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type=\u0022text\/css\u0022 rel=\u0022stylesheet\u0022 href=\u0022\/\/d282kpwvnogo5m.cloudfront.net\/sites\/default\/files\/cdn\/css\/http\/css_Xg7z6oCTVgud_Q0huYz9x9iiD5H_2YPSJ5z2ZViSWdY.css\u0022 media=\u0022all\u0022 \/\u003E\n\u003Clink rel=\u0027stylesheet\u0027 type=\u0027text\/css\u0027 href=\u0027\/sites\/all\/modules\/contrib\/panels\/plugins\/layouts\/onecol\/onecol.css\u0027 \/\u003E\u003C\/head\u003E\u003Cbody\u003E\u003Cdiv class=\u0022panels-ajax-tab-panel panels-ajax-tab-panel-sageoa-tab-art\u0022\u003E\u003Cdiv class=\u0022panel-display panel-1col clearfix\u0022 \u003E\n  \u003Cdiv class=\u0022panel-panel panel-col\u0022\u003E\n    \u003Cdiv\u003E\u003Cdiv class=\u0022panel-pane pane-highwire-markup\u0022 \u003E\n  \n      \n  \n  \u003Cdiv class=\u0022pane-content\u0022\u003E\n    \u003Cdiv class=\u0022highwire-markup\u0022\u003E\u003Cdiv xmlns=\u0022http:\/\/www.w3.org\/1999\/xhtml\u0022 id=\u0022content-block-markup\u0022 xmlns:xhtml=\u0022http:\/\/www.w3.org\/1999\/xhtml\u0022\u003E\u003Cdiv class=\u0022article fulltext-view \u0022\u003E\u003Cspan class=\u0022highwire-journal-article-marker-start\u0022\u003E\u003C\/span\u003E\u003Cdiv class=\u0022section abstract\u0022 id=\u0022abstract-1\u0022\u003E\u003Ch2\u003ESummary\u003C\/h2\u003E\n            \u003Cp id=\u0022p-1\u0022\u003EThis article discusses whether pharmacotherapy improves outcomes in patients with elevated triglycerides (TG) and normal low-density lipoprotein cholesterol. Limited data exist on the benefits of TG-lowering drugs on top of statins in high-risk patients.\u003C\/p\u003E\n         \u003C\/div\u003E\u003Cul class=\u0022kwd-group\u0022\u003E\u003Cli class=\u0022kwd\u0022\u003ELipid Disorders\u003C\/li\u003E\u003C\/ul\u003E\u003Cp id=\u0022p-2\u0022\u003EMarja-Riitta Taskinen, MD, Helsinki University Hospital, Helsinki, Finland, discussed whether pharmacotherapy improves outcomes in patients with elevated triglycerides (TG) and normal low-density lipoprotein cholesterol (LDL-C). Limited data exist on the benefits of TG-lowering drugs on top of statins in high-risk patients.\u003C\/p\u003E\u003Cp id=\u0022p-3\u0022\u003EA post hoc analysis of the PROVE IT-TIMI 22 trial, which randomized patients with acute coronary syndrome (ACS) to either intensive or standard statin therapy, showed that achievement of an on-treatment TG \u0026lt;150 mg\/dL was independently associated with a lower risk of recurrent coronary heart disease (CHD) events, lending support to the concept that achieving low TG may be an additional consideration beyond low LDL-C in patients after ACS [Miller M. \u003Cem\u003EJ Am Coll Cardiol\u003C\/em\u003E 2008].\u003C\/p\u003E\u003Cp id=\u0022p-4\u0022\u003EThe Fenofibrate Intervention and Event Lowering in Diabetes (FIELD) study, which randomized 9795 patients with type 2 diabetes mellitus (T2DM) and dyslipidemia to either fenofibrate or placebo, showed no reduction in the primary endpoint of coronary events with fenofibrate (p=0.16) [Keech A et al. \u003Cem\u003ELancet\u003C\/em\u003E 2005]. While the overall trial was neutral, there did appear to be benefit in an exploratory analysis of individuals with marked hypertriglyceridemia, especially among those with features of metabolic syndrome [Scott R. \u003Cem\u003EDiabetes Care\u003C\/em\u003E 2009]. Sacks et al. [Sacks FM et al. \u003Cem\u003EN Engl J Med\u003C\/em\u003E 2010] also found that fibrate treatment, combined with statin therapy, was not beneficial in reducing cardiovascular events compared with statin therapy alone in patients with T2DM in the primary results of the ACCORD trial. There was, however, a nonsignificant suggestion of heterogeneity in patients with high TG and low HDL (p-interaction 0.057).\u003C\/p\u003E\u003Cp id=\u0022p-5\u0022\u003EChapman et al. [Chapman MJ et al. \u003Cem\u003EEur Heart J\u003C\/em\u003E 2011] observed that even at the LDL-C goal, patients with cardiometabolic lipid abnormalities remain at a heightened risk of cardiovascular (CV) events. In the PROCAM study, about twice as many myocardial infarction (MI) survivors had elevated TG (200 mg\/dL) and\/or low HDL-C (\u0026lt;40 mg\/dL) versus matched controls. This dyslipidemic profile was associated with increased CV risk, even in patients who achieved low LDL-C levels [Assmann G et al. \u003Cem\u003EDiab Vasc Dis Res\u003C\/em\u003E 2010].\u003C\/p\u003E\u003Cp id=\u0022p-6\u0022\u003EProf. Taskinen noted that some high-risk individuals remain at a heightened risk of CV events even after achieving their LDL-C goal. Elevated TG, as a marker of triglyceride-rich lipoproteins (TRL) and their remnants, and low levels of HDL-C have been implicated in this residual excess CV risk. Prof Taskinen went on to note that elevated TG (\u2265150 mg\/dL) and\/or low HDL-C levels (\u0026lt;40 mg\/dL) should be factors in considering further treatment [Chapman MJ et al. \u003Cem\u003EEur Heart J\u003C\/em\u003E 2011].\u003C\/p\u003E\u003Cp id=\u0022p-7\u0022\u003EWhile there is observational and epidemiological evidence of an association between TG and outcomes, the benefits that have been observed with TG-specific therapies have been mixed and modest, especially in comparison with the proven benefits of statin therapy.\u003C\/p\u003E\u003Cdiv class=\u0022section\u0022 id=\u0022sec-1\u0022\u003E\n         \u003Ch2 class=\u0022\u0022\u003EHDL \u2013 Is It a Treatment Target?\u003C\/h2\u003E\n         \u003Cp id=\u0022p-8\u0022\u003EM. John Chapman, PhD, DSc, FESC, University Pierre and Marie Curie, Paris, France, discussed how both HDL quality and quantity may be important, noting that the role of HDL goes far beyond reverse cholesterol transport, and presented data on its antioxidant and anti-inflammatory properties.\u003C\/p\u003E\n         \u003Cp id=\u0022p-9\u0022\u003ECurrent observational evidence suggests a causal relationship between CV risk, elevated TRLs and their remnants, and low HDL-C [MJ Chapman. \u003Cem\u003EEur Heart J\u003C\/em\u003E 2011]. Wolfram et al. [Wolfram MR et al. \u003Cem\u003EAm J Cardiol\u003C\/em\u003E 2006] found that patients with low HDL-C (\u0026lt;40 mg\/dL in men; \u0026lt;45 mg\/dL in women) are 3 times more likely to die after ACS (RR, 0.33; p=0.033).\u003C\/p\u003E\n         \u003Cp id=\u0022p-10\u0022\u003EWhile statin treatment reduces the risk of CV events in patients with low HDL, it does not abrogate low HDL-associated CV risk. Barter et al. [Barter PJ et al. \u003Cem\u003EN Engl J Med\u003C\/em\u003E 2007] found that HDL-C levels predicted major CV events in patients who were treated with statins. Similarly, Sazonov et al. [Sazonov V. \u003Cem\u003EAtherosclerosis\u003C\/em\u003E 2010] found that in statin-treated patients, while overall rates of adverse events were lower than in nonstatin-treated patients, elevated LDL-C, reduced HDL-C, and\/or elevated TGs were still associated with a significantly increased relative risk of CV and\/or cerebrovascular events compared with patients who had lipid parameters at target (HR, 1.24; 95% CI, 1.06 to 1.46; p=0.006).\u003C\/p\u003E\n         \u003Cp id=\u0022p-11\u0022\u003EThe European Atherosclerosis Society Consensus Panel recently reviewed evidence for elevated TG-rich lipoproteins and low levels of HDL-C as CV risk factors [Chapman JM et al. \u003Cem\u003EEur Heart J\u003C\/em\u003E 2011]. They concluded that the data suggest that elevated TGs and their remnants, combined with low HDL-C, may play a causal role in premature coronary or peripheral atherosclerosis.\u003C\/p\u003E\n         \u003Cp id=\u0022p-12\u0022\u003ERecent applications of mass spectrometry-based proteomics have provided a new appreciation for the complexity of the HDL proteome by detecting more than 50 distinct HDL-associated proteins. Many proteins have known functions that do not fit easily into the randomized controlled trial paradigm (\u003Ca id=\u0022xref-fig-1-1\u0022 class=\u0022xref-fig\u0022 href=\u0022#F1\u0022\u003EFigure 1\u003C\/a\u003E) [Gordon SM et al. \u003Cem\u003ETrends Endocrinol Metab\u003C\/em\u003E 2011].\u003C\/p\u003E\n         \u003Cdiv id=\u0022F1\u0022 class=\u0022fig pos-float  odd\u0022\u003E\u003Cdiv class=\u0022highwire-figure\u0022\u003E\u003Cdiv class=\u0022fig-inline-img-wrapper\u0022\u003E\u003Cdiv class=\u0022fig-inline-img\u0022\u003E\u003Ca href=\u0022http:\/\/d282kpwvnogo5m.cloudfront.net\/content\/spmdc\/11\/10\/29\/F1.large.jpg?width=800\u0026amp;height=600\u0026amp;carousel=1\u0022 title=\u0022Atheroprotective and Vasculoprotective Functions of HDL.\u0022 class=\u0022fragment-images colorbox-load\u0022 rel=\u0022gallery-fragment-images-1835479831\u0022 data-figure-caption=\u0022Atheroprotective and Vasculoprotective Functions of HDL.\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003E\u003Cimg class=\u0022fragment-image\u0022 alt=\u0022Figure 1.\u0022 src=\u0022http:\/\/d282kpwvnogo5m.cloudfront.net\/content\/spmdc\/11\/10\/29\/F1.medium.gif\u0022\/\u003E\u003C\/a\u003E\u003C\/div\u003E\u003C\/div\u003E\u003Cul class=\u0022highwire-figure-links inline\u0022\u003E\u003Cli class=\u00220 first\u0022\u003E\u003Ca href=\u0022http:\/\/d282kpwvnogo5m.cloudfront.net\/content\/spmdc\/11\/10\/29\/F1.large.jpg?download=true\u0022 class=\u0022highwire-figure-link highwire-figure-link-download\u0022 title=\u0022Download Figure 1.\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EDownload figure\u003C\/a\u003E\u003C\/li\u003E\u003Cli class=\u00221\u0022\u003E\u003Ca href=\u0022http:\/\/d282kpwvnogo5m.cloudfront.net\/content\/spmdc\/11\/10\/29\/F1.large.jpg\u0022 class=\u0022highwire-figure-link highwire-figure-link-newtab\u0022 target=\u0022_blank\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EOpen in new tab\u003C\/a\u003E\u003C\/li\u003E\u003Cli class=\u00222 last\u0022\u003E\u003Ca href=\u0022\/highwire\/powerpoint\/12455\u0022 class=\u0022highwire-figure-link highwire-figure-link-ppt\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EDownload powerpoint\u003C\/a\u003E\u003C\/li\u003E\u003C\/ul\u003E\u003C\/div\u003E\u003Cdiv class=\u0022fig-caption attrib\u0022\u003E\u003Cspan class=\u0022fig-label\u0022\u003EFigure 1.\u003C\/span\u003E \n               \u003Cp id=\u0022p-13\u0022 class=\u0022first-child\u0022\u003EAtheroprotective and Vasculoprotective Functions of HDL.\u003C\/p\u003E\n            \u003Cq class=\u0022attrib\u0022 id=\u0022attrib-1\u0022\u003EReproduced with permission from M.J. Chapman, MD.\u003C\/q\u003E\u003Cdiv class=\u0022sb-div caption-clear\u0022\u003E\u003C\/div\u003E\u003C\/div\u003E\u003C\/div\u003E\n         \u003Cp id=\u0022p-14\u0022\u003EFindings link HDL to innate immunity and proteolytic pathways that are involved in inflammation and coagulation. The importance of these discoveries has been underscored by the demonstration that the proteomic profiles of HDL are altered in patients with CVD and can even be modified by lipid modification therapies [Gordon SM et al. \u003Cem\u003ETrends Endocrinol\u003C\/em\u003E Metab 2011].\u003C\/p\u003E\n      \u003C\/div\u003E\u003Cdiv class=\u0022section\u0022 id=\u0022sec-2\u0022\u003E\n         \u003Ch2 class=\u0022\u0022\u003ECETP Inhibition: Pros and Cons\u003C\/h2\u003E\n         \u003Cp id=\u0022p-15\u0022\u003EPhilip Barter, MD, PhD, The Heart Research Institute, Sydney, Australia, provided an update on a novel class of HDL-raising drugs, the cholesterol ester transfer protein (CETP) inhibitors.\u003C\/p\u003E\n         \u003Cp id=\u0022p-16\u0022\u003EDr. Barter explained that CETP inhibition increases HDL-C and apoA-1 levels, decreases LDL-C and apoB levels, and decreases the content of very low-density lipoprotein by transferring cholesteryl esters from HDL to other lipoproteins [Barter P et al. \u003Cem\u003EBiochem Biophys Acta\u003C\/em\u003E 1978]. It also plays a role in reverse cholesterol transport [Barter P. \u003Cem\u003EBiochem J\u003C\/em\u003E 1982].\u003C\/p\u003E\n         \u003Cp id=\u0022p-17\u0022\u003EA meta-analysis of CETP genotypes and subjects with CHD showed polymorphisms that are associated with lower CETP mass and activity, have higher HDL-C levels and a significantly reduced coronary risk [Thompson A et al. \u003Cem\u003EJAMA\u003C\/em\u003E 2008].\u003C\/p\u003E\n         \u003Cp id=\u0022p-18\u0022\u003EHowever, inhibiting CETP in humans with torcetrapib not only failed to reduce atherosclerosis in three imaging trials but also increased, rather than decreased, CV events in a large-scale endpoint trial (ILLUMINATE) [Barter P et al. \u003Cem\u003EN Engl J Med\u003C\/em\u003E 2007]. Possible explanations for the adverse outcomes are that torcetrapib had an adverse off-target effect that was mediated through aldosterone that manifested in elevated blood pressure or that CETP inhibition, as a mechanism for raising HDL, may be harmful.\u003C\/p\u003E\n         \u003Cp id=\u0022p-19\u0022\u003ECETP drugs that are currently being assessed in large outcome trials include dalcetrapib and anacetrapib. The dal-OUTCOMES trial is assessing the efficacy and safety of dalcetrapib in 15,600 patients with recent ACS [Schwartz GG et al. \u003Cem\u003EAm Heart J\u003C\/em\u003E 2009]. In the DEFINE trial, a Phase 2 safety trial of anacetrapib, treatment had no adverse effect on blood pressure, electrolytes, or aldosterone levels. The prespecified Bayesian analysis indicated that the event distribution in DEFINE provided a predictive probability (confidence) of 94% that anacetrapib would not be associated with the 25% increase in CV events that was seen in the torcetrapib trial [Cannon CP et al. \u003Cem\u003EN Engl J Med\u003C\/em\u003E 2010]. The efficacy and safety of anacetrapib are being evaluated in a large CV outcome trial, called REVEAL.\u003C\/p\u003E\n         \u003Cp id=\u0022p-20\u0022\u003EAccording to Dr. Barter, these CETP drugs hold promise as an addition to the lipid-lowering arsenal, but it will take a few years for the results of clinical outcome trials to determine whether that promise can be realized in clinical settings.\u003C\/p\u003E\n         \u003Cp id=\u0022p-21\u0022\u003EReaders should note that while there is strong observational and epidemiological data that show an association between low HDL and adverse CV events, there is still debate as to whether HDL is an actual mediator of vascular events or whether it is a potent integrative risk marker. To date, there have been no large outcomes trials that have shown a benefit of HDL-raising therapy, particularly on a background of statin therapy.\u003C\/p\u003E\n         \u003Cp id=\u0022p-22\u0022\u003ERecently, the Atherothrombosis Intervention in Metabolic Syndrome with Low HDL Cholesterol\/High Triglyceride and Impact on Global Health Outcomes (AIM-HIGH) study, which randomized 3414 patients with cardiovascular disease, high TG, and low HDL to high-dose extended-release niacin or placebo on a background of statin therapy, was halted prematurely (18 months ahead of schedule), because niacin offered no benefit. In addition, there were numerically more strokes with niacin (28 vs 12). Additional exploratory analyses from this trial will be important to understand if there are specific subgroups that did benefit from niacin.\u003C\/p\u003E\n         \u003Cp id=\u0022p-23\u0022\u003EOverall, while observational data show an association between elevated TG and adverse outcomes, and low HDL and adverse outcomes, data that support clinical benefits of medications that target these lipid abnormalities remain mixed. Statin therapy that is titrated to LDL reduction goals remains the most critical component of lipid therapy for patients who are at risk of CV events. Results of large outcomes studies that use CETP inhibitors, which lead to robust increases in HDL as well as LDL reduction, will provide important new information.\u003C\/p\u003E\n      \u003C\/div\u003E\u003Cul class=\u0022copyright-statement\u0022\u003E\u003Cli class=\u0022fn\u0022 id=\u0022copyright-statement-1\u0022\u003E\u00a9 2011 MD Conference Express\u003C\/li\u003E\u003C\/ul\u003E\u003Cspan class=\u0022highwire-journal-article-marker-end\u0022\u003E\u003C\/span\u003E\u003C\/div\u003E\u003Cspan id=\u0022related-urls\u0022\u003E\u003C\/span\u003E\u003C\/div\u003E\u003Ca href=\u0022http:\/\/mdc.sagepub.com\/content\/11\/10\/29.abstract\u0022 class=\u0022hw-link hw-link-article-abstract\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EView Summary\u003C\/a\u003E\u003C\/div\u003E  \u003C\/div\u003E\n\n  \n  \u003C\/div\u003E\n\u003C\/div\u003E\n  \u003C\/div\u003E\n\u003C\/div\u003E\n\u003C\/div\u003E\u003Cscript type=\u0022text\/javascript\u0022 src=\u0022http:\/\/mdc.sagepub.com\/sites\/all\/modules\/highwire\/highwire\/plugins\/highwire_markup_process\/js\/highwire_figures.js?nzmz8d\u0022\u003E\u003C\/script\u003E\n\u003Cscript type=\u0022text\/javascript\u0022 src=\u0022http:\/\/mdc.sagepub.com\/sites\/all\/modules\/highwire\/highwire\/plugins\/highwire_markup_process\/js\/highwire_openurl.js?nzmz8d\u0022\u003E\u003C\/script\u003E\n\u003C\/body\u003E\u003C\/html\u003E"}