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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\u003EAtherosclerosis is a diffuse process that starts early in childhood and progresses asymptomatically through adult life, often manifesting as coronary artery disease, stroke, transient ischemic attack, or peripheral arterial disease before the problem can be identified. Rupture of atherosclerotic plaque and its thrombotic complications are the major cause of acute coronary syndrome and cardiovascular death in the industrialized world. This article discusses some of the research that has advanced our understanding of the atherosclerotic process.\u003C\/p\u003E\n         \u003C\/div\u003E\u003Cul class=\u0022kwd-group\u0022\u003E\u003Cli class=\u0022kwd\u0022\u003Elipid disorders genomics\u003C\/li\u003E\u003Cli class=\u0022kwd\u0022\u003Ecoronary artery disease\u003C\/li\u003E\u003C\/ul\u003E\u003Cdiv class=\u0022section\u0022 id=\u0022sec-1\u0022\u003E\n         \n         \u003Cp id=\u0022p-2\u0022\u003EAtherosclerosis is a diffuse process that starts early in childhood and progresses asymptomatically through adult life, often manifesting as coronary artery disease, stroke, transient ischemic attack, or peripheral arterial disease before the problem can be identified. Rupture of atherosclerotic plaque and its thrombotic complications are the major cause of acute coronary syndrome (ACS) and cardiovascular (CV) death in the industrialized world. Valentin Fuster, MD, PhD, Mt. Sinai School of Medicine, New York, NY, discussed some of the research that has advanced our understanding of the atherosclerotic process.\u003C\/p\u003E\n         \u003Cp id=\u0022p-3\u0022\u003EAtherosclerotic plaques are a challenging imaging target due to their small size and tendency to change rapidly. By virtue of their enhanced spatial and temporal resolution, the new generation of imaging modalities (ie, magnetic resonance imaging, nuclear imaging, computed tomography, fluorescence imaging, intravascular ultrasonography, and optical coherence tomography) offers the possibility of identifying early atherosclerosis in at-risk individuals before the rupture occurs [Matter M et al. \u003Cem\u003EEur Heart J\u003C\/em\u003E 2009].\u003C\/p\u003E\n         \u003Cp id=\u0022p-4\u0022\u003EWe now know that peripheral blood mononuclear-derived endothelial progenitor cells (EPCs) bind platelets via the CD62P receptor and inhibit platelet activation, aggregation, and adhesion to collagen and thus prevent clot formation [Abou-Saleh H et al. \u003Cem\u003ECirculation\u003C\/em\u003E 2009]. We have also learned that exercise and pharmacological methods have the potential to increase and mobilize EPCs [Walther C et al. \u003Cem\u003ECirculation\u003C\/em\u003E 2009] which substitutes damaged endothelial cells as a result of risk factors [Moreno PR et al. \u003Cem\u003EJ Am Coll Cardiol\u003C\/em\u003E 2009]. Effective and protracted reduction of low-density lipoprotein cholesterol with statins is associated with a significant (p\u0026lt;0.01) regression of atherosclerotic lesions [Corti R et al. \u003Cem\u003ECirculation\u003C\/em\u003E 2002]. The reverse cholesterol transport (RCT) system has been shown to be the main mechanism for plaque regression [Moreno PR et al. \u003Cem\u003EJ Am Coll Cardiol\u003C\/em\u003E 2009]. In addition to raising high-density lipoprotein cholesterol, apolipoprotein A-I therapies and the promotion of cholesterol efflux from macrophages hold great promise and may be available for therapeutic application in the near future [Moreno PR et al. \u003Cem\u003EJ Am Coll Cardiol\u003C\/em\u003E 2009].\u003C\/p\u003E\n         \u003Cp id=\u0022p-5\u0022\u003EA number of independent studies now pinpoint inflammation as a key process that links multiple risk factors for atherosclerosis and its complications with altered arterial biology. Inflammasomes are multiprotein complexes that consist of caspase 1, PYCARD, a NALP, and sometimes caspase 5 or 11. Inflammasomes are responsible for activating inflammatory tissue responses. These cells are equipped with an array of signaling receptors that detect foreign molecular substances or altered endogenous molecules that appear under situations of stress [Stutz A et al. \u003Cem\u003EJ Clin Invest\u003C\/em\u003E 2009]. New insights into this process are coming from HIV research that show that the HIV infection may further increase cardiovascular disease risk via proatherosclerotic effects on smooth muscle cells and macrophages or by increasing inflammation [Currier JS. \u003Cem\u003ETop HIV Med\u003C\/em\u003E 2009].\u003C\/p\u003E\n         \u003Cp id=\u0022p-6\u0022\u003EDeath from cardiovascular disease (CVD) is and will remain for the foreseeable future the most significant cause of mortality worldwide; thus, the ability to determine an individual\u0027s risk of CVD and initiate treatment is essential. Christopher J. O\u0027Donnell, MD, Massachusetts General Hospital and Harvard Medical School, Boston, MA, discussed some of the advances that have made it possible to estimate individual risk and initiate earlier and, in some cases, personalized treatment.\u003C\/p\u003E\n         \u003Cp id=\u0022p-7\u0022\u003EThe Framingham Heart Study (FHS) is an ongoing multigenerational observational cohort study that has been used to identify CVD risk factors. Data from FHS participants were used to develop a coronary disease prediction algorithm to predict multivariate coronary heart disease (CHD) risk in patients without overt CHD [Wilson PW et al. \u003Cem\u003ECirculation\u003C\/em\u003E 1998]. Recently, D\u0027Agostino and colleagues reported on a new algorithm that expands on the Framingham CHD algorithm on the basis of a larger number of events, incorporates HDL cholesterol, and estimates absolute CVD risk [D\u0027Agostino RB et al. \u003Cem\u003ECirculation\u003C\/em\u003E 2008].\u003C\/p\u003E\n         \u003Cp id=\u0022p-8\u0022\u003EHigh-sensitivity C-reactive protein (hsCRP) is one of the most promising independent biomarkers for predicting future CV events. It also predicts the risk for hypertension and diabetes. Addition of hsCRP to established risk factors correctly reclassifies a substantial proportion of patients who are categorized as \u201cintermediate-risk\u201d by traditional risk scores into clinically relevant higher- or lower-risk categories [Ridker PM. \u003Cem\u003EJ Am Coll Cardiol\u003C\/em\u003E 2007]. Other biomarkers from different disease pathways, either alone or in combination, may further improve discrimination. In one study, the biomarkers that most strongly predicted major CV events were B-type natriuretic peptide level (adjusted hazard ratio, 1.25 per 1 SD increment in the log values) and urinary albumin-to-creatinine ratio (1.20) [Wang TJ et al. \u003Cem\u003EN Engl J Med\u003C\/em\u003E 2006]. In another study in the elderly, the simultaneous addition of several biomarkers of CV and renal abnormalities substantially improved the risk stratification for death from CV causes beyond that of a model that was based only on established risk factors (C statistic with biomarkers vs without biomarkers, 0.766 vs 0.664; p\u0026lt;0.001) [Zethelius B et al. \u003Cem\u003EN Engl J Med\u003C\/em\u003E 2008].\u003C\/p\u003E\n         \u003Cp id=\u0022p-9\u0022\u003EThe FHS is launching a major initiative to discover risk factors and markers that could lead to new blood tests to identify individuals without known CVD who are at high risk of atherosclerosis and metabolic diseases. This initiative, the Systems Approach to Biomarker Research in Cardiovascular Disease (SABRe CVD), will identify and validate new biomarkers, such as proteins, lipids, and messenger RNA molecules that are implicated in heart disease. The study will attempt to integrate proteomic, transcriptomic, lipomic, and metabolomic information to give a more complete picture of living organisms. The term \u201comic discovery\u201d is used to describe this process and refers to the comprehensive analysis of biological systems.\u003C\/p\u003E\n         \u003Cp id=\u0022p-10\u0022\u003EData suggest that parental CVD can predict offspring events that are independent of traditional risk factors [Lloyd-Jones, et al. \u003Cem\u003EJAMA\u003C\/em\u003E 2004]. The Human Genome Project has spawned several important \u201comic\u201d technologies that allow \u201cwhole-genome\u201d interrogation of sequence variation that will provide more exacting details of CVD mechanisms and, in some cases, are redefining its taxonomy. For instance, in one study, 42% of the residual variation in the quantity of coronary artery calcification was found to be attributable to genetic factors (p=0.0003) [Peyser P et al. \u003Cem\u003ECirculation\u003C\/em\u003E 2002].\u003C\/p\u003E\n         \u003Cp id=\u0022p-11\u0022\u003EAs of December 10, 2009, 443 genomewide association study papers have been published and 2083 single-nucleotide polymorphisms (SNPs) have been reported (\u003Ca href=\u0022http:\/\/www.genome.gov\/26525384\u0022\u003Ehttp:\/\/www.genome.gov\/26525384\u003C\/a\u003E). Genomewide association data have identified SNPs for most of the Framingham risk factors for CVD [Kathiresan S et al. \u003Cem\u003ENature Genetics\u003C\/em\u003E 2008, 2009]. A genotype score of nine validated SNPs that are associated with modulation in levels of LDL or HDL cholesterol has been found to be an independent risk factor for CVD. The score did not improve risk discrimination but did modestly improve clinical risk reclassification for individual subjects beyond standard clinical factors (\u003Ca id=\u0022xref-fig-1-1\u0022 class=\u0022xref-fig\u0022 href=\u0022#F1\u0022\u003EFigures 1A\u003C\/a\u003E and \u003Ca id=\u0022xref-fig-2-1\u0022 class=\u0022xref-fig\u0022 href=\u0022#F2\u0022\u003E1B\u003C\/a\u003E.) [Kathiresan S et al. \u003Cem\u003EN Engl J Med\u003C\/em\u003E 2008].\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\/9\/6\/4\/F1.large.jpg?width=800\u0026amp;height=600\u0026amp;carousel=1\u0022 title=\u0022Predictive Cumulative Freedom from MI, Ischemic Stroke, or Death From CHD According to Genotype Score.\u0022 class=\u0022fragment-images colorbox-load\u0022 rel=\u0022gallery-fragment-images-1439413222\u0022 data-figure-caption=\u0022Predictive Cumulative Freedom from MI, Ischemic Stroke, or Death From CHD According to Genotype Score.\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003E\u003Cimg class=\u0022fragment-image\u0022 alt=\u0022Figure 1A.\u0022 src=\u0022http:\/\/d282kpwvnogo5m.cloudfront.net\/content\/spmdc\/9\/6\/4\/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\/9\/6\/4\/F1.large.jpg?download=true\u0022 class=\u0022highwire-figure-link highwire-figure-link-download\u0022 title=\u0022Download Figure 1A.\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\/9\/6\/4\/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\/11537\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 1A.\u003C\/span\u003E \n               \u003Cp id=\u0022p-12\u0022 class=\u0022first-child\u0022\u003EPredictive Cumulative Freedom from MI, Ischemic Stroke, or Death From CHD According to Genotype Score.\u003C\/p\u003E\n            \u003Cq class=\u0022attrib\u0022 id=\u0022attrib-1\u0022\u003ECopyright \u00a9 2008 Massachusetts Medical Society. All rights reserved.\u003C\/q\u003E\u003Cdiv class=\u0022sb-div caption-clear\u0022\u003E\u003C\/div\u003E\u003C\/div\u003E\u003C\/div\u003E\n         \u003Cdiv id=\u0022F2\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\/9\/6\/4\/F2.large.jpg?width=800\u0026amp;height=600\u0026amp;carousel=1\u0022 title=\u0022ROC Curves for Incident MI, Ischemic Stroke, or Death From CHD During 10 Year Follow-Up.\u0022 class=\u0022fragment-images colorbox-load\u0022 rel=\u0022gallery-fragment-images-1439413222\u0022 data-figure-caption=\u0022ROC Curves for Incident MI, Ischemic Stroke, or Death From CHD During 10 Year Follow-Up.\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003E\u003Cimg class=\u0022fragment-image\u0022 alt=\u0022Figure 1B.\u0022 src=\u0022http:\/\/d282kpwvnogo5m.cloudfront.net\/content\/spmdc\/9\/6\/4\/F2.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\/9\/6\/4\/F2.large.jpg?download=true\u0022 class=\u0022highwire-figure-link highwire-figure-link-download\u0022 title=\u0022Download Figure 1B.\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\/9\/6\/4\/F2.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\/11541\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 1B.\u003C\/span\u003E \n               \u003Cp id=\u0022p-13\u0022 class=\u0022first-child\u0022\u003EROC Curves for Incident MI, Ischemic Stroke, or Death From CHD During 10 Year Follow-Up.\u003C\/p\u003E\n            \u003Cq class=\u0022attrib\u0022 id=\u0022attrib-2\u0022\u003ECopyright \u00a9 2008 Massachusetts Medical Society. All rights reserved.\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\u003EWhile genome sequencing is certainly the next frontier in personalized medicine, Dr. O\u0027Donnell concluded, we are still awaiting translation of this new information into effective prediction and prevention practices.\u003C\/p\u003E\n      \u003C\/div\u003E\u003Cul class=\u0022copyright-statement\u0022\u003E\u003Cli class=\u0022fn\u0022 id=\u0022copyright-statement-1\u0022\u003E\u00a9 2010 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\/9\/6\/4.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?nzmuu2\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?nzmuu2\u0022\u003E\u003C\/script\u003E\n\u003C\/body\u003E\u003C\/html\u003E"}