic, traumatic, and hypertensive vascular events in the brain. Twenty years ago Sparks et al showed a statistically significant correlation of increased density and prevalence of beta amyloid plaque in the parahippocampal gyrus of those with Alzheimer's disease and those with significant coronary artery disease. This finding was in contrast to lower and less-dense plaque in those without significant coronary artery disease. The Leiden + 85 study showed that cognitive impairment and dementia were increased 2.7 to 3.6 times from the greatest to lowest tertrile of high-density lipoprotein cholesterol, respectively.</description><dc:title>Letter to the Editor</dc:title><dc:creator>Douglas Trenkle</dc:creator><dc:identifier>10.1016/j.jacl.2010.02.010</dc:identifier><dc:source>Journal of Clinical Lipidology 4, 3 (2010)</dc:source><dc:date>2010-03-04</dc:date><prism:publicationName>Journal of Clinical Lipidology</prism:publicationName><prism:publicationDate>2010-03-04</prism:publicationDate><prism:volume>4</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1933-2874(10)X0004-6</prism:issueIdentifier><prism:section>Letters to the Editor</prism:section><prism:startingPage>196</prism:startingPage><prism:endingPage>196</prism:endingPage></item><item rdf:about="http://www.lipidjournal.com/article/PIIS1933287410000954/abstract?rss=yes"><title>Reply</title><link>http://www.lipidjournal.com/article/PIIS1933287410000954/abstract?rss=yes</link><description>I enjoyed reading the recent letter to the editor submitted by Dr. Trenkle, and I welcome the opportunity to respond for clarification. His reference to the work of Sparks et al refers to work more than a decade ago. Sparks more recently studied the use of atorvastatin and has not been followed by more positive trials recently.</description><dc:title>Reply</dc:title><dc:creator>David T. Nash</dc:creator><dc:identifier>10.1016/j.jacl.2010.03.001</dc:identifier><dc:source>Journal of Clinical Lipidology 4, 3 (2010)</dc:source><dc:date>2010-03-08</dc:date><prism:publicationName>Journal of Clinical Lipidology</prism:publicationName><prism:publicationDate>2010-03-08</prism:publicationDate><prism:volume>4</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1933-2874(10)X0004-6</prism:issueIdentifier><prism:section>Letters to the Editor</prism:section><prism:startingPage>196</prism:startingPage><prism:endingPage>197</prism:endingPage></item><item rdf:about="http://www.lipidjournal.com/article/PIIS193328741000108X/abstract?rss=yes"><title>Extended-Release Niacin/Laropiprant Lowers Serum Phosphorus Concentrations in Patients with Type 2 Diabetes and Mild Hyperphosphatemia</title><link>http://www.lipidjournal.com/article/PIIS193328741000108X/abstract?rss=yes</link><description>Synopsis: In type 2 diabetics (T2D) with normal renal function, serum phosphorus (P) concentrations have been reported as a strong, independent predictor of cardiovascular disease mortality. Calcium salts, despite their efficacy as a phosphate-lowering treatment in advanced chronic kidney disease (CKD), can enhance vascular calcification, which may be particularly problematic in T2D. Uncontrolled studies and two small, limited duration placebo-controlled trials indicate that niacin compounds lower serum P concentrations in patients with end-stage renal disease (ie, stage 5 CKD, an estimated glomerular filtration rate [eGFR] &lt; 15 ml/min/1.73 m2). Such data are complemented by mechanistic studies indicating that niacin causes direct inhibition of sodium-dependent, active intestinal phosphate transport.</description><dc:title>Extended-Release Niacin/Laropiprant Lowers Serum Phosphorus Concentrations in Patients with Type 2 Diabetes and Mild Hyperphosphatemia</dc:title><dc:creator>Andrew G. Bostom, Alexandra MacLean, Darbie Maccubbin, Diane Tipping, Hilde Gizek, William Hanlon</dc:creator><dc:identifier>10.1016/j.jacl.2010.03.009</dc:identifier><dc:source>Journal of Clinical Lipidology 4, 3 (2010)</dc:source><dc:date>2010-05-01</dc:date><prism:publicationName>Journal of Clinical Lipidology</prism:publicationName><prism:publicationDate>2010-05-01</prism:publicationDate><prism:volume>4</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1933-2874(10)X0004-6</prism:issueIdentifier><prism:section>Abstracts</prism:section><prism:startingPage>198</prism:startingPage><prism:endingPage>199</prism:endingPage></item><item rdf:about="http://www.lipidjournal.com/article/PIIS1933287410001091/abstract?rss=yes"><title>Efficacy and Selectivity of a Direct Absorption of Lipoproteins Apheresis System in Familial Hypercholesterolemic Omani Patients</title><link>http://www.lipidjournal.com/article/PIIS1933287410001091/abstract?rss=yes</link><description>Synopsis: Direct absorption of lipoproteins (DALI) has been shown as an effective means of apolipoprotein B (apoB)-containing lipoprotein removal from whole blood in patients with familial hypercholesterolemia.</description><dc:title>Efficacy and Selectivity of a Direct Absorption of Lipoproteins Apheresis System in Familial Hypercholesterolemic Omani Patients</dc:title><dc:creator>Khalid Humaid Alrasadi, Ali Talib Al-Hinai</dc:creator><dc:identifier>10.1016/j.jacl.2010.03.010</dc:identifier><dc:source>Journal of Clinical Lipidology 4, 3 (2010)</dc:source><dc:date>2010-05-01</dc:date><prism:publicationName>Journal of Clinical Lipidology</prism:publicationName><prism:publicationDate>2010-05-01</prism:publicationDate><prism:volume>4</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1933-2874(10)X0004-6</prism:issueIdentifier><prism:section>Abstracts</prism:section><prism:startingPage>199</prism:startingPage><prism:endingPage>199</prism:endingPage></item><item rdf:about="http://www.lipidjournal.com/article/PIIS1933287410001108/abstract?rss=yes"><title>A New Method to Evaluate the Hydrophility of Serum Lipoproteins</title><link>http://www.lipidjournal.com/article/PIIS1933287410001108/abstract?rss=yes</link><description>Synopsis: Serum lipoproteins are micellar structured particles with a hydrophobic core and a hydrated hydrophilic surface, caused by the dipolar character of water molecules. The structure of the vascular endothelium surface is similar: a hydrated layer with hydrophilic parts inside and hydrophobic parts outside the bloodstream. On the basis of the second thermodynamic law, the duration of contacts and the adherence between lipoproteins and the endothelium are prolonged at lower hydrophilic lipoproteins.</description><dc:title>A New Method to Evaluate the Hydrophility of Serum Lipoproteins</dc:title><dc:creator>Gűnter Schrot</dc:creator><dc:identifier>10.1016/j.jacl.2010.03.011</dc:identifier><dc:source>Journal of Clinical Lipidology 4, 3 (2010)</dc:source><dc:date>2010-05-01</dc:date><prism:publicationName>Journal of Clinical Lipidology</prism:publicationName><prism:publicationDate>2010-05-01</prism:publicationDate><prism:volume>4</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1933-2874(10)X0004-6</prism:issueIdentifier><prism:section>Abstracts</prism:section><prism:startingPage>199</prism:startingPage><prism:endingPage>199</prism:endingPage></item><item rdf:about="http://www.lipidjournal.com/article/PIIS193328741000111X/abstract?rss=yes"><title>Predicting the Risk of Atherothrombotic Disease with Lipid Ratios</title><link>http://www.lipidjournal.com/article/PIIS193328741000111X/abstract?rss=yes</link><description>Synopsis: The accumulation of cholesterol within the intima depends mainly on the balance between the cholesterol entering the intima (low-density lipoprotein [LDL]) and the cholesterol being removed from the intima by reverse cholesterol transport (high-density lipoprotein [HDL]). Because the accumulation of cholesterol within the intima is the main proximate cause of atherothrombotic disease (ATD), the population at risk of ATD should be predictable by the ratio between LDL and HDL—and specifically the cholesterol retention fraction (CRF, or [LDL-HDL]/LDL). The purpose of this presentation is to demonstrate that such is precisely the case and to show that the CRF is a better predictor of ATD than LDL by itself.</description><dc:title>Predicting the Risk of Atherothrombotic Disease with Lipid Ratios</dc:title><dc:creator>William E. Feeman</dc:creator><dc:identifier>10.1016/j.jacl.2010.03.012</dc:identifier><dc:source>Journal of Clinical Lipidology 4, 3 (2010)</dc:source><dc:date>2010-05-01</dc:date><prism:publicationName>Journal of Clinical Lipidology</prism:publicationName><prism:publicationDate>2010-05-01</prism:publicationDate><prism:volume>4</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1933-2874(10)X0004-6</prism:issueIdentifier><prism:section>Abstracts</prism:section><prism:startingPage>199</prism:startingPage><prism:endingPage>200</prism:endingPage></item><item rdf:about="http://www.lipidjournal.com/article/PIIS1933287410001121/abstract?rss=yes"><title>Response by Sex to Statin and Ezetimibe Versus Statin Monotherapy: Pooled Analysis from 22,913 Hyperlipidemic Patients</title><link>http://www.lipidjournal.com/article/PIIS1933287410001121/abstract?rss=yes</link><description>Synopsis: Coronary heart disease (CHD) remains the leading cause of mortality in women, highlighting the importance of preventive interventions in women.   Purpose: To assess sex-related efficacy of statin + ezetimibe (EZ) vs statin in a broad, pooled database.</description><dc:title>Response by Sex to Statin and Ezetimibe Versus Statin Monotherapy: Pooled Analysis from 22,913 Hyperlipidemic Patients</dc:title><dc:creator>Jennifer Robinson, Mary E. Hanson, Jianxin Lin, Arvind Shah, Andrew Tershakovec</dc:creator><dc:identifier>10.1016/j.jacl.2010.03.013</dc:identifier><dc:source>Journal of Clinical Lipidology 4, 3 (2010)</dc:source><dc:date>2010-05-01</dc:date><prism:publicationName>Journal of Clinical Lipidology</prism:publicationName><prism:publicationDate>2010-05-01</prism:publicationDate><prism:volume>4</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1933-2874(10)X0004-6</prism:issueIdentifier><prism:section>Abstracts</prism:section><prism:startingPage>200</prism:startingPage><prism:endingPage>200</prism:endingPage></item><item rdf:about="http://www.lipidjournal.com/article/PIIS1933287410001133/abstract?rss=yes"><title>Achievement of Specified Lipid and High-Sensitivity C-Reactive Protein Levels with Statin-Ezetimibe Versus Statin in Male and Female Patients Using Combined Data from 22,913 Patients</title><link>http://www.lipidjournal.com/article/PIIS1933287410001133/abstract?rss=yes</link><description>Synopsis: Despite documented benefits of lipid-lowering treatment in women, a considerable number of women are undertreated.   Purpose: To assess attainment of specified lipid and high-sensitivity C-reactive protein (hs-CRP) levels in men and women treated with statin + ezetimibe (EZ) vs statin in a broad, pooled database.</description><dc:title>Achievement of Specified Lipid and High-Sensitivity C-Reactive Protein Levels with Statin-Ezetimibe Versus Statin in Male and Female Patients Using Combined Data from 22,913 Patients</dc:title><dc:creator>Jennifer Robinson, Beth Abramson, Mary Hanson, Jianxin Lin, Arvind Shah, Andrew Tershakovec</dc:creator><dc:identifier>10.1016/j.jacl.2010.03.014</dc:identifier><dc:source>Journal of Clinical Lipidology 4, 3 (2010)</dc:source><dc:date>2010-05-01</dc:date><prism:publicationName>Journal of Clinical Lipidology</prism:publicationName><prism:publicationDate>2010-05-01</prism:publicationDate><prism:volume>4</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1933-2874(10)X0004-6</prism:issueIdentifier><prism:section>Abstracts</prism:section><prism:startingPage>200</prism:startingPage><prism:endingPage>201</prism:endingPage></item><item rdf:about="http://www.lipidjournal.com/article/PIIS1933287410001145/abstract?rss=yes"><title>Switching from Any Statin Brand to Ezetimibe/Simvastatin 10/20 mg is More Effective at Lowering Plasma Lipids Compared with Rosuvastatin 10 mg</title><link>http://www.lipidjournal.com/article/PIIS1933287410001145/abstract?rss=yes</link><description>Synopsis: Ezetimibe/simvastatin combination and rosuvastatin monotherapy represent two potent lipid-altering treatments for patients with hypercholesterolemia.   Purpose: This post-hoc analysis compared the effects of switching from statin monotherapy to ezetimibe/simvastatin 10/20 mg (EZE/SIMVA) vs rosuvastatin 10 mg (ROSUVA) in patient subgroups defined by the brand of prerandomization statin therapy.</description><dc:title>Switching from Any Statin Brand to Ezetimibe/Simvastatin 10/20 mg is More Effective at Lowering Plasma Lipids Compared with Rosuvastatin 10 mg</dc:title><dc:creator>Philippe Brudi, Maurizio Averna, Luc Missault, Michael Farnier, Helena Vaverkova, Margus Viigimaa, Qian Dong, Arvind Shah, William Taggart, Amy Johnson-Levonas</dc:creator><dc:identifier>10.1016/j.jacl.2010.03.015</dc:identifier><dc:source>Journal of Clinical Lipidology 4, 3 (2010)</dc:source><dc:date>2010-05-01</dc:date><prism:publicationName>Journal of Clinical Lipidology</prism:publicationName><prism:publicationDate>2010-05-01</prism:publicationDate><prism:volume>4</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1933-2874(10)X0004-6</prism:issueIdentifier><prism:section>Abstracts</prism:section><prism:startingPage>201</prism:startingPage><prism:endingPage>201</prism:endingPage></item><item rdf:about="http://www.lipidjournal.com/article/PIIS1933287410001157/abstract?rss=yes"><title>Prevalence and Pattern of Dyslipidemia in Omani Patients Undergoing Coronary Artery Bypass Surgery</title><link>http://www.lipidjournal.com/article/PIIS1933287410001157/abstract?rss=yes</link><description>Synopsis: Dyslipidemia is one of the most significant risk factors for rapid atherosclerotic attrition of saphenous vein grafts. Recent studies have shown an increased prevalence of dyslipidemia in the general population in Oman. However, no data are available in regard to the prevalence of dyslipidemia in patients undergoing coronary artery bypass graft surgery (CABG).</description><dc:title>Prevalence and Pattern of Dyslipidemia in Omani Patients Undergoing Coronary Artery Bypass Surgery</dc:title><dc:creator>Hilal Al-Sabti, Khalid H. Al-Rasadi, Mirdavron M. Mukaddirov, Ali Talib Al-Hinai</dc:creator><dc:identifier>10.1016/j.jacl.2010.03.016</dc:identifier><dc:source>Journal of Clinical Lipidology 4, 3 (2010)</dc:source><dc:date>2010-05-01</dc:date><prism:publicationName>Journal of Clinical Lipidology</prism:publicationName><prism:publicationDate>2010-05-01</prism:publicationDate><prism:volume>4</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1933-2874(10)X0004-6</prism:issueIdentifier><prism:section>Abstracts</prism:section><prism:startingPage>201</prism:startingPage><prism:endingPage>202</prism:endingPage></item><item rdf:about="http://www.lipidjournal.com/article/PIIS1933287410001169/abstract?rss=yes"><title>Aging: The New Cholesterol</title><link>http://www.lipidjournal.com/article/PIIS1933287410001169/abstract?rss=yes</link><description>Synopsis: Three generations ago, most physicians learned very little about cholesterol, and many doubted the value of treating elevated values. Six decades of double-blind controlled trials have converted cholesterol into a daily conversation piece, and a standard of care requirement for cardiovascular disease. In a similar manner today, we are faced with a global increase in aging with significant impacts on a large number of associated risk factors and illnesses that threaten to eventually overburden an already stretched healthcare system. Nevertheless, aging per se has not been examined with an appropriately intense investigational effort. Life expectancy is lengthening in every developed nation. Three quarters of babies will live to their 75th birthday, and many will reach 80 plus years.</description><dc:title>Aging: The New Cholesterol</dc:title><dc:creator>David T. Nash</dc:creator><dc:identifier>10.1016/j.jacl.2010.03.017</dc:identifier><dc:source>Journal of Clinical Lipidology 4, 3 (2010)</dc:source><dc:date>2010-05-01</dc:date><prism:publicationName>Journal of Clinical Lipidology</prism:publicationName><prism:publicationDate>2010-05-01</prism:publicationDate><prism:volume>4</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1933-2874(10)X0004-6</prism:issueIdentifier><prism:section>Abstracts</prism:section><prism:startingPage>202</prism:startingPage><prism:endingPage>202</prism:endingPage></item><item rdf:about="http://www.lipidjournal.com/article/PIIS1933287410001170/abstract?rss=yes"><title>Rise in Plasma Triglycerides: An Early Marker of Oxidative Stress in Urban Indians</title><link>http://www.lipidjournal.com/article/PIIS1933287410001170/abstract?rss=yes</link><description>Synopsis: Oxidative stress is implicated in the pathogenesis of noninsulin-dependent diabetes mellitus and coronary heart disease. At present, urban Indian subjects are at high risk for both of these conditions. Dyslipidemias characterized by 1) an increase in plasma triglycerides (TG); 2) a decrease in high-density lipoprotein cholesterol (HDL); and 3) elevated total cholesterol/HDL ratio frequently are found in this population. Urban Indians consume a high-fat diet with a high content of omega-6 fat.</description><dc:title>Rise in Plasma Triglycerides: An Early Marker of Oxidative Stress in Urban Indians</dc:title><dc:creator>Sharmila Dudani, Shivani Kalhan, Suparna Dubey, Sonia Sharma, B.S. Raheja</dc:creator><dc:identifier>10.1016/j.jacl.2010.03.018</dc:identifier><dc:source>Journal of Clinical Lipidology 4, 3 (2010)</dc:source><dc:date>2010-05-01</dc:date><prism:publicationName>Journal of Clinical Lipidology</prism:publicationName><prism:publicationDate>2010-05-01</prism:publicationDate><prism:volume>4</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1933-2874(10)X0004-6</prism:issueIdentifier><prism:section>Abstracts</prism:section><prism:startingPage>202</prism:startingPage><prism:endingPage>203</prism:endingPage></item><item rdf:about="http://www.lipidjournal.com/article/PIIS1933287410001182/abstract?rss=yes"><title>BGS Graph Predicts Better Than the Framingham Risk Score</title><link>http://www.lipidjournal.com/article/PIIS1933287410001182/abstract?rss=yes</link><description>Synopsis: The Framingham Risk Score (FRS) is a commonly used predictor of the risk of atherothrombotic disease (ATD). Multiple recent publications, which often use imaging techniques, have pointed out that the FRS fails to predict many people who already have subclinical ATD. The Bowling Green Study (BGS) has published a predictive graph that accurately predicts the population at risk of ATD, uses the same basic risk factors as does the FRS, and is determined on the basis of patient ATD outcomes.</description><dc:title>BGS Graph Predicts Better Than the Framingham Risk Score</dc:title><dc:creator>William E. Feeman</dc:creator><dc:identifier>10.1016/j.jacl.2010.03.019</dc:identifier><dc:source>Journal of Clinical Lipidology 4, 3 (2010)</dc:source><dc:date>2010-05-01</dc:date><prism:publicationName>Journal of Clinical Lipidology</prism:publicationName><prism:publicationDate>2010-05-01</prism:publicationDate><prism:volume>4</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1933-2874(10)X0004-6</prism:issueIdentifier><prism:section>Abstracts</prism:section><prism:startingPage>203</prism:startingPage><prism:endingPage>203</prism:endingPage></item><item rdf:about="http://www.lipidjournal.com/article/PIIS1933287410001194/abstract?rss=yes"><title>The Role of Innate Inflammatory Mediators in Acute Myocardial Infarction∗</title><link>http://www.lipidjournal.com/article/PIIS1933287410001194/abstract?rss=yes</link><description>Synopsis: Coronary heart disease currently accounts for 1 of every 6 deaths in the United States. In 2006, there were an estimated 1.3 million hospital admissions for acute coronary syndrome. These numbers have increased despite aggressive treatment and risk factor modification. Consequently, there is a need for better understanding of the mechanisms involved in the etiology, maturation, and destabilization of atherosclerotic plaques. Recent study has identified innate inflammatory mediators as a key component in atherosclerosis. These innate markers are markedly up-regulated in atherosclerotic tissue and receptor activation exhibits downstream atherogenic effects. During an acute myocardial infarction (AMI), the administration of a statin is associated with significant decrease in periprocedural mortality. This benefit is hypothesized to be secondary to the anti-inflammatory and/or antiplatelet pleiotropic effects of statins, including a reduction in interleukin-6 (IL-6) mRNA and protein expression. However, no data exist detailing the specific innate inflammatory mediators of an acutely ruptured plaque with resultant myocardial infarction.</description><dc:title>The Role of Innate Inflammatory Mediators in Acute Myocardial Infarction∗</dc:title><dc:creator>Joseph Thomas Poterucha, Scott W. Shurmur, Daniel R. Anderson</dc:creator><dc:identifier>10.1016/j.jacl.2010.03.020</dc:identifier><dc:source>Journal of Clinical Lipidology 4, 3 (2010)</dc:source><dc:date>2010-05-01</dc:date><prism:publicationName>Journal of Clinical Lipidology</prism:publicationName><prism:publicationDate>2010-05-01</prism:publicationDate><prism:volume>4</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1933-2874(10)X0004-6</prism:issueIdentifier><prism:section>Abstracts</prism:section><prism:startingPage>203</prism:startingPage><prism:endingPage>204</prism:endingPage></item><item rdf:about="http://www.lipidjournal.com/article/PIIS1933287410001200/abstract?rss=yes"><title>Blood Sugar Levels are Not Necessary to Predict the Population at Risk for Atherothrombotic Disease</title><link>http://www.lipidjournal.com/article/PIIS1933287410001200/abstract?rss=yes</link><description>Synopsis: Diabetes is considered to be a “coronary heart disease equivalent.” However, the risk of atherothrombotic disease (ATD) is not equal among all diabetics, and milder elevations of blood sugar are not in and of themselves causal for ATD. It is important to define the risk, if any, in patients with blood sugar elevations.</description><dc:title>Blood Sugar Levels are Not Necessary to Predict the Population at Risk for Atherothrombotic Disease</dc:title><dc:creator>William E. Feeman</dc:creator><dc:identifier>10.1016/j.jacl.2010.03.021</dc:identifier><dc:source>Journal of Clinical Lipidology 4, 3 (2010)</dc:source><dc:date>2010-05-01</dc:date><prism:publicationName>Journal of Clinical Lipidology</prism:publicationName><prism:publicationDate>2010-05-01</prism:publicationDate><prism:volume>4</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1933-2874(10)X0004-6</prism:issueIdentifier><prism:section>Abstracts</prism:section><prism:startingPage>204</prism:startingPage><prism:endingPage>204</prism:endingPage></item><item rdf:about="http://www.lipidjournal.com/article/PIIS1933287410001212/abstract?rss=yes"><title>Efficacy of Switching from Statin Monotherapy to Ezetimibe/Simvastatin 10/20 mg Versus Rosuvastatin 10 mg in High-Risk Patients Analyzed by Baseline LDL-C</title><link>http://www.lipidjournal.com/article/PIIS1933287410001212/abstract?rss=yes</link><description>Synopsis: Ezetimibe/simvastatin combination and rosuvastatin monotherapy represent two potent lipid-altering treatments for patients with hypercholesterolemia.   Purpose: This post-hoc analysis compared effects of switching from statins to ezetimibe/simvastatin 10/20 mg (EZE/SIMVA) vs rosuvastatin 10 mg (ROSUVA) in subgroups defined by LDL-C at baseline: Q1 (&lt;2.87 mmol/L) n = 165, Q2 (&gt;2.87 and &lt;3.19 mmol/L) n = 151, Q3 (&gt;3.19 and &lt;3.55 mmol/L) n = 150, and Q4 (&gt;3.55 mmol/L) n = 152.</description><dc:title>Efficacy of Switching from Statin Monotherapy to Ezetimibe/Simvastatin 10/20 mg Versus Rosuvastatin 10 mg in High-Risk Patients Analyzed by Baseline LDL-C</dc:title><dc:creator>Philippe Brudi, Maurizio Averna, Michael Farnier, Luc Missault, Helena Vaverkova, Margus Viigimaa, Qian Dong, Arvind Shah, William Taggart, Amy O. Johnson-Levonas</dc:creator><dc:identifier>10.1016/j.jacl.2010.03.022</dc:identifier><dc:source>Journal of Clinical Lipidology 4, 3 (2010)</dc:source><dc:date>2010-05-01</dc:date><prism:publicationName>Journal of Clinical Lipidology</prism:publicationName><prism:publicationDate>2010-05-01</prism:publicationDate><prism:volume>4</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1933-2874(10)X0004-6</prism:issueIdentifier><prism:section>Abstracts</prism:section><prism:startingPage>204</prism:startingPage><prism:endingPage>205</prism:endingPage></item><item rdf:about="http://www.lipidjournal.com/article/PIIS1933287410001224/abstract?rss=yes"><title>Switching from Statin Monotherapy to EZE/Simva or Rosuva Modifies Apo B, LDL-C, and non-HDL-C Correlations in Patients at High Risk of Coronary Disease</title><link>http://www.lipidjournal.com/article/PIIS1933287410001224/abstract?rss=yes</link><description>Synopsis: A consensus conference report issued by American Diabetes Association and the American College of Cardiology Foundation (ADA/ACCF) recommends LDL cholesterol (LDL-C), non-HDL cholesterol (non-HDL-C), and apolipoprotein B (apoB) treatment goals for patients with cardiometabolic risk.</description><dc:title>Switching from Statin Monotherapy to EZE/Simva or Rosuva Modifies Apo B, LDL-C, and non-HDL-C Correlations in Patients at High Risk of Coronary Disease</dc:title><dc:creator>Philippe Brudi, Helena Vaverkova, Michael Farnier, Qian Dong, Amy O. Johnson-Levonas, Arvind Shah</dc:creator><dc:identifier>10.1016/j.jacl.2010.03.023</dc:identifier><dc:source>Journal of Clinical Lipidology 4, 3 (2010)</dc:source><dc:date>2010-05-01</dc:date><prism:publicationName>Journal of Clinical Lipidology</prism:publicationName><prism:publicationDate>2010-05-01</prism:publicationDate><prism:volume>4</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1933-2874(10)X0004-6</prism:issueIdentifier><prism:section>Abstracts</prism:section><prism:startingPage>205</prism:startingPage><prism:endingPage>205</prism:endingPage></item><item rdf:about="http://www.lipidjournal.com/article/PIIS1933287410001236/abstract?rss=yes"><title>The Ability of Therapy with Ezetimibe/Simvastatin or Ezetimibe/Simvastatin/Fenofibrate to Achieve Lipid Targets in Mixed Dyslipidemic Patients</title><link>http://www.lipidjournal.com/article/PIIS1933287410001236/abstract?rss=yes</link><description>Synopsis: It has been recommended that high-risk patients with mixed hyperlipidemia be treated to a low-density lipoprotein-cholesterol (LDL-C) goal &lt;100 mg/dL, a non-high-density lipoprotein-cholesterol (non-HDL-C) goal &lt;130 mg/dL, and an apolipoprotein B (apoB) goal &lt;90 mg/dL. Aggressive treatments decreasing atherogenic lipoproteins can induce a shift in the correlations between apoB and LDL-C or non-HDL-C.</description><dc:title>The Ability of Therapy with Ezetimibe/Simvastatin or Ezetimibe/Simvastatin/Fenofibrate to Achieve Lipid Targets in Mixed Dyslipidemic Patients</dc:title><dc:creator>Michael Farnier, William Taggart, Jianxin Lin, Arvind Shah, Philippe Brudi</dc:creator><dc:identifier>10.1016/j.jacl.2010.03.024</dc:identifier><dc:source>Journal of Clinical Lipidology 4, 3 (2010)</dc:source><dc:date>2010-05-01</dc:date><prism:publicationName>Journal of Clinical Lipidology</prism:publicationName><prism:publicationDate>2010-05-01</prism:publicationDate><prism:volume>4</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1933-2874(10)X0004-6</prism:issueIdentifier><prism:section>Abstracts</prism:section><prism:startingPage>205</prism:startingPage><prism:endingPage>206</prism:endingPage></item><item rdf:about="http://www.lipidjournal.com/article/PIIS1933287410001248/abstract?rss=yes"><title>Improvements in Lipid Ratios with the Combination of Rosuvastatin 5 mg and Fenofibric Acid 135 mg in Patients with Mixed Dyslipidemia</title><link>http://www.lipidjournal.com/article/PIIS1933287410001248/abstract?rss=yes</link><description>Synopsis: Ratios of atherogenic to nonatherogenic lipid parameters are strong predictors of coronary heart disease (CHD) risk, particularly in patients with mixed dyslipidemia, and combination therapy may be needed to simultaneously improve multiple atherogenic parameters. A previous study showed that treatment with rosuvastatin (R) 10 mg + fenofibric acid 135 mg (FA) for 12 weeks significantly improved total cholesterol (TC)/high-density lipoprotein cholesterol (HDL-C; −43.3% vs −36.1% and −21.1%), non-HDL-C/HDL-C (−50.9% vs −42.3% and −24.8%) and TG/HDL-C (−53.2% vs −26.8% and −35.1%) ratios compared with R 10 mg and FA monotherapy, respectively. In the same study, greater improvements with R 20 mg + FA were noted in TC/HDL-C (−43.9% vs −41.7% and -21.1%), non-HDL-C/HDL-C (−51.6% vs −49.1% and −24.8%) and TG/HDL-C (−49.8% vs −28.4% and −35.1%) ratios compared with R 20 mg and FA monotherapy, respectively.</description><dc:title>Improvements in Lipid Ratios with the Combination of Rosuvastatin 5 mg and Fenofibric Acid 135 mg in Patients with Mixed Dyslipidemia</dc:title><dc:creator>Robert S. Rosenson, Maureen T. Kelly, Carolyn M. Setze, Alex Gold, Michael Cressman, James C. Stolzenbach, Laura A. Williams</dc:creator><dc:identifier>10.1016/j.jacl.2010.03.025</dc:identifier><dc:source>Journal of Clinical Lipidology 4, 3 (2010)</dc:source><dc:date>2010-05-01</dc:date><prism:publicationName>Journal of Clinical Lipidology</prism:publicationName><prism:publicationDate>2010-05-01</prism:publicationDate><prism:volume>4</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1933-2874(10)X0004-6</prism:issueIdentifier><prism:section>Abstracts</prism:section><prism:startingPage>206</prism:startingPage><prism:endingPage>206</prism:endingPage></item><item rdf:about="http://www.lipidjournal.com/article/PIIS193328741000125X/abstract?rss=yes"><title>Simultaneous Achievement of Optimal Lipid Targets with the Combination of Rosuvastatin 5 mg + Fenofibric Acid 135 mg in Patients with Mixed Dyslipidemia</title><link>http://www.lipidjournal.com/article/PIIS193328741000125X/abstract?rss=yes</link><description>Synopsis: Mixed dyslipidemia is characterized by multiple lipid abnormalities, including low high-density lipoprotein cholesterol (HDL-C) and high low-density lipoprotein cholesterol (LDL-C), triglyceride (TG), non-HDL-C, and apolipoprotein B (apoB). Along with LDL-C, guidelines advocate the use of combination therapy to treat other lipids that contribute to cardiovascular risk. The optimal targets are LDL-C &lt;100 mg/dL, non-HDL-C &lt;130 mg/dL, HDL-C &gt;40 mg/dL (&gt;50 mg/dL women), TG &lt;150 mg/dL, and apoB &lt;90 mg/dL. In a previous study, a greater percentage of patients treated with rosuvastatin (R) 10 mg + fenofibric acid 135 mg (FA) for 12 weeks simultaneously achieved targets of LDL-C and non-HDL-C (55.8% vs 47.3% and 3.1%); HDL-C, TG, and LDL-C (25.5% vs 8.2% and 2.7%); and HDL-C, TG, LDL-C, non-HDL-C, and apoB (23.4% vs 8.2% and 2.7%) than R 10 mg or FA monotherapy, respectively. In addition, a greater percentage of patients treated with R 20 mg + FA achieved targets of HDL-C, TG, and LDL-C (26.0% vs 9.1%); and HDL-C, TG, LDL-C, non-HDL-C, and apoB (25.5% vs 8.7%) than R 20 mg.</description><dc:title>Simultaneous Achievement of Optimal Lipid Targets with the Combination of Rosuvastatin 5 mg + Fenofibric Acid 135 mg in Patients with Mixed Dyslipidemia</dc:title><dc:creator>Robert S. Rosenson, Maureen T. Kelly, Carolyn M. Setze, Alex Gold, Michael Cressman, James C. Stolzenbach, Laura A. Williams</dc:creator><dc:identifier>10.1016/j.jacl.2010.03.026</dc:identifier><dc:source>Journal of Clinical Lipidology 4, 3 (2010)</dc:source><dc:date>2010-05-01</dc:date><prism:publicationName>Journal of Clinical Lipidology</prism:publicationName><prism:publicationDate>2010-05-01</prism:publicationDate><prism:volume>4</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1933-2874(10)X0004-6</prism:issueIdentifier><prism:section>Abstracts</prism:section><prism:startingPage>206</prism:startingPage><prism:endingPage>207</prism:endingPage></item><item rdf:about="http://www.lipidjournal.com/article/PIIS1933287410001261/abstract?rss=yes"><title>Stability of Lipid Responses to Prescription Omega-3 Acid Ethyl Esters Plus Simvastatin Over Two Years</title><link>http://www.lipidjournal.com/article/PIIS1933287410001261/abstract?rss=yes</link><description>Synopsis: Combination therapy of prescription omega-3 acid ethyl esters (P-OM3) with simvastatin is effective for improving the lipid profile in subjects with mixed dyslipidemia. A recent investigation demonstrated the efficacy of combined therapy using simvastatin 80 mg/d for 6 weeks, but limited data are available on long-term treatment.</description><dc:title>Stability of Lipid Responses to Prescription Omega-3 Acid Ethyl Esters Plus Simvastatin Over Two Years</dc:title><dc:creator>Kevin Carl Maki, William S. Harris, Barry C. Lubin, Matthew S. Reeves, Mary R. Dicklin</dc:creator><dc:identifier>10.1016/j.jacl.2010.03.027</dc:identifier><dc:source>Journal of Clinical Lipidology 4, 3 (2010)</dc:source><dc:date>2010-05-01</dc:date><prism:publicationName>Journal of Clinical Lipidology</prism:publicationName><prism:publicationDate>2010-05-01</prism:publicationDate><prism:volume>4</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1933-2874(10)X0004-6</prism:issueIdentifier><prism:section>Abstracts</prism:section><prism:startingPage>207</prism:startingPage><prism:endingPage>207</prism:endingPage></item><item rdf:about="http://www.lipidjournal.com/article/PIIS1933287410001273/abstract?rss=yes"><title>Ezetimibe/Simvastatin 10/20 mg Versus Rosuvastatin 10 mg in High Risk Hypercholesterolemic Patients Stratified by Previous Statin Treatment Potency</title><link>http://www.lipidjournal.com/article/PIIS1933287410001273/abstract?rss=yes</link><description>Synopsis: Despite substantial low-density lipoprotein cholesterol (LDL-C) lowering associated with the use of statins, a considerable number of patients require LDL-C lowering beyond that achieved by currently used statin therapies.</description><dc:title>Ezetimibe/Simvastatin 10/20 mg Versus Rosuvastatin 10 mg in High Risk Hypercholesterolemic Patients Stratified by Previous Statin Treatment Potency</dc:title><dc:creator>Michael Farnier, Margus Viigimaa, Helena Vaverkova, Maurizio Averna, Luc Missault, Qian Dong, Arvind Shah, Mary E. Hanson, Andrew M. Tershakovec</dc:creator><dc:identifier>10.1016/j.jacl.2010.03.028</dc:identifier><dc:source>Journal of Clinical Lipidology 4, 3 (2010)</dc:source><dc:date>2010-05-01</dc:date><prism:publicationName>Journal of Clinical Lipidology</prism:publicationName><prism:publicationDate>2010-05-01</prism:publicationDate><prism:volume>4</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1933-2874(10)X0004-6</prism:issueIdentifier><prism:section>Abstracts</prism:section><prism:startingPage>207</prism:startingPage><prism:endingPage>208</prism:endingPage></item><item rdf:about="http://www.lipidjournal.com/article/PIIS1933287410001285/abstract?rss=yes"><title>Clinical Pharmacist Services Significantly Increase Low-Density Lipoprotein Cholesterol Goal Attainment in an Outpatient-Based Lipid Clinic</title><link>http://www.lipidjournal.com/article/PIIS1933287410001285/abstract?rss=yes</link><description>Synopsis: The L-TAP study demonstrated that only 38% of all patients and only 18% of patients with coronary heart disease (CHD) achieved their target low-density lipoprotein cholesterol (LDL-C) goals. Eight years later, the NEPTUNE II study demonstrated increased rates of LDL-C goal attainment to 67% overall. Of that number, 89% of the low-risk patients (0–1 NCEP III risk factors), 76% of moderate to moderately high-risk patients (≥2 risk factors), and 57% of high-risk patients (CHD or CHD risk equivalent) achieved their LDL-C goals. Only 18% of very-high-risk patients achieved their LDL-C goals; however, this was a relatively new concept at the time the NEPTUNE II study was published. Although this is a vast improvement since the L-TAP study, there is still room to do better, especially in our high-risk and very-high-risk patients. Perhaps a collaborative care model with clinical pharmacists can improve LDL-C goal attainment.</description><dc:title>Clinical Pharmacist Services Significantly Increase Low-Density Lipoprotein Cholesterol Goal Attainment in an Outpatient-Based Lipid Clinic</dc:title><dc:creator>Eric K. Gupta</dc:creator><dc:identifier>10.1016/j.jacl.2010.03.029</dc:identifier><dc:source>Journal of Clinical Lipidology 4, 3 (2010)</dc:source><dc:date>2010-05-01</dc:date><prism:publicationName>Journal of Clinical Lipidology</prism:publicationName><prism:publicationDate>2010-05-01</prism:publicationDate><prism:volume>4</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1933-2874(10)X0004-6</prism:issueIdentifier><prism:section>Abstracts</prism:section><prism:startingPage>208</prism:startingPage><prism:endingPage>208</prism:endingPage></item><item rdf:about="http://www.lipidjournal.com/article/PIIS1933287410001297/abstract?rss=yes"><title>Effects of Vitamin D Supplementation on 25-Hydroxyvitamin D and Markers of Cardiovascular Disease Risk in Subjects with High Waist Circumference</title><link>http://www.lipidjournal.com/article/PIIS1933287410001297/abstract?rss=yes</link><description>Synopsis: Observational studies have shown an inverse relationship between circulating 25-hydroxyvitamin D [25(OH)D] and the incidence of cardiovascular disease (CVD), and we recently reported a strong positive relationship between serum 25(OH)D and high-density lipoprotein cholesterol (HDL-C) concentration.</description><dc:title>Effects of Vitamin D Supplementation on 25-Hydroxyvitamin D and Markers of Cardiovascular Disease Risk in Subjects with High Waist Circumference</dc:title><dc:creator>Kevin Carl Maki, Martyn R. Rubin, Les G. Wong, Jamie F. McManus, Christopher D. Jensen, Rachel Hubacher, Andrea Lawless</dc:creator><dc:identifier>10.1016/j.jacl.2010.03.030</dc:identifier><dc:source>Journal of Clinical Lipidology 4, 3 (2010)</dc:source><dc:date>2010-05-01</dc:date><prism:publicationName>Journal of Clinical Lipidology</prism:publicationName><prism:publicationDate>2010-05-01</prism:publicationDate><prism:volume>4</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1933-2874(10)X0004-6</prism:issueIdentifier><prism:section>Abstracts</prism:section><prism:startingPage>208</prism:startingPage><prism:endingPage>209</prism:endingPage></item><item rdf:about="http://www.lipidjournal.com/article/PIIS1933287410001303/abstract?rss=yes"><title>Predictors of Anterior and Posterior Wall Carotid Intima Media Thickness Progression in Men and Women at Moderate Risk of Coronary Heart Disease</title><link>http://www.lipidjournal.com/article/PIIS1933287410001303/abstract?rss=yes</link><description>Synopsis: Early detection of arterial wall thickening, the subclinical phase of atherosclerosis, may be useful for identifying individuals at risk for future cardiovascular events. Carotid intima media thickness (CIMT)-assessed rate of atherosclerosis progression is a risk factor for clinical cardiovascular events, but the relationships between various coronary heart disease (CHD) risk factors and CIMT progression are unclear.</description><dc:title>Predictors of Anterior and Posterior Wall Carotid Intima Media Thickness Progression in Men and Women at Moderate Risk of Coronary Heart Disease</dc:title><dc:creator>Kevin Carl Maki, Michael H. Davidson, Mary R. Dicklin, Marjorie Bell</dc:creator><dc:identifier>10.1016/j.jacl.2010.03.031</dc:identifier><dc:source>Journal of Clinical Lipidology 4, 3 (2010)</dc:source><dc:date>2010-05-01</dc:date><prism:publicationName>Journal of Clinical Lipidology</prism:publicationName><prism:publicationDate>2010-05-01</prism:publicationDate><prism:volume>4</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1933-2874(10)X0004-6</prism:issueIdentifier><prism:section>Abstracts</prism:section><prism:startingPage>209</prism:startingPage><prism:endingPage>209</prism:endingPage></item><item rdf:about="http://www.lipidjournal.com/article/PIIS1933287410001315/abstract?rss=yes"><title>Omega-3 Fatty Acid Nutritional Labeling Content of Dietary Fish Oil Supplements: A Systematic Review∗</title><link>http://www.lipidjournal.com/article/PIIS1933287410001315/abstract?rss=yes</link><description>Synopsis: Prescription grade omega-3 fatty acids (P-OM3 FA) are approved by the Food and Drug Administration (FDA) for the treatment of hypertriglyceridemia (&gt;500 mg/dL). However, not all managed-care organizations have P-OM3 FA on their medication formulary or it may be considered step-therapy where the copayment may be cost-prohibitive for certain patients. Thus, patients are often left to purchase dietary fish oil supplements as a non-FDA approved alternative. The content of EPA and DHA in the dietary fish oil products varies widely and these products are not regulated by the FDA. As a result, patients' lipid responses may be suboptimal due to inadequate doses of EPA and DHA.</description><dc:title>Omega-3 Fatty Acid Nutritional Labeling Content of Dietary Fish Oil Supplements: A Systematic Review∗</dc:title><dc:creator>Atanaz Zargar, Matthew K. Ito</dc:creator><dc:identifier>10.1016/j.jacl.2010.03.032</dc:identifier><dc:source>Journal of Clinical Lipidology 4, 3 (2010)</dc:source><dc:date>2010-05-01</dc:date><prism:publicationName>Journal of Clinical Lipidology</prism:publicationName><prism:publicationDate>2010-05-01</prism:publicationDate><prism:volume>4</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1933-2874(10)X0004-6</prism:issueIdentifier><prism:section>Abstracts</prism:section><prism:startingPage>209</prism:startingPage><prism:endingPage>210</prism:endingPage></item><item rdf:about="http://www.lipidjournal.com/article/PIIS1933287410001327/abstract?rss=yes"><title>Atherogenic High-Density Lipoprotein in Subjects with Hyperalphalipoproteinemia</title><link>http://www.lipidjournal.com/article/PIIS1933287410001327/abstract?rss=yes</link><description>Synopsis: We have identified a high-density lipoprotein (HDL) phenotype in a cohort of adult patients with coronary heart disease and hyperalphalipoproteinemia (HALP) that appears to promote atherosclerosis on the basis of its in vitro properties.</description><dc:title>Atherogenic High-Density Lipoprotein in Subjects with Hyperalphalipoproteinemia</dc:title><dc:creator>Catherine Janise McNeal, Craig Larner, Subroto Chatterjee, London Worthy, Ronald Macfarlane, Simon Sheather, Petar Alaupovic</dc:creator><dc:identifier>10.1016/j.jacl.2010.03.033</dc:identifier><dc:source>Journal of Clinical Lipidology 4, 3 (2010)</dc:source><dc:date>2010-05-01</dc:date><prism:publicationName>Journal of Clinical Lipidology</prism:publicationName><prism:publicationDate>2010-05-01</prism:publicationDate><prism:volume>4</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1933-2874(10)X0004-6</prism:issueIdentifier><prism:section>Abstracts</prism:section><prism:startingPage>210</prism:startingPage><prism:endingPage>210</prism:endingPage></item><item rdf:about="http://www.lipidjournal.com/article/PIIS1933287410001339/abstract?rss=yes"><title>Long-Term Efficacy of Rosuvastatin and Fenofibric Acid 20 mg/135 mg in Dyslipidemic Patients Initially Treated with Rosuvastatin and Fenofibric Acid 10 mg/135 mg</title><link>http://www.lipidjournal.com/article/PIIS1933287410001339/abstract?rss=yes</link><description>Synopsis: The efficacy and safety of combination therapy with rosuvastatin and fenofibric acid were demonstrated in a 12-week, controlled study of patients with mixed dyslipidemia randomized to rosuvastatin 10, 20, or 40 mg; fenofibric acid 135 mg; or the combination of rosuvastatin and fenofibric acid (R/FA; 10/135 or 20/135 mg). A subsequent 52-week open-label extension study included an evaluation of the long-term efficacy and safety of R/FA 20/135 mg.</description><dc:title>Long-Term Efficacy of Rosuvastatin and Fenofibric Acid 20 mg/135 mg in Dyslipidemic Patients Initially Treated with Rosuvastatin and Fenofibric Acid 10 mg/135 mg</dc:title><dc:creator>Keith C. Ferdinand, Michael H. Davidson, Maureen T. Kelly, Carolyn M. Setze, Rick Schiebinger, Darryl J. Sleep</dc:creator><dc:identifier>10.1016/j.jacl.2010.03.034</dc:identifier><dc:source>Journal of Clinical Lipidology 4, 3 (2010)</dc:source><dc:date>2010-05-01</dc:date><prism:publicationName>Journal of Clinical Lipidology</prism:publicationName><prism:publicationDate>2010-05-01</prism:publicationDate><prism:volume>4</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1933-2874(10)X0004-6</prism:issueIdentifier><prism:section>Abstracts</prism:section><prism:startingPage>210</prism:startingPage><prism:endingPage>211</prism:endingPage></item><item rdf:about="http://www.lipidjournal.com/article/PIIS1933287410001340/abstract?rss=yes"><title>Effects of an Insoluble Fraction of Soy Protein Versus Milk Protein on Plasma Lipids and Fecal Bile Acids in Men and Women with Hypercholesterolemia</title><link>http://www.lipidjournal.com/article/PIIS1933287410001340/abstract?rss=yes</link><description>Synopsis: Soy protein consumption is associated with reductions in plasma cholesterol. Some studies have also indicated that consumption of low-fat dairy products can reduce plasma lipids, but the mechanisms for these effects are poorly understood.</description><dc:title>Effects of an Insoluble Fraction of Soy Protein Versus Milk Protein on Plasma Lipids and Fecal Bile Acids in Men and Women with Hypercholesterolemia</dc:title><dc:creator>Kevin Carl Maki, Dustie N. Butteiger, Tia M. Rains, Matthew S. Reeves, Chuck Schasteen, Elaine S. Krul</dc:creator><dc:identifier>10.1016/j.jacl.2010.03.035</dc:identifier><dc:source>Journal of Clinical Lipidology 4, 3 (2010)</dc:source><dc:date>2010-05-01</dc:date><prism:publicationName>Journal of Clinical Lipidology</prism:publicationName><prism:publicationDate>2010-05-01</prism:publicationDate><prism:volume>4</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1933-2874(10)X0004-6</prism:issueIdentifier><prism:section>Abstracts</prism:section><prism:startingPage>211</prism:startingPage><prism:endingPage>211</prism:endingPage></item><item rdf:about="http://www.lipidjournal.com/article/PIIS1933287410001352/abstract?rss=yes"><title>A Plant Sterol/Stanol Supplement in Tablet Form Lowers Low-Density Lipoprotein and Non-High-Density Lipoprotein Cholesterol in Men and Women with Primary Hypercholesterolemia</title><link>http://www.lipidjournal.com/article/PIIS1933287410001352/abstract?rss=yes</link><description>Synopsis: Plant sterols and stanols (1.0 to 3.0 g/d) have been shown to lower total cholesterol (TC), non−high-density lipoprotein cholesterol (non-HDL-C) and low-density lipoprotein cholesterol (LDL-C). Meta-analyses suggest LDL-C reductions of ∼4% per g of plant sterol/stanol. Most previous studies have administered plant sterols/stanols in food forms.</description><dc:title>A Plant Sterol/Stanol Supplement in Tablet Form Lowers Low-Density Lipoprotein and Non-High-Density Lipoprotein Cholesterol in Men and Women with Primary Hypercholesterolemia</dc:title><dc:creator>Kevin Carl Maki, Andrea Lawless, Matthew S. Reeves, Mary R. Dicklin, Belinda H. Jenks, Ed Shneyvas, James Brooks</dc:creator><dc:identifier>10.1016/j.jacl.2010.03.036</dc:identifier><dc:source>Journal of Clinical Lipidology 4, 3 (2010)</dc:source><dc:date>2010-05-01</dc:date><prism:publicationName>Journal of Clinical Lipidology</prism:publicationName><prism:publicationDate>2010-05-01</prism:publicationDate><prism:volume>4</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1933-2874(10)X0004-6</prism:issueIdentifier><prism:section>Abstracts</prism:section><prism:startingPage>211</prism:startingPage><prism:endingPage>212</prism:endingPage></item><item rdf:about="http://www.lipidjournal.com/article/PIIS1933287410001364/abstract?rss=yes"><title>A Variant of the LPA Gene Predicts Cardiovascular Event Reduction by Aspirin Therapy in a Primary Prevention Setting</title><link>http://www.lipidjournal.com/article/PIIS1933287410001364/abstract?rss=yes</link><description>Synopsis: The risk/benefit ratio of aspirin therapy in primary prevention of cardiovascular disease does not justify the use of aspirin. The 4399Met variant of the LPA gene—a gene that encodes apolipoprotein(a)—can help identify those who may have an acceptable risk/benefit ratio for aspirin therapy in a primary prevention setting.</description><dc:title>A Variant of the LPA Gene Predicts Cardiovascular Event Reduction by Aspirin Therapy in a Primary Prevention Setting</dc:title><dc:creator>Robert H. Superko, Dov Shiffman, James J. Devlin</dc:creator><dc:identifier>10.1016/j.jacl.2010.03.037</dc:identifier><dc:source>Journal of Clinical Lipidology 4, 3 (2010)</dc:source><dc:date>2010-05-01</dc:date><prism:publicationName>Journal of Clinical Lipidology</prism:publicationName><prism:publicationDate>2010-05-01</prism:publicationDate><prism:volume>4</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1933-2874(10)X0004-6</prism:issueIdentifier><prism:section>Abstracts</prism:section><prism:startingPage>212</prism:startingPage><prism:endingPage>212</prism:endingPage></item><item rdf:about="http://www.lipidjournal.com/article/PIIS1933287410001376/abstract?rss=yes"><title>Adding Niacin Extended-Release (NER) to Simvastatin Improves Apolipoprotein B (apoB), apoA-I, the apoB:A-I Ratio, and Lipid Goal Attainment in the Highest-Risk Cardiometabolic Patients</title><link>http://www.lipidjournal.com/article/PIIS1933287410001376/abstract?rss=yes</link><description>Synopsis: Several studies suggest that apolipoprotein B (apoB) and the apoB:A-I ratio provide a better assessment of cardiovascular disease risk than LDL-C alone. This may be particularly important in patients with diabetic or atherogenic dyslipidemia characterized by decreased HDL-C and increased numbers of small dense LDL particles as identified by increased apoB levels. A treatment goal of apoB &lt;80 mg/dL is recommended by the 2008 ADD/ACC consensus statement for patients at highest cardiometabolic risk, defined as having known CVD or diabetes and ≥1 major CVD risk factors.</description><dc:title>Adding Niacin Extended-Release (NER) to Simvastatin Improves Apolipoprotein B (apoB), apoA-I, the apoB:A-I Ratio, and Lipid Goal Attainment in the Highest-Risk Cardiometabolic Patients</dc:title><dc:creator>Thao T. Doan, Ping Jiang, Roopal B. Thakkar, Moti L. Kashyap, Michael H. Davidson</dc:creator><dc:identifier>10.1016/j.jacl.2010.03.038</dc:identifier><dc:source>Journal of Clinical Lipidology 4, 3 (2010)</dc:source><dc:date>2010-05-01</dc:date><prism:publicationName>Journal of Clinical Lipidology</prism:publicationName><prism:publicationDate>2010-05-01</prism:publicationDate><prism:volume>4</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1933-2874(10)X0004-6</prism:issueIdentifier><prism:section>Abstracts</prism:section><prism:startingPage>212</prism:startingPage><prism:endingPage>213</prism:endingPage></item><item rdf:about="http://www.lipidjournal.com/article/PIIS1933287410001388/abstract?rss=yes"><title>Efficacy and Safety of Fixed-Dose Rosuvastatin/Fenofibric Acid Versus Simvastatin Monotherapy in Patients with Elevated Low-Density Lipoprotein Cholesterol and Triglycerides</title><link>http://www.lipidjournal.com/article/PIIS1933287410001388/abstract?rss=yes</link><description>Synopsis: Combination therapy with a statin and a fibrate is one of the treatment options to manage multiple lipid abnormalities in patients with hypercholesterolemia and elevated triglycerides (TG).</description><dc:title>Efficacy and Safety of Fixed-Dose Rosuvastatin/Fenofibric Acid Versus Simvastatin Monotherapy in Patients with Elevated Low-Density Lipoprotein Cholesterol and Triglycerides</dc:title><dc:creator>Eli M. Roth, James M. McKenney, Maureen T. Kelly, Carolyn M. Setze, Dawn M. Carlson, Alex Gold, Michael Cressman, James C. Stolzenbach, Laura A. Williams, Peter H. Jones</dc:creator><dc:identifier>10.1016/j.jacl.2010.03.039</dc:identifier><dc:source>Journal of Clinical Lipidology 4, 3 (2010)</dc:source><dc:date>2010-05-01</dc:date><prism:publicationName>Journal of Clinical Lipidology</prism:publicationName><prism:publicationDate>2010-05-01</prism:publicationDate><prism:volume>4</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1933-2874(10)X0004-6</prism:issueIdentifier><prism:section>Abstracts</prism:section><prism:startingPage>213</prism:startingPage><prism:endingPage>213</prism:endingPage></item><item rdf:about="http://www.lipidjournal.com/article/PIIS193328741000139X/abstract?rss=yes"><title>Aspirin Reduces Transient Flushing and Glucose Increases During Therapy with Niacin Extended-Release</title><link>http://www.lipidjournal.com/article/PIIS193328741000139X/abstract?rss=yes</link><description>Synopsis: Proprietary niacin extended-release reduces most proatherogenic lipids while increasing antiatherogenic lipids. Therapy with niacin has been associated with flushing and a transient increase in blood glucose levels, although long-term effects on HbA1c are not usually observed. Both flushing and increases in blood glucose may be mediated via associated pathways. Aspirin has been demonstrated to mitigate flushing during adaptation to niacin extended-release therapy.</description><dc:title>Aspirin Reduces Transient Flushing and Glucose Increases During Therapy with Niacin Extended-Release</dc:title><dc:creator>Robert J. Padley, Roopal B. Thakkar, Ping Jiang, Scott L. Krause, Michael H. Davidson, Henry A. Punzi</dc:creator><dc:identifier>10.1016/j.jacl.2010.03.040</dc:identifier><dc:source>Journal of Clinical Lipidology 4, 3 (2010)</dc:source><dc:date>2010-05-01</dc:date><prism:publicationName>Journal of Clinical Lipidology</prism:publicationName><prism:publicationDate>2010-05-01</prism:publicationDate><prism:volume>4</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1933-2874(10)X0004-6</prism:issueIdentifier><prism:section>Abstracts</prism:section><prism:startingPage>213</prism:startingPage><prism:endingPage>214</prism:endingPage></item><item rdf:about="http://www.lipidjournal.com/article/PIIS1933287410001406/abstract?rss=yes"><title>Aspirin Improves Niacin-Associated Flushing and its Impact on Dyslipidemic Patients' Quality of Life</title><link>http://www.lipidjournal.com/article/PIIS1933287410001406/abstract?rss=yes</link><description>Synopsis: Flushing occurs primarily during initiation of niacin therapy and is typically short-lived. Aspirin (ASA) significantly reduces the incidence and intensity of niacin-associated flushing and may improve flushing's impact on quality of life.</description><dc:title>Aspirin Improves Niacin-Associated Flushing and its Impact on Dyslipidemic Patients' Quality of Life</dc:title><dc:creator>Thao T. Dong, Ping Jiang, Rhea Parreno, Roopal B. Thakkar, Scott L. Krause, Robert J. Padley</dc:creator><dc:identifier>10.1016/j.jacl.2010.03.041</dc:identifier><dc:source>Journal of Clinical Lipidology 4, 3 (2010)</dc:source><dc:date>2010-05-01</dc:date><prism:publicationName>Journal of Clinical Lipidology</prism:publicationName><prism:publicationDate>2010-05-01</prism:publicationDate><prism:volume>4</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1933-2874(10)X0004-6</prism:issueIdentifier><prism:section>Abstracts</prism:section><prism:startingPage>214</prism:startingPage><prism:endingPage>214</prism:endingPage></item><item rdf:about="http://www.lipidjournal.com/article/PIIS1933287410001418/abstract?rss=yes"><title>Sex and Ethnic Disparities in High-Density Lipoprotein Subclasses∗</title><link>http://www.lipidjournal.com/article/PIIS1933287410001418/abstract?rss=yes</link><description>Synopsis: Several epidemiological studies have shown race and sex differences in conventional lipoprotein parameters. Descriptive studies on these differences in novel lipid subfractions, high-density lipoprotein (HDL) subclasses in particular, are very scant. Previous studies were performed only on biracial groups and in high-risk populations.</description><dc:title>Sex and Ethnic Disparities in High-Density Lipoprotein Subclasses∗</dc:title><dc:creator>Palaniappan Manickam, Ankit Rathod, Praveen Guntipalli, Pawan Hari, Vikas Veeranna, Sony Jacob, Luis Afonso</dc:creator><dc:identifier>10.1016/j.jacl.2010.03.042</dc:identifier><dc:source>Journal of Clinical Lipidology 4, 3 (2010)</dc:source><dc:date>2010-05-01</dc:date><prism:publicationName>Journal of Clinical Lipidology</prism:publicationName><prism:publicationDate>2010-05-01</prism:publicationDate><prism:volume>4</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1933-2874(10)X0004-6</prism:issueIdentifier><prism:section>Abstracts</prism:section><prism:startingPage>214</prism:startingPage><prism:endingPage>215</prism:endingPage></item><item rdf:about="http://www.lipidjournal.com/article/PIIS193328741000142X/abstract?rss=yes"><title>The Lipid-Altering Effects of Extended-Release Niacin/Laropiprant Among Different Patient Subgroups</title><link>http://www.lipidjournal.com/article/PIIS193328741000142X/abstract?rss=yes</link><description>Synopsis: Extended-release niacin/laropiprant (ERN/LRPT) improves key lipid parameters associated with increased cardiovascular disease (CVD) risk in patients with primary hypercholesterolemia or mixed dyslipidemia.</description><dc:title>The Lipid-Altering Effects of Extended-Release Niacin/Laropiprant Among Different Patient Subgroups</dc:title><dc:creator>Harold Edward Bays, Alexandra MacLean, Arvind Shah, Christine McCrary Sisk, Qian Dong, Darbie Maccubbin</dc:creator><dc:identifier>10.1016/j.jacl.2010.03.043</dc:identifier><dc:source>Journal of Clinical Lipidology 4, 3 (2010)</dc:source><dc:date>2010-05-01</dc:date><prism:publicationName>Journal of Clinical Lipidology</prism:publicationName><prism:publicationDate>2010-05-01</prism:publicationDate><prism:volume>4</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1933-2874(10)X0004-6</prism:issueIdentifier><prism:section>Abstracts</prism:section><prism:startingPage>215</prism:startingPage><prism:endingPage>215</prism:endingPage></item><item rdf:about="http://www.lipidjournal.com/article/PIIS1933287410001431/abstract?rss=yes"><title>Effect of Hepatic Impairment on the Pharmacokinetics of Dalcetrapib</title><link>http://www.lipidjournal.com/article/PIIS1933287410001431/abstract?rss=yes</link><description>Synopsis: Dalcetrapib acts to raise high-density lipoprotein cholesterol (HDL-C) concentrations by reducing cholesteryl ester transfer protein (CETP) activity, with the expectation that increasing HDL-C will reduce cardiovascular risk. Patients with high cardiovascular risk often have comorbidities, and, because dalcetrapib is extensively metabolized, dose adjustment could be required in individuals with hepatic dysfunction.</description><dc:title>Effect of Hepatic Impairment on the Pharmacokinetics of Dalcetrapib</dc:title><dc:creator>Mary Phelan, Olaf Kuhlmann, Judith Anzures-Cabrera, Bimaljit Matharu, Darren Bentley</dc:creator><dc:identifier>10.1016/j.jacl.2010.03.044</dc:identifier><dc:source>Journal of Clinical Lipidology 4, 3 (2010)</dc:source><dc:date>2010-05-01</dc:date><prism:publicationName>Journal of Clinical Lipidology</prism:publicationName><prism:publicationDate>2010-05-01</prism:publicationDate><prism:volume>4</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1933-2874(10)X0004-6</prism:issueIdentifier><prism:section>Abstracts</prism:section><prism:startingPage>215</prism:startingPage><prism:endingPage>216</prism:endingPage></item><item rdf:about="http://www.lipidjournal.com/article/PIIS1933287410001443/abstract?rss=yes"><title>No Clinically Relevant Drug-Drug Interactions Between Dalcetrapib and a Monophasic Oral Contraceptive (Microgynon-30®)</title><link>http://www.lipidjournal.com/article/PIIS1933287410001443/abstract?rss=yes</link><description>Synopsis: Dalcetrapib will be prescribed to increase high-density lipoprotein cholesterol by reducing cholesteryl ester transfer protein activity, and potentially reduce residual cardiovascular risk. Patients administered dalcetrapib will most likely include women co-prescribed an oral contraceptive (OC). We investigated the potential for drug-drug-interaction in women co-administered dalcetrapib 900 mg once daily ([QD] a supratherapeutic dose greater than 600 mg tested in phase 3 trials) and Microgynon-30 QD, a widely prescribed monophasic OC.</description><dc:title>No Clinically Relevant Drug-Drug Interactions Between Dalcetrapib and a Monophasic Oral Contraceptive (Microgynon-30®)</dc:title><dc:creator>Anne-Marie Young, Adam Foley-Comer, Judith Anzures-Cabrera, Michael Derks</dc:creator><dc:identifier>10.1016/j.jacl.2010.03.045</dc:identifier><dc:source>Journal of Clinical Lipidology 4, 3 (2010)</dc:source><dc:date>2010-05-01</dc:date><prism:publicationName>Journal of Clinical Lipidology</prism:publicationName><prism:publicationDate>2010-05-01</prism:publicationDate><prism:volume>4</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1933-2874(10)X0004-6</prism:issueIdentifier><prism:section>Abstracts</prism:section><prism:startingPage>216</prism:startingPage><prism:endingPage>216</prism:endingPage></item><item rdf:about="http://www.lipidjournal.com/article/PIIS1933287410001455/abstract?rss=yes"><title>Prognostic Factors that Influence the Risk of Intensification of Anti-Hyperglycemic Medication Among Patients with Type 2 Diabetes</title><link>http://www.lipidjournal.com/article/PIIS1933287410001455/abstract?rss=yes</link><description>Synopsis: Niacin improves diabetic dyslipidemia but also increases blood glucose levels in some patients. Compared with placebo (PBO), type 2 diabetes (DM-2) patients treated with ER niacin/laropiprant (ERN/LRPT) were more likely to require an intensification of their anti-hyperglycemic medications (AHA; 8.2% vs 17.6%).</description><dc:title>Prognostic Factors that Influence the Risk of Intensification of Anti-Hyperglycemic Medication Among Patients with Type 2 Diabetes</dc:title><dc:creator>Darbie Maccubbin, Alexandra MacLean, Hilde Giezek, Christine McCray Sisk</dc:creator><dc:identifier>10.1016/j.jacl.2010.03.046</dc:identifier><dc:source>Journal of Clinical Lipidology 4, 3 (2010)</dc:source><dc:date>2010-05-01</dc:date><prism:publicationName>Journal of Clinical Lipidology</prism:publicationName><prism:publicationDate>2010-05-01</prism:publicationDate><prism:volume>4</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1933-2874(10)X0004-6</prism:issueIdentifier><prism:section>Abstracts</prism:section><prism:startingPage>216</prism:startingPage><prism:endingPage>216</prism:endingPage></item><item rdf:about="http://www.lipidjournal.com/article/PIIS1933287410001467/abstract?rss=yes"><title>Extended-Release Nicotinic Acid Versus Inositol Hexanicotinate for the Treatment of Dyslipidemia</title><link>http://www.lipidjournal.com/article/PIIS1933287410001467/abstract?rss=yes</link><description>Synopsis: This was a comparison of the efficacy, safety, and tolerability of two forms of nicotinic acid (NA), wax-matrix, extended release, nicotinic acid (WMNA), and Inositol Hexanicotinate (IHN), or “no flush” niacin in persons with dyslipidemia.</description><dc:title>Extended-Release Nicotinic Acid Versus Inositol Hexanicotinate for the Treatment of Dyslipidemia</dc:title><dc:creator>Joseph Keenan</dc:creator><dc:identifier>10.1016/j.jacl.2010.03.047</dc:identifier><dc:source>Journal of Clinical Lipidology 4, 3 (2010)</dc:source><dc:date>2010-05-01</dc:date><prism:publicationName>Journal of Clinical Lipidology</prism:publicationName><prism:publicationDate>2010-05-01</prism:publicationDate><prism:volume>4</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1933-2874(10)X0004-6</prism:issueIdentifier><prism:section>Abstracts</prism:section><prism:startingPage>216</prism:startingPage><prism:endingPage>217</prism:endingPage></item><item rdf:about="http://www.lipidjournal.com/article/PIIS1933287410001479/abstract?rss=yes"><title>Prognostic Utility of Lipid Parameters in Prediction of New-Onset Microalbuminuria in Hypertensive Patients∗</title><link>http://www.lipidjournal.com/article/PIIS1933287410001479/abstract?rss=yes</link><description>Synopsis: Microalbuminuria has been recognized as a potential marker of future cardiovascular disease (CVD) in hypertensive patients. Comparative data on the prognostic utility of conventional lipid parameters in predicting new-onset microalbuminuria (NOM) in hypertensives is scant.</description><dc:title>Prognostic Utility of Lipid Parameters in Prediction of New-Onset Microalbuminuria in Hypertensive Patients∗</dc:title><dc:creator>Palaniappan Manickam, Praveen Guntipalli, Ankit Rathod, Pawan Kumar Hari, Rajeev Sudhaker, Vikas Veerenna, Sony Jacob, Luis Afonso</dc:creator><dc:identifier>10.1016/j.jacl.2010.03.048</dc:identifier><dc:source>Journal of Clinical Lipidology 4, 3 (2010)</dc:source><dc:date>2010-05-01</dc:date><prism:publicationName>Journal of Clinical Lipidology</prism:publicationName><prism:publicationDate>2010-05-01</prism:publicationDate><prism:volume>4</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1933-2874(10)X0004-6</prism:issueIdentifier><prism:section>Abstracts</prism:section><prism:startingPage>217</prism:startingPage><prism:endingPage>217</prism:endingPage></item><item rdf:about="http://www.lipidjournal.com/article/PIIS1933287410001480/abstract?rss=yes"><title>Acute Reduction of Lipoprotein (a) After Low-Density Lipoprotein Apheresis May Improve Symptoms of Angina∗</title><link>http://www.lipidjournal.com/article/PIIS1933287410001480/abstract?rss=yes</link><description>Synopsis: Low-density lipoprotein apheresis (LDL-a) therapy rapidly reduces plasma levels of low density lipoprotein-cholesterol (LDL-C) by more than 60% in patients with homozygous or severe heterozygous familial hypercholesterolemia (FH) who are intolerant to lipid lowering therapy. LDL-a also reduces plasma levels of lipoprotein(a), Lp(a), an atherothrombotic particle capable of increasing the risk of coronary heart disease (CHD). In addition to reducing CHD, LDL-a treatment for FH patients has demonstrated improvement in symptoms of angina and peripheral arterial disease (PAD). However, the evidence supporting LDL therapy in patients with normal LDL levels and elevated Lp(a) is lacking. This is the first case study examining the acute clinical benefits of LDL-a for a patient with CHD, cerebrovascular disease, and angina while having normal LDL-C but abnormally high levels of Lp(a).</description><dc:title>Acute Reduction of Lipoprotein (a) After Low-Density Lipoprotein Apheresis May Improve Symptoms of Angina∗</dc:title><dc:creator>Deepti Bulchandani, Patrick Moriarty</dc:creator><dc:identifier>10.1016/j.jacl.2010.03.049</dc:identifier><dc:source>Journal of Clinical Lipidology 4, 3 (2010)</dc:source><dc:date>2010-05-01</dc:date><prism:publicationName>Journal of Clinical Lipidology</prism:publicationName><prism:publicationDate>2010-05-01</prism:publicationDate><prism:volume>4</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1933-2874(10)X0004-6</prism:issueIdentifier><prism:section>Abstracts</prism:section><prism:startingPage>217</prism:startingPage><prism:endingPage>218</prism:endingPage></item><item rdf:about="http://www.lipidjournal.com/article/PIIS1933287410001492/abstract?rss=yes"><title>Predictors of Combination Therapy for the Treatment of Dyslipidemia in the Actual Clinical Practice-Setting</title><link>http://www.lipidjournal.com/article/PIIS1933287410001492/abstract?rss=yes</link><description>Synopsis: Several factors play a role in the selection of treatment for patients with dyslipidemia in the actual clinical-practice setting.   Purpose: To determine the predictors for prescribing combination therapy versus monotherapy to control lipid abnormalities in a clinical-practice setting.</description><dc:title>Predictors of Combination Therapy for the Treatment of Dyslipidemia in the Actual Clinical Practice-Setting</dc:title><dc:creator>Radhika Nair, Woodie Zachry</dc:creator><dc:identifier>10.1016/j.jacl.2010.03.050</dc:identifier><dc:source>Journal of Clinical Lipidology 4, 3 (2010)</dc:source><dc:date>2010-05-01</dc:date><prism:publicationName>Journal of Clinical Lipidology</prism:publicationName><prism:publicationDate>2010-05-01</prism:publicationDate><prism:volume>4</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1933-2874(10)X0004-6</prism:issueIdentifier><prism:section>Abstracts</prism:section><prism:startingPage>218</prism:startingPage><prism:endingPage>218</prism:endingPage></item><item rdf:about="http://www.lipidjournal.com/article/PIIS1933287410001509/abstract?rss=yes"><title>The Treatment of Dyslipidemia in Actual Practice Settings That Use Similar Inclusion Criteria to the ACCORD Lipid Trial</title><link>http://www.lipidjournal.com/article/PIIS1933287410001509/abstract?rss=yes</link><description>Synopsis: Although clinical trials are a crucial source of information, it is important to understand the applicability of the results within the context of an actual practice setting in a non-randomized patient population.</description><dc:title>The Treatment of Dyslipidemia in Actual Practice Settings That Use Similar Inclusion Criteria to the ACCORD Lipid Trial</dc:title><dc:creator>Radhika Nair, Woodie Zachry</dc:creator><dc:identifier>10.1016/j.jacl.2010.03.051</dc:identifier><dc:source>Journal of Clinical Lipidology 4, 3 (2010)</dc:source><dc:date>2010-05-01</dc:date><prism:publicationName>Journal of Clinical Lipidology</prism:publicationName><prism:publicationDate>2010-05-01</prism:publicationDate><prism:volume>4</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1933-2874(10)X0004-6</prism:issueIdentifier><prism:section>Abstracts</prism:section><prism:startingPage>218</prism:startingPage><prism:endingPage>219</prism:endingPage></item><item rdf:about="http://www.lipidjournal.com/article/PIIS1933287410001510/abstract?rss=yes"><title>Associations Between Switches to Simvastatin and Low-Density Lipoprotein Goal Attainment Among High-Risk Patients in a US Managed-Care Population</title><link>http://www.lipidjournal.com/article/PIIS1933287410001510/abstract?rss=yes</link><description>Synopsis: The availability of generic simvastatin has prompted substantial changes in formulary recommendations.   Purpose: The goal of this retrospective, observational study was to examine the impact of switches to simvastatin on low-density lipoprotein cholesterol (LDL-C) goal attainment among coronary heart disease (CHD)/CHD risk equivalent patients in a large national managed care claims database.</description><dc:title>Associations Between Switches to Simvastatin and Low-Density Lipoprotein Goal Attainment Among High-Risk Patients in a US Managed-Care Population</dc:title><dc:creator>David Robert Neff, Kaan Tunceli, Shiva Sajjan, Dena Ramey, Andrew M. Tershakovec, Henry X. Hu, JoAnne M. Foody</dc:creator><dc:identifier>10.1016/j.jacl.2010.03.052</dc:identifier><dc:source>Journal of Clinical Lipidology 4, 3 (2010)</dc:source><dc:date>2010-05-01</dc:date><prism:publicationName>Journal of Clinical Lipidology</prism:publicationName><prism:publicationDate>2010-05-01</prism:publicationDate><prism:volume>4</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1933-2874(10)X0004-6</prism:issueIdentifier><prism:section>Abstracts</prism:section><prism:startingPage>219</prism:startingPage><prism:endingPage>219</prism:endingPage></item><item rdf:about="http://www.lipidjournal.com/article/PIIS1933287410001522/abstract?rss=yes"><title>Changes in Prescription Patterns for Ezetimibe/Simvastatin, Ezetimibe and Statin, and Statin Therapies and Expected Effects on LDL-C Reduction</title><link>http://www.lipidjournal.com/article/PIIS1933287410001522/abstract?rss=yes</link><description>Synopsis: Recent trends in managed care databases have suggested decreased use of ezetimibe/simvastatin (E/S) combination and coadministered E and statin therapies.   Purpose: This analysis evaluated changes in prescription (Rx) patterns for E/S, E and statins, and statin therapies in a managed care database and expected effects on LDL-C lowering during 2007–2008.</description><dc:title>Changes in Prescription Patterns for Ezetimibe/Simvastatin, Ezetimibe and Statin, and Statin Therapies and Expected Effects on LDL-C Reduction</dc:title><dc:creator>Peter Paul Toth, Christie M. Ballantyne, Michael H. Davidson, Dena Ramey, David Neff, Andrew M. Tershakovec, Henry X. Hu, Joanne E. Tomassini, Kaan Tunceli</dc:creator><dc:identifier>10.1016/j.jacl.2010.03.053</dc:identifier><dc:source>Journal of Clinical Lipidology 4, 3 (2010)</dc:source><dc:date>2010-05-01</dc:date><prism:publicationName>Journal of Clinical Lipidology</prism:publicationName><prism:publicationDate>2010-05-01</prism:publicationDate><prism:volume>4</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1933-2874(10)X0004-6</prism:issueIdentifier><prism:section>Abstracts</prism:section><prism:startingPage>219</prism:startingPage><prism:endingPage>220</prism:endingPage></item><item rdf:about="http://www.lipidjournal.com/article/PIIS1933287410001534/abstract?rss=yes"><title>Colesevelam HCl to Treat Hypercholesterolemia and Improve Glycemia in Prediabetes: A Randomized, Prospective Study</title><link>http://www.lipidjournal.com/article/PIIS1933287410001534/abstract?rss=yes</link><description>Synopsis: Prediabetes (impaired glucose tolerance and/or impaired fasting glucose) increases the risk of developing microvascular/macrovascular disease and progression to type 2 diabetes.</description><dc:title>Colesevelam HCl to Treat Hypercholesterolemia and Improve Glycemia in Prediabetes: A Randomized, Prospective Study</dc:title><dc:creator>Sam Misir, Yehuda Handelsman, Timothy W. Garvey, Vivian A. Fonseca, Julio Rosenstock, Michael R. Jones, Yu-Ling Lai, Xiaoping Jin, Sukumar Nagendran, Stacey L. Abby</dc:creator><dc:identifier>10.1016/j.jacl.2010.03.054</dc:identifier><dc:source>Journal of Clinical Lipidology 4, 3 (2010)</dc:source><dc:date>2010-05-01</dc:date><prism:publicationName>Journal of Clinical Lipidology</prism:publicationName><prism:publicationDate>2010-05-01</prism:publicationDate><prism:volume>4</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1933-2874(10)X0004-6</prism:issueIdentifier><prism:section>Abstracts</prism:section><prism:startingPage>220</prism:startingPage><prism:endingPage>220</prism:endingPage></item><item rdf:about="http://www.lipidjournal.com/article/PIIS1933287410001546/abstract?rss=yes"><title>Mipomersen, a First-in-Class Apolipoprotein B Synthesis Inhibitor, Lowers Lipoprotein (a) in Patients with Homozygous Familial Hypercholesterolemia</title><link>http://www.lipidjournal.com/article/PIIS1933287410001546/abstract?rss=yes</link><description>Synopsis: Despite available lipid-lowering therapy (LLT), adequate treatment of patients with homozygous familial hypercholesterolemia (HoFH) remains an unmet medical need. Mipomersen (ISIS301012) is an apolipoprotein A (apoB) synthesis inhibitor based on antisense oligonucleotide technology. In lipoprotein (a) (Lp[a]) transgenic mice, the use of mipomersen reduced Lp(a) levels without having an impact on apo(a) synthesis. Reductions in Lp(a) also were observed in a pilot study in 3 patients with HoFH.</description><dc:title>Mipomersen, a First-in-Class Apolipoprotein B Synthesis Inhibitor, Lowers Lipoprotein (a) in Patients with Homozygous Familial Hypercholesterolemia</dc:title><dc:creator>William C. Cromwell, Raul D. Santos, Dirk J. Blom, David A. Marais, Robin H. Lachmann, Daniel Gaudet, Ju L. Tan, Scott Chasan-Taber, Diane L. Tribble, JoAnn Flaim, Frederick J. Raal, Min-Ji Charng</dc:creator><dc:identifier>10.1016/j.jacl.2010.03.055</dc:identifier><dc:source>Journal of Clinical Lipidology 4, 3 (2010)</dc:source><dc:date>2010-05-01</dc:date><prism:publicationName>Journal of Clinical Lipidology</prism:publicationName><prism:publicationDate>2010-05-01</prism:publicationDate><prism:volume>4</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1933-2874(10)X0004-6</prism:issueIdentifier><prism:section>Abstracts</prism:section><prism:startingPage>221</prism:startingPage><prism:endingPage>221</prism:endingPage></item><item rdf:about="http://www.lipidjournal.com/article/PIIS1933287410001558/abstract?rss=yes"><title>Change Heart and Vascular Risk with Attitude, Nutrition, Goals, and Exercise (CHANGE)</title><link>http://www.lipidjournal.com/article/PIIS1933287410001558/abstract?rss=yes</link><description>Synopsis: Cardiovascular disease is the number one cause of death in the United States. Traditional risk factors account for more than 90% of the risk of an initial heart attack. Forty-four percent of the reduction in death from heart disease in recent decades is attributed to risk factor modification. Many individuals are aware of their risk factors; however, they are not aware of their treatment goals. Low-risk individuals identified by the Framingham risk score account for the majority of cardiovascular events. Identification of lifetime risk rather than Framingham risk identifies individuals appropriate for early aggressive risk factor management.</description><dc:title>Change Heart and Vascular Risk with Attitude, Nutrition, Goals, and Exercise (CHANGE)</dc:title><dc:creator>Edward Mark Goldenberg, Elisabeth Bradley, Deanna Hoosty, Bernadette Baker, Catherine Johnson, Melissa Steward, Dionne Thompson, Penny Vigneau</dc:creator><dc:identifier>10.1016/j.jacl.2010.03.056</dc:identifier><dc:source>Journal of Clinical Lipidology 4, 3 (2010)</dc:source><dc:date>2010-05-01</dc:date><prism:publicationName>Journal of Clinical Lipidology</prism:publicationName><prism:publicationDate>2010-05-01</prism:publicationDate><prism:volume>4</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1933-2874(10)X0004-6</prism:issueIdentifier><prism:section>Abstracts</prism:section><prism:startingPage>221</prism:startingPage><prism:endingPage>222</prism:endingPage></item><item rdf:about="http://www.lipidjournal.com/article/PIIS193328741000156X/abstract?rss=yes"><title>Attainment of Dual Treatment Levels for High-Sensitivity C-Reactive Protein and Lipids in Older (&gt;65 Years) Patients with Cardiovascular Disease Risk: Ezetimibe/Simvastatin Versus Atorvastatin</title><link>http://www.lipidjournal.com/article/PIIS193328741000156X/abstract?rss=yes</link><description>Synopsis: Although low-density lipoprotein cholesterol (LDL-C) lowering remains the primary aim of lipid-lowering therapy in patients with cardiovascular disease (CVD), guidelines additionally recommend non-high-density lipoprotein cholesterol (HDL-C) and apolipoprotein B (apoB) as secondary treatment targets in greater-risk patients. High-sensitivity C-reactive protein (hsCRP) is an inflammatory marker considered to be predictive of CVD. However, few data exist regarding the relationships between therapeutic changes in lipoproteins and reduction of hsCRP or achievement of dual targets in older patients.</description><dc:title>Attainment of Dual Treatment Levels for High-Sensitivity C-Reactive Protein and Lipids in Older (&gt;65 Years) Patients with Cardiovascular Disease Risk: Ezetimibe/Simvastatin Versus Atorvastatin</dc:title><dc:creator>Franklin Joseph Zieve, W. Virgil Brown, JoAnne M. Foody, Charlotte Jones-Burton, Qian Dong, Joanne F. Tomassini, Arvind Shah, Andrew M. Tershakovec</dc:creator><dc:identifier>10.1016/j.jacl.2010.03.057</dc:identifier><dc:source>Journal of Clinical Lipidology 4, 3 (2010)</dc:source><dc:date>2010-05-01</dc:date><prism:publicationName>Journal of Clinical Lipidology</prism:publicationName><prism:publicationDate>2010-05-01</prism:publicationDate><prism:volume>4</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1933-2874(10)X0004-6</prism:issueIdentifier><prism:section>Abstracts</prism:section><prism:startingPage>222</prism:startingPage><prism:endingPage>222</prism:endingPage></item><item rdf:about="http://www.lipidjournal.com/article/PIIS1933287410001571/abstract?rss=yes"><title>Fibrates Lower the Risk of Myocardial Infarction but Not Stroke or Mortality in Patients with Cardiovascular Disease: A Meta-Analysis and Systematic Review∗</title><link>http://www.lipidjournal.com/article/PIIS1933287410001571/abstract?rss=yes</link><description>Synopsis: Fibric acid derivatives (fibrates) are effective in lowering serum triglycerides and increasing serum HDL cholesterol. However, studies evaluating the impact of fibrate therapy on major clinical events in patients with cardiovascular disease have shown inconsistent results. The long-term benefits of fibrate therapy remain undetermined.</description><dc:title>Fibrates Lower the Risk of Myocardial Infarction but Not Stroke or Mortality in Patients with Cardiovascular Disease: A Meta-Analysis and Systematic Review∗</dc:title><dc:creator>Firas Al Badarin, James O'Keefe</dc:creator><dc:identifier>10.1016/j.jacl.2010.03.058</dc:identifier><dc:source>Journal of Clinical Lipidology 4, 3 (2010)</dc:source><dc:date>2010-05-01</dc:date><prism:publicationName>Journal of Clinical Lipidology</prism:publicationName><prism:publicationDate>2010-05-01</prism:publicationDate><prism:volume>4</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1933-2874(10)X0004-6</prism:issueIdentifier><prism:section>Abstracts</prism:section><prism:startingPage>222</prism:startingPage><prism:endingPage>223</prism:endingPage></item><item rdf:about="http://www.lipidjournal.com/article/PIIS1933287410001583/abstract?rss=yes"><title>Inverse Relationship Between High-Density Lipoprotein Cholesterol Raising and High-Sensitivity C-Reactive Protein Reduction in Older Patients Treated with Lipid-Lowering Therapy</title><link>http://www.lipidjournal.com/article/PIIS1933287410001583/abstract?rss=yes</link><description>Synopsis: Little is known regarding relationships between hsCRP and lipoproteins other than low-density lipoprotein cholesterol (LDL-C), particularly high-density lipoprotein cholesterol (HDL-C), which has both anti-inflammatory and cholesterol-mediating effects. Moreover, these relationships have not been well-studied in older patients.</description><dc:title>Inverse Relationship Between High-Density Lipoprotein Cholesterol Raising and High-Sensitivity C-Reactive Protein Reduction in Older Patients Treated with Lipid-Lowering Therapy</dc:title><dc:creator>W. Virgil Brown, JoAnne M. Foody, Franklin Zieve, Charlotte Jones-Burton, Qian Dong, Joanne E. Tomassini, Arvind Shah, Andrew M. Tershakovec</dc:creator><dc:identifier>10.1016/j.jacl.2010.03.059</dc:identifier><dc:source>Journal of Clinical Lipidology 4, 3 (2010)</dc:source><dc:date>2010-05-01</dc:date><prism:publicationName>Journal of Clinical Lipidology</prism:publicationName><prism:publicationDate>2010-05-01</prism:publicationDate><prism:volume>4</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1933-2874(10)X0004-6</prism:issueIdentifier><prism:section>Abstracts</prism:section><prism:startingPage>223</prism:startingPage><prism:endingPage>223</prism:endingPage></item><item rdf:about="http://www.lipidjournal.com/article/PIIS1933287410001595/abstract?rss=yes"><title>Comparison of Attainment of Diabetes Goals and Knowledge Between Traditional Practice Settings and a Dietitian/Nurse Practitioner-Run Lipid Clinic</title><link>http://www.lipidjournal.com/article/PIIS1933287410001595/abstract?rss=yes</link><description>Synopsis: Management of diabetes requires continuous medical care and ardent patient self-management to reduce the risk of long-term complications. Despite guideline recommendations for diabetes management, only 7% of adult patients with diabetes in a recent study were at their A1c, blood pressure, and cholesterol goals. Multidisciplinary collaboration can improve patient outcomes; however, there is limited data around the benefits achieved when a dietitian/CDE collaborates with a nurse practitioner (NP) to manage diabetes.</description><dc:title>Comparison of Attainment of Diabetes Goals and Knowledge Between Traditional Practice Settings and a Dietitian/Nurse Practitioner-Run Lipid Clinic</dc:title><dc:creator>Kristina M. Lloyd, Thomas Algozzine, Carolyn Finocchiaro</dc:creator><dc:identifier>10.1016/j.jacl.2010.03.060</dc:identifier><dc:source>Journal of Clinical Lipidology 4, 3 (2010)</dc:source><dc:date>2010-05-01</dc:date><prism:publicationName>Journal of Clinical Lipidology</prism:publicationName><prism:publicationDate>2010-05-01</prism:publicationDate><prism:volume>4</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1933-2874(10)X0004-6</prism:issueIdentifier><prism:section>Abstracts</prism:section><prism:startingPage>223</prism:startingPage><prism:endingPage>224</prism:endingPage></item><item rdf:about="http://www.lipidjournal.com/article/PIIS1933287410001601/abstract?rss=yes"><title>Relationships Between Low-Density Lipoprotein Cholesterol, Apolipoprotein B, and Non-High-Density Lipoprotein Cholesterol with High-Sensitivity C-Reactive Protein in Hypercholesterolemic Patients at Risk for Cardiovascular Disease</title><link>http://www.lipidjournal.com/article/PIIS1933287410001601/abstract?rss=yes</link><description>Synopsis: Low-density lipoprotein cholesterol (LDL-C) and high-sensitivity C-reactive protein (hsCRP) are important markers of cardiovascular disease risk. Lipid-lowering therapy (LLT) with statins (St) and ezetimibe coadministered with statins (E+St) results in reduction of LDL-C and hsCRP levels. Associations between percent changes in LDL-C and hsCRP after LLT are generally small. Non-high-density lipoprotein cholesterol (HDL-C) and apolipoprotein B (apoB) are also risk markers altered by LLT, but less is known about the relationships between hsCRP and these markers.</description><dc:title>Relationships Between Low-Density Lipoprotein Cholesterol, Apolipoprotein B, and Non-High-Density Lipoprotein Cholesterol with High-Sensitivity C-Reactive Protein in Hypercholesterolemic Patients at Risk for Cardiovascular Disease</dc:title><dc:creator>James H. O Keefe, Mohammad Abuannadi, Jianxin Lin, Arvind Shah, David Neff, Joanne E. Tomassini, Andrew M. Tershakovec</dc:creator><dc:identifier>10.1016/j.jacl.2010.03.061</dc:identifier><dc:source>Journal of Clinical Lipidology 4, 3 (2010)</dc:source><dc:date>2010-05-01</dc:date><prism:publicationName>Journal of Clinical Lipidology</prism:publicationName><prism:publicationDate>2010-05-01</prism:publicationDate><prism:volume>4</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1933-2874(10)X0004-6</prism:issueIdentifier><prism:section>Abstracts</prism:section><prism:startingPage>224</prism:startingPage><prism:endingPage>224</prism:endingPage></item><item rdf:about="http://www.lipidjournal.com/article/PIIS1933287410001613/abstract?rss=yes"><title>Effects of Ezetimibe Added to Atorvastatin Versus Atorvastatin Up-Titration on Attainment of Single and Dual Levels for Low-Density Lipoprotein Cholesterol and Non-High-Density Lipoprotein Cholesterol, Apolipoprotein B, or High-Sensitivity C-Reactive Protein in Older Adults with High Coronary Heart Disease Risk</title><link>http://www.lipidjournal.com/article/PIIS1933287410001613/abstract?rss=yes</link><description>Synopsis: Few clinical studies have focused on the efficacy of lipid-lowering therapies in the growing population of men and women 65 years and older.   Purpose: This post-hoc analysis evaluated the effect of ezetimibe added to atorvastatin versus atorvastatin up-titration on the attainment of suggested single/dual levels of low-density lipoprotein cholesterol (LDL-C; &lt;70, &lt;100 mg/dL) and non-high-density lipoprotein cholesterol (HDL-C; &lt;100, &lt;130 mg/dL) or apolipoprotein B (apoB; &lt;80, &lt;90 mg/dL) in patients ≥65 years of age with hypercholesterolemia, high coronary heart disease (CHD) risk, and LDL-C levels greater than prespecified targets during atorvastatin 10 mg/day therapy (&lt;70 mg/dL for patients with atherosclerotic vascular disease [AVD], &lt;100 mg/dL for patients without AVD). hs-CRP is a CHD risk marker, and attainment of levels &lt;2 mg/L either alone or together with LDL-C was also assessed.</description><dc:title>Effects of Ezetimibe Added to Atorvastatin Versus Atorvastatin Up-Titration on Attainment of Single and Dual Levels for Low-Density Lipoprotein Cholesterol and Non-High-Density Lipoprotein Cholesterol, Apolipoprotein B, or High-Sensitivity C-Reactive Protein in Older Adults with High Coronary Heart Disease Risk</dc:title><dc:creator>Christian Constance, Ori Ben-Yehuda, Nanette K. Wenger, Franklin Zieve, Jianxin Lin, Arvind Shah, William Taggart, Robert Lowe, Charlotte Jones-Burton, Andrew M. Tershakovec</dc:creator><dc:identifier>10.1016/j.jacl.2010.03.062</dc:identifier><dc:source>Journal of Clinical Lipidology 4, 3 (2010)</dc:source><dc:date>2010-05-01</dc:date><prism:publicationName>Journal of Clinical Lipidology</prism:publicationName><prism:publicationDate>2010-05-01</prism:publicationDate><prism:volume>4</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1933-2874(10)X0004-6</prism:issueIdentifier><prism:section>Abstracts</prism:section><prism:startingPage>224</prism:startingPage><prism:endingPage>225</prism:endingPage></item><item rdf:about="http://www.lipidjournal.com/article/PIIS1933287410001625/abstract?rss=yes"><title>Safety and Efficacy of Ezetimibe/Simvastatin Combination Versus Atorvastatin in Patients 65 Years of Age and Older</title><link>http://www.lipidjournal.com/article/PIIS1933287410001625/abstract?rss=yes</link><description>Synopsis: More than 80% of coronary heart disease (CHD)-related mortality occurs in patients 65 years of age or older. The use of statins to mitigate CHD risk has been suboptimal, in part because of concerns of increased side effects in older patients. Few clinical studies have focused on the efficacy and safety of lipid-lowering strategies in this population.</description><dc:title>Safety and Efficacy of Ezetimibe/Simvastatin Combination Versus Atorvastatin in Patients 65 Years of Age and Older</dc:title><dc:creator>Franklin Joseph Zieve, Joanne M. Foody, W. Virgil Brown, Adeniyi J. Adewale, Doreen Flaim, Robert S. Lowe, Charlotte Jones-Burton, Andrew M. Tershakovec</dc:creator><dc:identifier>10.1016/j.jacl.2010.03.063</dc:identifier><dc:source>Journal of Clinical Lipidology 4, 3 (2010)</dc:source><dc:date>2010-05-01</dc:date><prism:publicationName>Journal of Clinical Lipidology</prism:publicationName><prism:publicationDate>2010-05-01</prism:publicationDate><prism:volume>4</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1933-2874(10)X0004-6</prism:issueIdentifier><prism:section>Abstracts</prism:section><prism:startingPage>225</prism:startingPage><prism:endingPage>225</prism:endingPage></item><item rdf:about="http://www.lipidjournal.com/article/PIIS1933287410001637/abstract?rss=yes"><title>Long-Term Outcomes from the Utilization of a Novel Web-Based Lipid Management Software in a Single Specialty Cardiology Practice</title><link>http://www.lipidjournal.com/article/PIIS1933287410001637/abstract?rss=yes</link><description>Synopsis: The cardiovascular disease (CVD) evaluator is a web-based expert system written in Visual Basic 6 and DotNet and patented by USPO. The system basically comes up with specific diagnostic and therapeutic recommendations for the individual patient from clinical information, lipid profile, emerging risk factors (if available), and advanced lipid profile, including genetic risk factors. It uses published CV disease risk-scoring systems such as Framingham and published guidelines such as NCEP, ITF, ADA, and NKF. The diagnostic and therapeutic recommendations are determined on the basis of clinical trials, which are cited in the reference section of the output and the relevant journal articles can instantly be linked to through an HTML web page.</description><dc:title>Long-Term Outcomes from the Utilization of a Novel Web-Based Lipid Management Software in a Single Specialty Cardiology Practice</dc:title><dc:creator>Demir Baykal</dc:creator><dc:identifier>10.1016/j.jacl.2010.03.064</dc:identifier><dc:source>Journal of Clinical Lipidology 4, 3 (2010)</dc:source><dc:date>2010-05-01</dc:date><prism:publicationName>Journal of Clinical Lipidology</prism:publicationName><prism:publicationDate>2010-05-01</prism:publicationDate><prism:volume>4</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1933-2874(10)X0004-6</prism:issueIdentifier><prism:section>Abstracts</prism:section><prism:startingPage>225</prism:startingPage><prism:endingPage>226</prism:endingPage></item><item rdf:about="http://www.lipidjournal.com/article/PIIS1933287410001649/abstract?rss=yes"><title>Hepatic Lipase Deficiency in a Middle-Eastern/Arabic Male∗</title><link>http://www.lipidjournal.com/article/PIIS1933287410001649/abstract?rss=yes</link><description>Synopsis: Hepatic lipase (HL) deficiency is a rare genetic disorder that has been associated with premature atherosclerosis despite high plasma high-density lipoprotein (HDL) cholesterol concentrations in the affected patients. We describe the clinical and biochemical features of HL deficiency in a young male of Middle-Eastern/Arabic origin. This is the first report of cholesterol ester transfer protein (CETP) activity and mass in HL deficiency in a patient from this ethnic group.</description><dc:title>Hepatic Lipase Deficiency in a Middle-Eastern/Arabic Male∗</dc:title><dc:creator>Nafila Bazdawi Al-Riyami, Abdullah M. Al Ali, Ahmad J. Al-Sarraf, John Hill, Robert Hegele, Kristina Sachs-Barrable, Kishor M. Wasan, Jiri Frohlich</dc:creator><dc:identifier>10.1016/j.jacl.2010.03.065</dc:identifier><dc:source>Journal of Clinical Lipidology 4, 3 (2010)</dc:source><dc:date>2010-05-01</dc:date><prism:publicationName>Journal of Clinical Lipidology</prism:publicationName><prism:publicationDate>2010-05-01</prism:publicationDate><prism:volume>4</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1933-2874(10)X0004-6</prism:issueIdentifier><prism:section>Abstracts</prism:section><prism:startingPage>226</prism:startingPage><prism:endingPage>227</prism:endingPage></item><item rdf:about="http://www.lipidjournal.com/article/PIIS1933287410001650/abstract?rss=yes"><title>Simple Changes in Diet and Exercise: A Longitudinal, Retrospective Analysis</title><link>http://www.lipidjournal.com/article/PIIS1933287410001650/abstract?rss=yes</link><description>Synopsis: Residency training limits opportunities for physical activity. Given the many hours spent at the hospital, there are also often limited choices regarding healthy food choices. These factors can contribute to adverse effects on the lipid profile. At the end of residency, the author was overweight and had a less than ideal lipid profile.</description><dc:title>Simple Changes in Diet and Exercise: A Longitudinal, Retrospective Analysis</dc:title><dc:creator>Kari Uusinarkaus</dc:creator><dc:identifier>10.1016/j.jacl.2010.03.066</dc:identifier><dc:source>Journal of Clinical Lipidology 4, 3 (2010)</dc:source><dc:date>2010-05-01</dc:date><prism:publicationName>Journal of Clinical Lipidology</prism:publicationName><prism:publicationDate>2010-05-01</prism:publicationDate><prism:volume>4</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1933-2874(10)X0004-6</prism:issueIdentifier><prism:section>Abstracts</prism:section><prism:startingPage>227</prism:startingPage><prism:endingPage>227</prism:endingPage></item><item rdf:about="http://www.lipidjournal.com/article/PIIS1933287410001662/abstract?rss=yes"><title>High Low-Density Lipoprotein Associated with a Higher Early Viral Response (EVR) Rates in Genotype 1 Chronic Hepatitis C (CHC)∗</title><link>http://www.lipidjournal.com/article/PIIS1933287410001662/abstract?rss=yes</link><description>Synopsis: Hepatitis C virus (HCV) interacts with low-density lipoprotein (LDL) receptors and has also been postulated to cause insulin resistance. Previous studies have suggested that lipids as well as insulin resistance may play a role in regulating HCV clearance. Genotype 1 is the commonest genotype in the United States and has been associated with the lowest response rates to treatment among all genotypes.</description><dc:title>High Low-Density Lipoprotein Associated with a Higher Early Viral Response (EVR) Rates in Genotype 1 Chronic Hepatitis C (CHC)∗</dc:title><dc:creator>Jagdish S. Nachnani, Deepti G. Bulchandani, Laura M. Alba</dc:creator><dc:identifier>10.1016/j.jacl.2010.03.067</dc:identifier><dc:source>Journal of Clinical Lipidology 4, 3 (2010)</dc:source><dc:date>2010-05-01</dc:date><prism:publicationName>Journal of Clinical Lipidology</prism:publicationName><prism:publicationDate>2010-05-01</prism:publicationDate><prism:volume>4</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1933-2874(10)X0004-6</prism:issueIdentifier><prism:section>Abstracts</prism:section><prism:startingPage>227</prism:startingPage><prism:endingPage>228</prism:endingPage></item><item rdf:about="http://www.lipidjournal.com/article/PIIS1933287410001674/abstract?rss=yes"><title>Can Hypoglycemia be Used as a Marker of Outcome in Hospitalized Non-Diabetics∗</title><link>http://www.lipidjournal.com/article/PIIS1933287410001674/abstract?rss=yes</link><description>Synopsis: Hypoglycemia is a common complication in hospitalized patients. Affected patients tend to have an increase in cost and duration of their stay. Previous research revealed that these effects are markedly stronger in nondiabetics than in diabetics. Current data outline multiple risk factors for hypoglycemia in diabetics. However, to date there is only limited information concerning risk factors in nondiabetics.</description><dc:title>Can Hypoglycemia be Used as a Marker of Outcome in Hospitalized Non-Diabetics∗</dc:title><dc:creator>Annette Kristina Blosch, Arthur Chernoff, Prabhjot Singh Nijjar</dc:creator><dc:identifier>10.1016/j.jacl.2010.03.068</dc:identifier><dc:source>Journal of Clinical Lipidology 4, 3 (2010)</dc:source><dc:date>2010-05-01</dc:date><prism:publicationName>Journal of Clinical Lipidology</prism:publicationName><prism:publicationDate>2010-05-01</prism:publicationDate><prism:volume>4</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1933-2874(10)X0004-6</prism:issueIdentifier><prism:section>Abstracts</prism:section><prism:startingPage>228</prism:startingPage><prism:endingPage>228</prism:endingPage></item><item rdf:about="http://www.lipidjournal.com/article/PIIS1933287410001686/abstract?rss=yes"><title>A Readiness Analysis of the NCQA Diabetes Physician Recognition Program Standards Attainment for a Chicagoland Family Practice Group</title><link>http://www.lipidjournal.com/article/PIIS1933287410001686/abstract?rss=yes</link><description>Synopsis: Diabetes mellitus is a disorder that affects an estimated 18 million Americans. Approximately 50% of affected individuals have not yet been diagnosed. The Diabetes Physician Recognition Program (DPRP) is designed to recognize doctors who excel in managing diabetes. It is also designed to support efforts that reward physicians for delivering high-quality care.</description><dc:title>A Readiness Analysis of the NCQA Diabetes Physician Recognition Program Standards Attainment for a Chicagoland Family Practice Group</dc:title><dc:creator>Scott E. Glosner, George Litsas</dc:creator><dc:identifier>10.1016/j.jacl.2010.03.069</dc:identifier><dc:source>Journal of Clinical Lipidology 4, 3 (2010)</dc:source><dc:date>2010-05-01</dc:date><prism:publicationName>Journal of Clinical Lipidology</prism:publicationName><prism:publicationDate>2010-05-01</prism:publicationDate><prism:volume>4</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1933-2874(10)X0004-6</prism:issueIdentifier><prism:section>Abstracts</prism:section><prism:startingPage>228</prism:startingPage><prism:endingPage>229</prism:endingPage></item><item rdf:about="http://www.lipidjournal.com/article/PIIS1933287410001698/abstract?rss=yes"><title>Low-Density Lipoprotein (LDL) Particle Number is Heterogeneous among Persons with and Without Type 2 Diabetes and LDL Cholesterol &lt;100 mg/dL</title><link>http://www.lipidjournal.com/article/PIIS1933287410001698/abstract?rss=yes</link><description>Synopsis: Patients with diabetes have relatively normal levels of low-density lipoprotein cholesterol (LDL-C) and elevated levels of other atherogenic lipoproteins. Differences in lipoprotein subclasses between persons with type 2 diabetes (T2DM) and persons without diabetes (NKDM) and the impact of inflammation have not been extensively examined. This study assessed variations in lipids, lipoprotein particle concentration/subclass, and inflammation by diabetes status.</description><dc:title>Low-Density Lipoprotein (LDL) Particle Number is Heterogeneous among Persons with and Without Type 2 Diabetes and LDL Cholesterol &lt;100 mg/dL</dc:title><dc:creator>Ray Pourfarzib, Tara Dall</dc:creator><dc:identifier>10.1016/j.jacl.2010.03.070</dc:identifier><dc:source>Journal of Clinical Lipidology 4, 3 (2010)</dc:source><dc:date>2010-05-01</dc:date><prism:publicationName>Journal of Clinical Lipidology</prism:publicationName><prism:publicationDate>2010-05-01</prism:publicationDate><prism:volume>4</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1933-2874(10)X0004-6</prism:issueIdentifier><prism:section>Abstracts</prism:section><prism:startingPage>229</prism:startingPage><prism:endingPage>229</prism:endingPage></item><item rdf:about="http://www.lipidjournal.com/article/PIIS1933287410001704/abstract?rss=yes"><title>Long-Term Outcomes in Patients with Severe Hypertriglyceridemia—Simulation Using the Archimedes Model</title><link>http://www.lipidjournal.com/article/PIIS1933287410001704/abstract?rss=yes</link><description>Synopsis: Individuals with elevated triglyceride (TG) levels are at greater risk for coronary heart disease (CHD). However, there is a lack of long-term data to quantitatively demonstrate the risk in patients with severe (≥500 mg/dL) hypertriglyceridemia (SHTG).</description><dc:title>Long-Term Outcomes in Patients with Severe Hypertriglyceridemia—Simulation Using the Archimedes Model</dc:title><dc:creator>Bhakti Arondekar, Stuart Samuel, Ian Blumenfeld, Barbara Peskin, Montiago LeBute, Glenda Stone, Peter Alperin</dc:creator><dc:identifier>10.1016/j.jacl.2010.03.071</dc:identifier><dc:source>Journal of Clinical Lipidology 4, 3 (2010)</dc:source><dc:date>2010-05-01</dc:date><prism:publicationName>Journal of Clinical Lipidology</prism:publicationName><prism:publicationDate>2010-05-01</prism:publicationDate><prism:volume>4</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1933-2874(10)X0004-6</prism:issueIdentifier><prism:section>Abstracts</prism:section><prism:startingPage>229</prism:startingPage><prism:endingPage>230</prism:endingPage></item><item rdf:about="http://www.lipidjournal.com/article/PIIS1933287410001716/abstract?rss=yes"><title>Cost Effectiveness of Prescription Strength Omega-3 in Individuals with Severe Hypertriglyceridemia</title><link>http://www.lipidjournal.com/article/PIIS1933287410001716/abstract?rss=yes</link><description>Synopsis: Clinical trials in individuals with severe (≥500 mg/dL) hypertriglyceridemia (SHTG) have demonstrated that 4 g/day of prescription-strength omega-3 (P OM-3) can reduce triglyceride (TG) levels by 45%. Individuals with increased TG levels are at greater risk for coronary heart disease (CHD). However, a study is lacking to support the potential cost effectiveness (CE) of P OM-3 in individuals with SHTG.</description><dc:title>Cost Effectiveness of Prescription Strength Omega-3 in Individuals with Severe Hypertriglyceridemia</dc:title><dc:creator>Bhakti Arondekar, Stuart Samuel, Ian Blumenfeld, Barbara Peskin, Montiago LeBute, Glenda Stone, Peter Alperin</dc:creator><dc:identifier>10.1016/j.jacl.2010.03.072</dc:identifier><dc:source>Journal of Clinical Lipidology 4, 3 (2010)</dc:source><dc:date>2010-05-01</dc:date><prism:publicationName>Journal of Clinical Lipidology</prism:publicationName><prism:publicationDate>2010-05-01</prism:publicationDate><prism:volume>4</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1933-2874(10)X0004-6</prism:issueIdentifier><prism:section>Abstracts</prism:section><prism:startingPage>230</prism:startingPage><prism:endingPage>230</prism:endingPage></item><item rdf:about="http://www.lipidjournal.com/article/PIIS1933287410001728/abstract?rss=yes"><title>28-Year Experience with Plasma Exchange and Low-Density Lipoprotein Apheresis in Managing a Patient with Familial Hypercholesterolemia: A Case Report</title><link>http://www.lipidjournal.com/article/PIIS1933287410001728/abstract?rss=yes</link><description>Synopsis: Patients with homozygous familial hypercholesterolemia (FH) have severe hypercholesterolemia since birth, which, if untreated, leads to early onset accelerated atherosclerosis with cardiovascular manifestations. Usual diet and medication management regimens are ineffective in lowering cholesterol in these patients. Apheresis procedures that help in removal of cholesterol from circulation have been used. In therapeutic plasma exchange (TPE), whole plasma, with cholesterol along with all other plasma constituents, is removed and replaced with albumin. Selective low-density lipoprotein (LDL)-removal systems were approved late the 1990s.With these systems, plasma separated from cellular elements is perfused through columns to selectively remove LDL and treated plasma is returned to the patient along with cells. No additional replacement solution is required.</description><dc:title>28-Year Experience with Plasma Exchange and Low-Density Lipoprotein Apheresis in Managing a Patient with Familial Hypercholesterolemia: A Case Report</dc:title><dc:creator>Ramakrishna L. Reddy</dc:creator><dc:identifier>10.1016/j.jacl.2010.03.073</dc:identifier><dc:source>Journal of Clinical Lipidology 4, 3 (2010)</dc:source><dc:date>2010-05-01</dc:date><prism:publicationName>Journal of Clinical Lipidology</prism:publicationName><prism:publicationDate>2010-05-01</prism:publicationDate><prism:volume>4</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1933-2874(10)X0004-6</prism:issueIdentifier><prism:section>Abstracts</prism:section><prism:startingPage>230</prism:startingPage><prism:endingPage>231</prism:endingPage></item></rdf:RDF>