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	High density lipoprotein (HDL) therapy in cardiovascular disease management 

Introduction
Dyslipidaemia is a significant risk factor, and a common finding in patients with advanced atherosclerosis. Patients typically have high LDL, triglycerides and low HDL. Over the past two decades the focus of dyslipidaemia treatment was LDL lowering, particularly with statins. Despite the dramatic improvement in primary and secondary prevention of atherosclerotic clinical sequelae with statins, it is apparent that other approaches are needed.
Evidence that low plasma HDL is a causative factor in atherogenesis is growing, and there is increasing interest in HDL based therapy. HDL molecules have been shown to possess acute plaque stabilising properties. Evidence from early clinical studies utilising infusion of HDL support a compelling argument for its use as an acute therapeutic modality targeting the unstable atherosclerotic plaque. 

HDL and the risk of cardiovascular disease
It has been long established that plasma concentrations of HDL are inversely related to the risk of cardiovascular disease (CVD)  ADDIN EN.CITE <EndNote><Cite><Author>Rhoads</Author><Year>1976</Year><RecNum>900</RecNum><DisplayText><style face="superscript">1</style></DisplayText><record><rec-number>900</rec-number><foreign-keys><key app="EN" db-id="90dsvsxdjxwazqe0xdmpzaxsdea20t2fdvvt" timestamp="0">900</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Rhoads, G. G.</author><author>Gulbrandsen, C. L.</author><author>Kagan, A.</author></authors></contributors><titles><title>Serum lipoproteins and coronary heart disease in a population study of Hawaii Japanese men</title><secondary-title>N Engl J Med</secondary-title></titles><pages>293-8</pages><volume>294</volume><number>6</number><edition>1976/02/05</edition><keywords><keyword>Aged</keyword><keyword>Cholesterol/*blood</keyword><keyword>Coronary Disease/blood/*epidemiology</keyword><keyword>*Ethnic Groups</keyword><keyword>Hawaii</keyword><keyword>Humans</keyword><keyword>Hyperlipidemias/epidemiology</keyword><keyword>Japan/ethnology</keyword><keyword>Lipoproteins/*blood</keyword><keyword>Lipoproteins, HDL/blood</keyword><keyword>Lipoproteins, LDL/blood</keyword><keyword>Lipoproteins, VLDL/blood</keyword><keyword>Male</keyword><keyword>Middle Aged</keyword><keyword>Risk</keyword><keyword>Triglycerides/*blood</keyword></keywords><dates><year>1976</year><pub-dates><date>Feb 5</date></pub-dates></dates><isbn>0028-4793 (Print)</isbn><accession-num>173994</accession-num><urls><related-urls><url>http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&amp;db=PubMed&amp;dopt=Citation&amp;list_uids=173994</url></related-urls></urls><language>eng</language></record></Cite></EndNote>1. Low plasma HDL concentration is the most common lipid abnormality observed in men with coronary heart disease (CHD)  ADDIN EN.CITE <EndNote><Cite><Author>Genest</Author><Year>1991</Year><RecNum>899</RecNum><DisplayText><style face="superscript">2</style></DisplayText><record><rec-number>899</rec-number><foreign-keys><key app="EN" db-id="90dsvsxdjxwazqe0xdmpzaxsdea20t2fdvvt" timestamp="0">899</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Genest, J. J.</author><author>McNamara, J. R.</author><author>Salem, D. N.</author><author>Schaefer, E. J.</author></authors></contributors><auth-address>Lipid Metabolism Laboratory, United States Department of Agriculture Human Nutrition Research Center on Aging, Tufts University, Boston, Massachusetts.</auth-address><titles><title>Prevalence of risk factors in men with premature coronary artery disease</title><secondary-title>Am J Cardiol</secondary-title></titles><pages>1185-9</pages><volume>67</volume><number>15</number><edition>1991/06/01</edition><keywords><keyword>Adult</keyword><keyword>Cholesterol, HDL/blood</keyword><keyword>Cholesterol, LDL/blood</keyword><keyword>Coronary Disease/*epidemiology</keyword><keyword>Diabetes Mellitus/epidemiology</keyword><keyword>Humans</keyword><keyword>Hypertension/epidemiology</keyword><keyword>Male</keyword><keyword>Massachusetts/epidemiology</keyword><keyword>Middle Aged</keyword><keyword>Prevalence</keyword><keyword>Risk Factors</keyword><keyword>Smoking/epidemiology</keyword></keywords><dates><year>1991</year><pub-dates><date>Jun 1</date></pub-dates></dates><isbn>0002-9149 (Print)</isbn><accession-num>2035438</accession-num><urls><related-urls><url>http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&amp;db=PubMed&amp;dopt=Citation&amp;list_uids=2035438</url></related-urls></urls><electronic-resource-num>0002-9149(91)90924-A [pii]</electronic-resource-num><language>eng</language></record></Cite></EndNote>2. As shown in the Framingham study, this inverse relationship is independent of LDL levels  ADDIN EN.CITE <EndNote><Cite><Author>Castelli</Author><Year>1988</Year><RecNum>897</RecNum><DisplayText><style face="superscript">3</style></DisplayText><record><rec-number>897</rec-number><foreign-keys><key app="EN" db-id="90dsvsxdjxwazqe0xdmpzaxsdea20t2fdvvt" timestamp="0">897</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Castelli, W. P.</author></authors></contributors><auth-address>National Heart, Lung and Blood Institute, Framingham, Massachusetts 01701.</auth-address><titles><title>Cholesterol and lipids in the risk of coronary artery disease--the Framingham Heart Study</title><secondary-title>Can J Cardiol</secondary-title></titles><pages>5A-10A</pages><volume>4 Suppl A</volume><edition>1988/07/01</edition><keywords><keyword>Adult</keyword><keyword>Cholesterol/*blood</keyword><keyword>Coronary Disease/blood/*prevention &amp; control</keyword><keyword>Female</keyword><keyword>Follow-Up Studies</keyword><keyword>Humans</keyword><keyword>Lipids/*blood</keyword><keyword>Male</keyword><keyword>Mass Screening</keyword><keyword>Massachusetts</keyword><keyword>Middle Aged</keyword><keyword>Prospective Studies</keyword><keyword>Risk Factors</keyword><keyword>Time Factors</keyword></keywords><dates><year>1988</year><pub-dates><date>Jul</date></pub-dates></dates><isbn>0828-282X (Print)</isbn><accession-num>3179802</accession-num><urls><related-urls><url>http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&amp;db=PubMed&amp;dopt=Citation&amp;list_uids=3179802</url></related-urls></urls><language>eng</language></record></Cite></EndNote>3. 
Low plasma HDL concentration has been redefined as < 40 mg/dL for men and < 50 mg/dL for women  ADDIN EN.CITE <EndNote><Cite><Author>Toth</Author><Year>2005</Year><RecNum>898</RecNum><DisplayText><style face="superscript">4</style></DisplayText><record><rec-number>898</rec-number><foreign-keys><key app="EN" db-id="90dsvsxdjxwazqe0xdmpzaxsdea20t2fdvvt" timestamp="0">898</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Toth, Peter P.</author></authors></contributors><titles><title>The &quot;Good Cholesterol&quot;: High-Density Lipoprotein</title><secondary-title>Circulation</secondary-title></titles><pages>e89-91</pages><volume>111</volume><number>5</number><dates><year>2005</year><pub-dates><date>February 8, 2005</date></pub-dates></dates><urls><related-urls><url>http://circ.ahajournals.org</url></related-urls></urls><electronic-resource-num>10.1161/01.cir.0000154555.07002.ca</electronic-resource-num></record></Cite></EndNote>4. Epidemiological studies have shown that for every 1mg/dL rise in HDL the risk for developing CVD decreases by 2% in men and 3% in women  ADDIN EN.CITE <EndNote><Cite><Author>Gordon</Author><Year>1989</Year><RecNum>896</RecNum><DisplayText><style face="superscript">5</style></DisplayText><record><rec-number>896</rec-number><foreign-keys><key app="EN" db-id="90dsvsxdjxwazqe0xdmpzaxsdea20t2fdvvt" timestamp="0">896</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Gordon, D. J.</author><author>Probstfield, J. L.</author><author>Garrison, R. J.</author><author>Neaton, J. D.</author><author>Castelli, W. P.</author><author>Knoke, J. D.</author><author>Jacobs, D. R., Jr.</author><author>Bangdiwala, S.</author><author>Tyroler, H. A.</author></authors></contributors><auth-address>Lipid Metabolism-Atherogenesis Branch, National Institutes of Health, Bethesda, Maryland, MD 20892.</auth-address><titles><title>High-density lipoprotein cholesterol and cardiovascular disease. Four prospective American studies</title><secondary-title>Circulation</secondary-title></titles><pages>8-15</pages><volume>79</volume><number>1</number><edition>1989/01/01</edition><keywords><keyword>Adult</keyword><keyword>Aged</keyword><keyword>Cardiovascular Diseases/*blood</keyword><keyword>Cholesterol, HDL/*blood</keyword><keyword>Clinical Trials as Topic</keyword><keyword>Cohort Studies</keyword><keyword>Female</keyword><keyword>Humans</keyword><keyword>Male</keyword><keyword>Middle Aged</keyword><keyword>Prospective Studies</keyword><keyword>Regression Analysis</keyword><keyword>Risk Factors</keyword><keyword>Sex Factors</keyword><keyword>Statistics as Topic</keyword></keywords><dates><year>1989</year><pub-dates><date>Jan</date></pub-dates></dates><isbn>0009-7322 (Print)</isbn><accession-num>2642759</accession-num><urls><related-urls><url>http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&amp;db=PubMed&amp;dopt=Citation&amp;list_uids=2642759</url></related-urls></urls><language>eng</language></record></Cite></EndNote>5.
Given this measurable impact of HDL dyslipidaemia on CVD risk, HDL-based therapy has become an obvious approach to decreasing the risk of atherosclerosis. 



HDL structure and the reverse cholesterol transport
HDLs represent a class of small, high density lipoproteins. Apolipoprotein-A1 (Apo- A1) is the main component in HDL, accounting for 70% of HDL�s protein content. Other proteins associated with HDL, which are involved in lipid metabolism or with possible antioxidant activities include enzymes such as lecithin�cholesterol acyltransferase (LCAT), lipoprotein-associated phospholipase A2 (also called platelet-activating factor-acetylhydrolase, PAF-AH), paraoxonase 1 (PON1) and glutathione selenoperoxidase (GPX)  ADDIN EN.CITE <EndNote><Cite><Author>Kontush</Author><Year>2006</Year><RecNum>902</RecNum><DisplayText><style face="superscript">6</style></DisplayText><record><rec-number>902</rec-number><foreign-keys><key app="EN" db-id="90dsvsxdjxwazqe0xdmpzaxsdea20t2fdvvt" timestamp="0">902</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Kontush, A.</author><author>Chapman, M. J.</author></authors></contributors><auth-address>Dyslipoproteinemia and Atherosclerosis Research Unit, National Institute for Health and Medical Research, Hopital de la Pitie, 83 boulevard de l&apos;Hopital, 75651 Paris Cedex 13, France. kontush@chups.jussieu.fr</auth-address><titles><title>Functionally defective high-density lipoprotein: a new therapeutic target at the crossroads of dyslipidemia, inflammation, and atherosclerosis</title><secondary-title>Pharmacol Rev</secondary-title></titles><pages>342-74</pages><volume>58</volume><number>3</number><edition>2006/09/14</edition><keywords><keyword>Animals</keyword><keyword>Atherosclerosis/*drug therapy</keyword><keyword>Dyslipidemias/*drug therapy</keyword><keyword>Humans</keyword><keyword>Inflammation/*drug therapy</keyword><keyword>Lipoproteins, HDL/*genetics/*physiology</keyword><keyword>Metabolic Diseases/etiology</keyword><keyword>Models, Biological</keyword></keywords><dates><year>2006</year><pub-dates><date>Sep</date></pub-dates></dates><isbn>0031-6997 (Print)</isbn><accession-num>16968945</accession-num><urls><related-urls><url>http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&amp;db=PubMed&amp;dopt=Citation&amp;list_uids=16968945</url></related-urls></urls><electronic-resource-num>58/3/342 [pii]&#xD;10.1124/pr.58.3.1</electronic-resource-num><language>eng</language></record></Cite></EndNote>6. 
HDL functions as a transporter of cholesterol from peripheral tissue to the liver for excretion. This process is known as reverse cholesterol transport (RCT) (Figure 1): 
HDL molecules are synthesised in the liver (70%) and small intestine (30%) as primary protein-rich, lipid-poor disc-shaped particles known as nascent native HDL. 
These lipid poor discoidal molecules are able to take up cholesterol from arterial wall and macrophages via the ATP-binding cassette A-1 (ABCA-1) receptor. 
Cholesterol is transferred into the lipid poor HDL and is then esterified by LCAT. When cholesterol is esterified and packed into the core of discoidal HDL, it forms mature spherical HDL.
HDL facilitates cholesterol excretion by the liver through two pathways:
Direct pathway: HDL transports cholesterol directly to the liver via scavenger receptor class-B type-1 (SR-B1).
Indirect pathway: Cholesteryl ester is transferred to VLDL and LDL by interacting with cholesteryl ester transfer protein (CETP). Cholesterol is then transported to the liver through the endogenous pathway described above.
RCT was one of the earliest recognised properties of HDL. A lot of the antiatherogenic properties of HDL were initially attributed to this process. More recent work showed that HDL and its reconstituted particles have other properties that could contribute to the antiatherogenic effects, independent of RCT. 



Other antiatherogenic functions of HDL
There are several mechanisms apart from RCT by which HDL protects against atherosclerosis. These include antioxidant effects, anti-inflammatory effects, antithrombotic effects, and modification of endothelial function (Figure 2).
HDL and its mimetic peptides have been shown to limit LDL oxidation  ADDIN EN.CITE <EndNote><Cite><Author>Parthasarathy</Author><Year>1994</Year><RecNum>905</RecNum><DisplayText><style face="superscript">7</style></DisplayText><record><rec-number>905</rec-number><foreign-keys><key app="EN" db-id="90dsvsxdjxwazqe0xdmpzaxsdea20t2fdvvt" timestamp="0">905</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Parthasarathy, S.</author><author>Santanam, N.</author></authors></contributors><auth-address>Department of Gynecology and Obstetrics, Emory University School of Medicine, Atlanta, Georgia.</auth-address><titles><title>Mechanisms of oxidation, antioxidants, and atherosclerosis</title><secondary-title>Curr Opin Lipidol</secondary-title></titles><pages>371-5</pages><volume>5</volume><number>5</number><edition>1994/10/01</edition><keywords><keyword>Animals</keyword><keyword>*Antioxidants</keyword><keyword>Arachidonate 15-Lipoxygenase/metabolism</keyword><keyword>Arteriosclerosis/*metabolism</keyword><keyword>Humans</keyword><keyword>Lipoproteins, LDL/metabolism</keyword><keyword>Metals/metabolism</keyword><keyword>Nitric Oxide/physiology</keyword><keyword>Oxidation-Reduction</keyword><keyword>Peroxidases/metabolism</keyword><keyword>Sulfhydryl Compounds/metabolism</keyword><keyword>Superoxides/metabolism</keyword></keywords><dates><year>1994</year><pub-dates><date>Oct</date></pub-dates></dates><isbn>0957-9672 (Print)</isbn><accession-num>7858912</accession-num><urls><related-urls><url>http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&amp;db=PubMed&amp;dopt=Citation&amp;list_uids=7858912</url></related-urls></urls><language>eng</language></record></Cite></EndNote>7. Antioxidant properties are mediated through paraoxonases (PONs), which circulate the blood bound to HDL  ADDIN EN.CITE <EndNote><Cite><Author>Durrington</Author><Year>2001</Year><RecNum>906</RecNum><DisplayText><style face="superscript">8</style></DisplayText><record><rec-number>906</rec-number><foreign-keys><key app="EN" db-id="90dsvsxdjxwazqe0xdmpzaxsdea20t2fdvvt" timestamp="0">906</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Durrington, P. N.</author><author>Mackness, B.</author><author>Mackness, M. I.</author></authors></contributors><auth-address>University of Manchester Department of Medicine, Manchester Royal Infirmary, Manchester, England. pdurrington@hq.cmht.nwest.nhs.uk</auth-address><titles><title>Paraoxonase and atherosclerosis</title><secondary-title>Arterioscler Thromb Vasc Biol</secondary-title></titles><pages>473-80</pages><volume>21</volume><number>4</number><edition>2001/04/17</edition><keywords><keyword>Antioxidants/pharmacology</keyword><keyword>Arteriosclerosis/metabolism/*physiopathology/prevention &amp; control</keyword><keyword>Aryldialkylphosphatase</keyword><keyword>Cholesterol, HDL/drug effects/physiology</keyword><keyword>Coronary Disease/metabolism/physiopathology/prevention &amp; control</keyword><keyword>Esterases/*physiology</keyword><keyword>Humans</keyword><keyword>Lipid Peroxidation/drug effects/physiology</keyword><keyword>Oxidative Stress/drug effects/physiology</keyword></keywords><dates><year>2001</year><pub-dates><date>Apr</date></pub-dates></dates><isbn>1524-4636 (Electronic)</isbn><accession-num>11304460</accession-num><urls><related-urls><url>http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&amp;db=PubMed&amp;dopt=Citation&amp;list_uids=11304460</url></related-urls></urls><language>eng</language></record></Cite></EndNote>8. Other enzymes such as PAF-AH and LCAT have also been implicated in contributing to HDL�s antioxidant properties  ADDIN EN.CITE <EndNote><Cite><Author>Van Lenten</Author><Year>2001</Year><RecNum>907</RecNum><DisplayText><style face="superscript">9</style></DisplayText><record><rec-number>907</rec-number><foreign-keys><key app="EN" db-id="90dsvsxdjxwazqe0xdmpzaxsdea20t2fdvvt" timestamp="0">907</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Van Lenten, B. J.</author><author>Navab, M.</author><author>Shih, D.</author><author>Fogelman, A. M.</author><author>Lusis, A. J.</author></authors></contributors><auth-address>Department of Medicine, University of California, Los Angeles, California, USA. bvanlent@mednet.ucla.edu</auth-address><titles><title>The role of high-density lipoproteins in oxidation and inflammation</title><secondary-title>Trends Cardiovasc Med</secondary-title></titles><pages>155-61</pages><volume>11</volume><number>3-4</number><edition>2001/11/01</edition><keywords><keyword>Animals</keyword><keyword>Humans</keyword><keyword>Inflammation/metabolism</keyword><keyword>Inflammation Mediators/*physiology</keyword><keyword>Lipid Peroxidation/*physiology</keyword><keyword>Lipoproteins, HDL/*physiology</keyword></keywords><dates><year>2001</year><pub-dates><date>Apr-May</date></pub-dates></dates><isbn>1050-1738 (Print)</isbn><accession-num>11686006</accession-num><urls><related-urls><url>http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&amp;db=PubMed&amp;dopt=Citation&amp;list_uids=11686006</url></related-urls></urls><electronic-resource-num>S1050-1738(01)00095-0 [pii]</electronic-resource-num><language>eng</language></record></Cite></EndNote>9. These enzymes have been shown to limit phospholipids� oxidation and accumulation in LDL  ADDIN EN.CITE  ADDIN EN.CITE.DATA 10.
Some of the anti-inflammatory effects of HDL have been attributed to inhibition of cytokine induced expression of adhesion molecules and chemokines such MCP-1  ADDIN EN.CITE  ADDIN EN.CITE.DATA 11-13. Other anti-inflammatory functions of HDL are related to its role in the hydrolysis of ox-LDL  ADDIN EN.CITE  ADDIN EN.CITE.DATA 14.
HDL is antithrombogenic through the reduction of platelet aggregation  ADDIN EN.CITE <EndNote><Cite><Author>Chen</Author><Year>1994</Year><RecNum>914</RecNum><DisplayText><style face="superscript">15</style></DisplayText><record><rec-number>914</rec-number><foreign-keys><key app="EN" db-id="90dsvsxdjxwazqe0xdmpzaxsdea20t2fdvvt" timestamp="0">914</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Chen, L. Y.</author><author>Mehta, J. L.</author></authors></contributors><auth-address>Department of Medicine, College of Medicine, University of Florida, Gainesville 32610-0277.</auth-address><titles><title>Inhibitory effect of high-density lipoprotein on platelet function is mediated by increase in nitric oxide synthase activity in platelets</title><secondary-title>Life Sci</secondary-title></titles><pages>1815-21</pages><volume>55</volume><number>23</number><edition>1994/01/01</edition><keywords><keyword>Amino Acid Oxidoreductases/drug effects/*metabolism</keyword><keyword>Blood Platelets/drug effects/enzymology/*physiology</keyword><keyword>Humans</keyword><keyword>Lipoproteins, HDL/*pharmacology</keyword><keyword>Nitric Oxide Synthase</keyword><keyword>Nitrites/metabolism</keyword><keyword>Platelet Aggregation Inhibitors/*pharmacology</keyword><keyword>Serotonin/metabolism</keyword></keywords><dates><year>1994</year></dates><isbn>0024-3205 (Print)</isbn><accession-num>7526105</accession-num><urls><related-urls><url>http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&amp;db=PubMed&amp;dopt=Citation&amp;list_uids=7526105</url></related-urls></urls><language>eng</language></record></Cite></EndNote>15, reversing LDL-induced inhibition of fibrinolysis  ADDIN EN.CITE <EndNote><Cite><Author>Ren</Author><Year>2000</Year><RecNum>915</RecNum><DisplayText><style face="superscript">16</style></DisplayText><record><rec-number>915</rec-number><foreign-keys><key app="EN" db-id="90dsvsxdjxwazqe0xdmpzaxsdea20t2fdvvt" timestamp="0">915</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Ren, S.</author><author>Shen, G. X.</author></authors></contributors><auth-address>Departments of Internal Medicine and Physiology, University of Manitoba, Winnipeg, Canada.</auth-address><titles><title>Impact of antioxidants and HDL on glycated LDL-induced generation of fibrinolytic regulators from vascular endothelial cells</title><secondary-title>Arterioscler Thromb Vasc Biol</secondary-title></titles><pages>1688-93</pages><volume>20</volume><number>6</number><edition>2000/06/10</edition><keywords><keyword>Antioxidants/*pharmacology</keyword><keyword>Butylated Hydroxytoluene/pharmacology</keyword><keyword>Endothelium, Vascular/*drug effects/metabolism</keyword><keyword>Humans</keyword><keyword>Lipid Peroxidation/drug effects</keyword><keyword>Lipoproteins, HDL/*pharmacology</keyword><keyword>Lipoproteins, LDL/*pharmacology</keyword><keyword>Plasminogen Activator Inhibitor 1/*metabolism</keyword><keyword>Tissue Plasminogen Activator/*metabolism</keyword><keyword>Vitamin E/pharmacology</keyword></keywords><dates><year>2000</year><pub-dates><date>Jun</date></pub-dates></dates><isbn>1079-5642 (Print)</isbn><accession-num>10845890</accession-num><urls><related-urls><url>http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&amp;db=PubMed&amp;dopt=Citation&amp;list_uids=10845890</url></related-urls></urls><language>eng</language></record></Cite></EndNote>16, inhibiting tissue factors (factors Va, VIIIa and X)  ADDIN EN.CITE  ADDIN EN.CITE.DATA 17, 18 and increasing the activity of protein S and activated protein C  ADDIN EN.CITE <EndNote><Cite><Author>Griffin</Author><Year>1999</Year><RecNum>918</RecNum><DisplayText><style face="superscript">19</style></DisplayText><record><rec-number>918</rec-number><foreign-keys><key app="EN" db-id="90dsvsxdjxwazqe0xdmpzaxsdea20t2fdvvt" timestamp="0">918</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Griffin, J. H.</author><author>Kojima, K.</author><author>Banka, C. L.</author><author>Curtiss, L. K.</author><author>Fernandez, J. A.</author></authors></contributors><auth-address>Department of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, California 92037, USA. jgriffin@scripps.edu</auth-address><titles><title>High-density lipoprotein enhancement of anticoagulant activities of plasma protein S and activated protein C</title><secondary-title>J Clin Invest</secondary-title></titles><pages>219-27</pages><volume>103</volume><number>2</number><edition>1999/01/23</edition><keywords><keyword>Anticoagulants/*metabolism</keyword><keyword>Apolipoproteins A/blood</keyword><keyword>Blood Coagulation/drug effects/physiology</keyword><keyword>Coronary Disease/metabolism</keyword><keyword>Enzyme Activation</keyword><keyword>Factor Va/metabolism</keyword><keyword>Humans</keyword><keyword>Lipoproteins, HDL/*pharmacology</keyword><keyword>Lipoproteins, LDL/pharmacology</keyword><keyword>Partial Thromboplastin Time</keyword><keyword>Phospholipids/pharmacology</keyword><keyword>Protein C/*metabolism</keyword><keyword>Protein S/*metabolism</keyword><keyword>Prothrombin Time</keyword></keywords><dates><year>1999</year><pub-dates><date>Jan</date></pub-dates></dates><isbn>0021-9738 (Print)</isbn><accession-num>9916134</accession-num><urls><related-urls><url>http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&amp;db=PubMed&amp;dopt=Citation&amp;list_uids=9916134</url></related-urls></urls><electronic-resource-num>10.1172/JCI5006</electronic-resource-num><language>eng</language></record></Cite></EndNote>19.
Experimental studies showed that vasculopathy related to endothelial dysfunction is negatively correlated with serum HDL levels. This could be linked to HDL�s effect on increasing the bioavailability of endothelium derived nitric oxide (NO) and prostacyclin  ADDIN EN.CITE  ADDIN EN.CITE.DATA 20, 21.  
The clinical significance of these proposed protective mechanisms of HDL have not been thoroughly evaluated.  

Clinical Strategies to Elevate HDL
Nonpharmacologic therapy

Diet � High-carbohydrate, low-fat diets may be associated with low serum HDL levels.
Obesity � HDL levels decline with obesity and reduction in body mass index has been associated with increases in HDL levels  ADDIN EN.CITE <EndNote><Cite><Author>Wilsgaard</Author><Year>2004</Year><RecNum>919</RecNum><DisplayText><style face="superscript">22</style></DisplayText><record><rec-number>919</rec-number><foreign-keys><key app="EN" db-id="90dsvsxdjxwazqe0xdmpzaxsdea20t2fdvvt" timestamp="0">919</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Wilsgaard, T.</author><author>Arnesen, E.</author></authors></contributors><auth-address>Institute of Community Medicine, University of Tromso, Tromso, Norway. tom.wilsgaard@ism.uit.no</auth-address><titles><title>Change in serum lipids and body mass index by age, sex, and smoking status: the Tromso study 1986-1995</title><secondary-title>Ann Epidemiol</secondary-title></titles><pages>265-73</pages><volume>14</volume><number>4</number><edition>2004/04/07</edition><keywords><keyword>Adult</keyword><keyword>Age Distribution</keyword><keyword>*Body Mass Index</keyword><keyword>Body Weight/physiology</keyword><keyword>Cholesterol, HDL/blood</keyword><keyword>Cohort Studies</keyword><keyword>Female</keyword><keyword>Humans</keyword><keyword>Linear Models</keyword><keyword>Lipids/*blood</keyword><keyword>Male</keyword><keyword>Middle Aged</keyword><keyword>Norway/epidemiology</keyword><keyword>Obesity/blood/*epidemiology</keyword><keyword>Sex Factors</keyword><keyword>Smoking/*epidemiology</keyword><keyword>Triglycerides/blood</keyword></keywords><dates><year>2004</year><pub-dates><date>Apr</date></pub-dates></dates><isbn>1047-2797 (Print)</isbn><accession-num>15066606</accession-num><urls><related-urls><url>http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&amp;db=PubMed&amp;dopt=Citation&amp;list_uids=15066606</url></related-urls></urls><electronic-resource-num>10.1016/j.annepidem.2003.08.004&#xD;S1047279703002801 [pii]</electronic-resource-num><language>eng</language></record></Cite></EndNote>22.
Exercise � Regular aerobic exercise can raise HDL levels by up to 25%  ADDIN EN.CITE <EndNote><Cite><Author>Spate-Douglas</Author><Year>1999</Year><RecNum>920</RecNum><DisplayText><style face="superscript">23</style></DisplayText><record><rec-number>920</rec-number><foreign-keys><key app="EN" db-id="90dsvsxdjxwazqe0xdmpzaxsdea20t2fdvvt" timestamp="0">920</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Spate-Douglas, T.</author><author>Keyser, R. E.</author></authors></contributors><auth-address>School of Health Sciences, Grand Valley State University, Allendale, MI, USA.</auth-address><titles><title>Exercise intensity: its effect on the high-density lipoprotein profile</title><secondary-title>Arch Phys Med Rehabil</secondary-title></titles><pages>691-5</pages><volume>80</volume><number>6</number><edition>1999/06/23</edition><keywords><keyword>Adult</keyword><keyword>*Exercise</keyword><keyword>Female</keyword><keyword>Heart Rate</keyword><keyword>Humans</keyword><keyword>Lipoproteins, HDL/*blood</keyword><keyword>Physical Fitness</keyword></keywords><dates><year>1999</year><pub-dates><date>Jun</date></pub-dates></dates><isbn>0003-9993 (Print)</isbn><accession-num>10378497</accession-num><urls><related-urls><url>http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&amp;db=PubMed&amp;dopt=Citation&amp;list_uids=10378497</url></related-urls></urls><electronic-resource-num>S0003-9993(99)90174-0 [pii]</electronic-resource-num><language>eng</language></record></Cite></EndNote>23.
Smoking � Smokers have been noted to have lower HDL levels and smoking cessation has been associated with a significant increase (approximately 4 mg/dL) in HDL  ADDIN EN.CITE <EndNote><Cite><Author>Maeda</Author><Year>2003</Year><RecNum>921</RecNum><DisplayText><style face="superscript">24</style></DisplayText><record><rec-number>921</rec-number><foreign-keys><key app="EN" db-id="90dsvsxdjxwazqe0xdmpzaxsdea20t2fdvvt" timestamp="0">921</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Maeda, K.</author><author>Noguchi, Y.</author><author>Fukui, T.</author></authors></contributors><auth-address>Department of General Medicine and Clinical Epidemiology, Kyoto University Graduate School of Medicine, Kyoto, Japan.</auth-address><titles><title>The effects of cessation from cigarette smoking on the lipid and lipoprotein profiles: a meta-analysis</title><secondary-title>Prev Med</secondary-title></titles><pages>283-90</pages><volume>37</volume><number>4</number><edition>2003/09/26</edition><keywords><keyword>Cholesterol/*blood</keyword><keyword>Cholesterol, HDL/blood</keyword><keyword>Cholesterol, LDL/blood</keyword><keyword>Humans</keyword><keyword>*Smoking Cessation</keyword><keyword>Triglycerides/*blood</keyword></keywords><dates><year>2003</year><pub-dates><date>Oct</date></pub-dates></dates><isbn>0091-7435 (Print)</isbn><accession-num>14507483</accession-num><urls><related-urls><url>http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&amp;db=PubMed&amp;dopt=Citation&amp;list_uids=14507483</url></related-urls></urls><electronic-resource-num>S0091743503001105 [pii]</electronic-resource-num><language>eng</language></record></Cite></EndNote>24.
Alcohol � Moderate alcohol consumption can significantly increase HDL levels  ADDIN EN.CITE  ADDIN EN.CITE.DATA 25, 26.

Pharmacologic therapy
Statins:
Statins elevate HDL levels by approximately 5-15%. This modest effect of statins may be attributed to their function in activating PPAR-( receptors and inhibiting the CETP pathway  ADDIN EN.CITE  ADDIN EN.CITE.DATA 27, 28.
Statins confer the strongest cardioprotective effects on patients with low HDL as demonstrated by the WOSCOPS (West of Scotland Coronary Prevention Study) and the AFCAPS/TexCAPS (Air Force/Texas Coronary Atherosclerosis Prevention Study)  ADDIN EN.CITE  ADDIN EN.CITE.DATA 29, 30. This highlights the clinical significance of HDL elevation in treating CVD. 
Current recommendations indicate that statins should be used as first line agents in patients with low HDL levels in isolation or in combination with high LDL  ADDIN EN.CITE <EndNote><Cite><Author>Toth</Author><Year>2004</Year><RecNum>928</RecNum><DisplayText><style face="superscript">31</style></DisplayText><record><rec-number>928</rec-number><foreign-keys><key app="EN" db-id="90dsvsxdjxwazqe0xdmpzaxsdea20t2fdvvt" timestamp="0">928</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Toth, P. P.</author></authors></contributors><auth-address>Sterling Rock Falls Clinic, 101 E Miller Rd, Sterling, Ill, USA. peter.toth@srfc.com</auth-address><titles><title>High-density lipoprotein and cardiovascular risk</title><secondary-title>Circulation</secondary-title></titles><pages>1809-12</pages><volume>109</volume><number>15</number><edition>2004/04/21</edition><keywords><keyword>Adult</keyword><keyword>Coronary Artery Disease/complications/*epidemiology</keyword><keyword>Female</keyword><keyword>Humans</keyword><keyword>Hypolipoproteinemias/*complications/drug therapy</keyword><keyword>Lipoproteins, HDL/*blood/physiology</keyword><keyword>Male</keyword><keyword>Risk Factors</keyword></keywords><dates><year>2004</year><pub-dates><date>Apr 20</date></pub-dates></dates><isbn>1524-4539 (Electronic)</isbn><accession-num>15096460</accession-num><urls><related-urls><url>http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&amp;db=PubMed&amp;dopt=Citation&amp;list_uids=15096460</url></related-urls></urls><electronic-resource-num>10.1161/01.CIR.0000126889.97626.B8&#xD;109/15/1809 [pii]</electronic-resource-num><language>eng</language></record></Cite></EndNote>31.

Fibrates:
 Fibrates are weak PPAP-( receptor agonists that elevate HDL levels by 10-20%, while lowering triglycerides and both total and LDL cholesterol. They upregulate expression of apo-A1 and apo-A2, the two main constituents of HDL  ADDIN EN.CITE <EndNote><Cite><Author>Wierzbicki</Author><Year>2003</Year><RecNum>932</RecNum><DisplayText><style face="superscript">32</style></DisplayText><record><rec-number>932</rec-number><foreign-keys><key app="EN" db-id="90dsvsxdjxwazqe0xdmpzaxsdea20t2fdvvt" timestamp="0">932</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Wierzbicki, A. S.</author><author>Mikhailidis, D. P.</author><author>Wray, R.</author><author>Schacter, M.</author><author>Cramb, R.</author><author>Simpson, W. G.</author><author>Byrne, C. B.</author></authors></contributors><auth-address>Department of Chemical Pathology, St. Thomas&apos; Hospital, London, UK. Anthony.Wierzbicki@kcl.ac.uk</auth-address><titles><title>Statin-fibrate combination: therapy for hyperlipidemia: a review</title><secondary-title>Curr Med Res Opin</secondary-title></titles><pages>155-68</pages><volume>19</volume><number>3</number><edition>2003/06/20</edition><keywords><keyword>Anticholesteremic Agents/*administration &amp; dosage/pharmacology</keyword><keyword>Antilipemic Agents/*administration &amp; dosage/pharmacology</keyword><keyword>Drug Interactions</keyword><keyword>Drug Therapy, Combination</keyword><keyword>Humans</keyword><keyword>Hyperlipidemias/*drug therapy</keyword><keyword>Stroke/prevention &amp; control</keyword></keywords><dates><year>2003</year></dates><isbn>0300-7995 (Print)</isbn><accession-num>12814127</accession-num><urls><related-urls><url>http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&amp;db=PubMed&amp;dopt=Citation&amp;list_uids=12814127</url></related-urls></urls><language>eng</language></record></Cite></EndNote>32. Fibrates also downregulate Apo-C3 expression and increase the expression of lipoprotein lipase, both of which result in reduced triglycerides and LDL particles. In addition to lipid regulation, fibrates have been shown to decrease the levels of fibrinogen and CRP  ADDIN EN.CITE <EndNote><Cite><Author>Joy</Author><Year>2008</Year><RecNum>933</RecNum><DisplayText><style face="superscript">33</style></DisplayText><record><rec-number>933</rec-number><foreign-keys><key app="EN" db-id="90dsvsxdjxwazqe0xdmpzaxsdea20t2fdvvt" timestamp="0">933</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Joy, T.</author><author>Hegele, R. A.</author></authors></contributors><auth-address>Robarts Research Institute and Schulich School of Medicine and Dentistry, University of Western Ontario, London, Ontario, Canada, N6A 5K8.</auth-address><titles><title>Is raising HDL a futile strategy for atheroprotection?</title><secondary-title>Nat Rev Drug Discov</secondary-title></titles><pages>143-55</pages><volume>7</volume><number>2</number><edition>2008/02/02</edition><keywords><keyword>Animals</keyword><keyword>Anticholesteremic Agents/*therapeutic use</keyword><keyword>Apolipoprotein A-I/genetics/metabolism</keyword><keyword>Atherosclerosis/genetics/metabolism/*prevention &amp; control</keyword><keyword>Cholesterol Ester Transfer Proteins/antagonists &amp; inhibitors</keyword><keyword>Clinical Trials as Topic</keyword><keyword>Humans</keyword><keyword>Lipoproteins, HDL/chemistry/*metabolism/physiology</keyword><keyword>Phospholipids/therapeutic use</keyword><keyword>Quinolines/therapeutic use</keyword><keyword>Sulfhydryl Compounds/therapeutic use</keyword><keyword>Treatment Outcome</keyword></keywords><dates><year>2008</year><pub-dates><date>Feb</date></pub-dates></dates><isbn>1474-1784 (Electronic)</isbn><accession-num>18239670</accession-num><urls><related-urls><url>http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&amp;db=PubMed&amp;dopt=Citation&amp;list_uids=18239670</url></related-urls></urls><electronic-resource-num>nrd2489 [pii]&#xD;10.1038/nrd2489</electronic-resource-num><language>eng</language></record></Cite></EndNote>33.
Many large trials including The Helsinki Heart Study, DAIS (Diabetes Atherosclerosis Intervention Study) and VA-HIT, have demonstrated that fibrate treatment significantly elevated HDL cholesterol and reduced progression of atherosclerosis or the risk for CVD  ADDIN EN.CITE  ADDIN EN.CITE.DATA 34-36.

Niacin:
Niacin therapy raises HDL levels by 15-35%, making it the most effective agent currently available. The beneficial effects of niacin are linked to promoting hepatic apo-A1 production and slowing hepatic clearance of apo-A1 and HDL, through mechanisms not yet well understood  ADDIN EN.CITE <EndNote><Cite><Author>Malik</Author><Year>2003</Year><RecNum>934</RecNum><DisplayText><style face="superscript">37</style></DisplayText><record><rec-number>934</rec-number><foreign-keys><key app="EN" db-id="90dsvsxdjxwazqe0xdmpzaxsdea20t2fdvvt" timestamp="0">934</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Malik, S.</author><author>Kashyap, M. L.</author></authors></contributors><auth-address>Atherosclerosis Research Center, Department of Veterans Affairs Healthcare System, Division of Cardiology, University of California at Irvine, 5901 East Seventh Street (11-111-I), Long Beach, CA 90822, USA.</auth-address><titles><title>Niacin, lipids, and heart disease</title><secondary-title>Curr Cardiol Rep</secondary-title></titles><pages>470-6</pages><volume>5</volume><number>6</number><edition>2003/10/16</edition><keywords><keyword>Antilipemic Agents/*administration &amp; dosage</keyword><keyword>Drug Therapy, Combination</keyword><keyword>Heart Diseases/*prevention &amp; control</keyword><keyword>Humans</keyword><keyword>Lipoproteins/*drug effects</keyword><keyword>Niacin/*administration &amp; dosage</keyword></keywords><dates><year>2003</year><pub-dates><date>Nov</date></pub-dates></dates><isbn>1523-3782 (Print)</isbn><accession-num>14558989</accession-num><urls><related-urls><url>http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&amp;db=PubMed&amp;dopt=Citation&amp;list_uids=14558989</url></related-urls></urls><language>eng</language></record></Cite></EndNote>37. Experimental studies suggest that niacins may raise HDL levels through inhibition of the CETP pathway  ADDIN EN.CITE <EndNote><Cite><Author>Hernandez</Author><Year>2007</Year><RecNum>935</RecNum><DisplayText><style face="superscript">38</style></DisplayText><record><rec-number>935</rec-number><foreign-keys><key app="EN" db-id="90dsvsxdjxwazqe0xdmpzaxsdea20t2fdvvt" timestamp="0">935</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Hernandez, M.</author><author>Wright, S. D.</author><author>Cai, T. Q.</author></authors></contributors><auth-address>Department of Cardiovascular Diseases, Merck Research Laboratories, RY80L-126, 126 East Lincoln Avenue, Rahway, NJ 07065, USA.</auth-address><titles><title>Critical role of cholesterol ester transfer protein in nicotinic acid-mediated HDL elevation in mice</title><secondary-title>Biochem Biophys Res Commun</secondary-title></titles><pages>1075-80</pages><volume>355</volume><number>4</number><edition>2007/03/06</edition><keywords><keyword>Animals</keyword><keyword>Apolipoprotein B-100/genetics/metabolism</keyword><keyword>Cholesterol Ester Transfer Proteins/genetics/*metabolism</keyword><keyword>Cholesterol, HDL/*metabolism</keyword><keyword>Humans</keyword><keyword>Male</keyword><keyword>Mice</keyword><keyword>Mice, Transgenic</keyword><keyword>Niacin/*pharmacology</keyword></keywords><dates><year>2007</year><pub-dates><date>Apr 20</date></pub-dates></dates><isbn>0006-291X (Print)</isbn><accession-num>17335774</accession-num><urls><related-urls><url>http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&amp;db=PubMed&amp;dopt=Citation&amp;list_uids=17335774</url></related-urls></urls><electronic-resource-num>S0006-291X(07)00370-1 [pii]&#xD;10.1016/j.bbrc.2007.02.079</electronic-resource-num><language>eng</language></record></Cite></EndNote>38. Niacins also bind and activate adipose nicotinic cell receptors. Activation of these receptors leads to decreased lipolysis through inhibition of adenyl cyclase in adipose cells. As a result, free fatty acid levels decrease, leading to decreased triglyceride production  ADDIN EN.CITE <EndNote><Cite><Author>Meyers</Author><Year>2004</Year><RecNum>936</RecNum><DisplayText><style face="superscript">39</style></DisplayText><record><rec-number>936</rec-number><foreign-keys><key app="EN" db-id="90dsvsxdjxwazqe0xdmpzaxsdea20t2fdvvt" timestamp="0">936</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Meyers, C. D.</author><author>Kamanna, V. S.</author><author>Kashyap, M. L.</author></authors></contributors><auth-address>Endocrinology Section, VA Long Beach Healthcare System, Department of Medicine, University of California, Irvine, California, USA.</auth-address><titles><title>Niacin therapy in atherosclerosis</title><secondary-title>Curr Opin Lipidol</secondary-title></titles><pages>659-65</pages><volume>15</volume><number>6</number><edition>2004/11/06</edition><keywords><keyword>Anti-Inflammatory Agents/pharmacology</keyword><keyword>Arteriosclerosis/*drug therapy/prevention &amp; control</keyword><keyword>Diabetes Mellitus, Type 2/drug therapy</keyword><keyword>Drug Therapy, Combination</keyword><keyword>Humans</keyword><keyword>Lovastatin/pharmacology</keyword><keyword>Niacin/pharmacology/*therapeutic use</keyword><keyword>Randomized Controlled Trials as Topic</keyword></keywords><dates><year>2004</year><pub-dates><date>Dec</date></pub-dates></dates><isbn>0957-9672 (Print)</isbn><accession-num>15529025</accession-num><urls><related-urls><url>http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&amp;db=PubMed&amp;dopt=Citation&amp;list_uids=15529025</url></related-urls></urls><electronic-resource-num>00041433-200412000-00006 [pii]</electronic-resource-num><language>eng</language></record></Cite></EndNote>39. Furthermore, niacins have been shown to reduce CRP, fibrinogen and LDL oxidation  ADDIN EN.CITE <EndNote><Cite><Author>Malik</Author><Year>2003</Year><RecNum>934</RecNum><DisplayText><style face="superscript">37</style></DisplayText><record><rec-number>934</rec-number><foreign-keys><key app="EN" db-id="90dsvsxdjxwazqe0xdmpzaxsdea20t2fdvvt" timestamp="0">934</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Malik, S.</author><author>Kashyap, M. L.</author></authors></contributors><auth-address>Atherosclerosis Research Center, Department of Veterans Affairs Healthcare System, Division of Cardiology, University of California at Irvine, 5901 East Seventh Street (11-111-I), Long Beach, CA 90822, USA.</auth-address><titles><title>Niacin, lipids, and heart disease</title><secondary-title>Curr Cardiol Rep</secondary-title></titles><pages>470-6</pages><volume>5</volume><number>6</number><edition>2003/10/16</edition><keywords><keyword>Antilipemic Agents/*administration &amp; dosage</keyword><keyword>Drug Therapy, Combination</keyword><keyword>Heart Diseases/*prevention &amp; control</keyword><keyword>Humans</keyword><keyword>Lipoproteins/*drug effects</keyword><keyword>Niacin/*administration &amp; dosage</keyword></keywords><dates><year>2003</year><pub-dates><date>Nov</date></pub-dates></dates><isbn>1523-3782 (Print)</isbn><accession-num>14558989</accession-num><urls><related-urls><url>http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&amp;db=PubMed&amp;dopt=Citation&amp;list_uids=14558989</url></related-urls></urls><language>eng</language></record></Cite></EndNote>37.
Although niacins are effective in HDL elevation, their widespread use has been limited by unfavourable side effects, including intense flushing, impaired glucose tolerance, increased uric acid levels and liver toxicity. The combination of extended release niacin and a selective prostaglandin D2 receptor 1 antagonist, has been shown to reduce niacin related flushing by about 50%  ADDIN EN.CITE  ADDIN EN.CITE.DATA 40. However, the extended release forms of niacin have an increased risk of liver toxicity  ADDIN EN.CITE <EndNote><Cite><Author>Etchason</Author><Year>1991</Year><RecNum>937</RecNum><DisplayText><style face="superscript">41</style></DisplayText><record><rec-number>937</rec-number><foreign-keys><key app="EN" db-id="90dsvsxdjxwazqe0xdmpzaxsdea20t2fdvvt" timestamp="0">937</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Etchason, J. A.</author><author>Miller, T. D.</author><author>Squires, R. W.</author><author>Allison, T. G.</author><author>Gau, G. T.</author><author>Marttila, J. K.</author><author>Kottke, B. A.</author></authors></contributors><auth-address>Department of Internal Medicine, Mayo Clinic, Rochester, MN 55905.</auth-address><titles><title>Niacin-induced hepatitis: a potential side effect with low-dose time-release niacin</title><secondary-title>Mayo Clin Proc</secondary-title></titles><pages>23-8</pages><volume>66</volume><number>1</number><edition>1991/01/01</edition><keywords><keyword>Adult</keyword><keyword>Delayed-Action Preparations</keyword><keyword>Female</keyword><keyword>Hepatitis, Toxic/*etiology</keyword><keyword>Humans</keyword><keyword>Hyperlipidemias/drug therapy</keyword><keyword>Male</keyword><keyword>Middle Aged</keyword><keyword>Niacin/administration &amp; dosage/*adverse effects</keyword></keywords><dates><year>1991</year><pub-dates><date>Jan</date></pub-dates></dates><isbn>0025-6196 (Print)</isbn><accession-num>1988755</accession-num><urls><related-urls><url>http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&amp;db=PubMed&amp;dopt=Citation&amp;list_uids=1988755</url></related-urls></urls><language>eng</language></record></Cite></EndNote>41. 
Most of the niacin related trials looked into its use as an adjunct to statins. In HATS (HDL-Atherosclerosis Treatment Study), the combination of niacin and simvastatin in patients with CHD, reduced event recurrence by 60�90% compared with the placebo group  ADDIN EN.CITE  ADDIN EN.CITE.DATA 42. These results were further supported by the ARBITER (Arterial Biology for the Investigation of the Treatment Effects of Reducing Cholesterol) 2 study  ADDIN EN.CITE  ADDIN EN.CITE.DATA 43. In this study, niacin-plus-statin combination therapy in CHD patients reduced atherosclerotic disease progression (measured by carotid intima�media thickness) when compared with statin monotherapy. Although the study was not powered to show differences in cardiovascular event endpoints (only 167 patients), there was a trend towards greater reduction in clinical cardiovascular events in the statin-plus-niacin patients (3.8% vs. 9.6% in the statin monotherapy group; p=0.20).
It is clear that niacins can exert their protective effects through multiple cardioprotective mechanisms. The observed clinical efficacy from both HATS and ARBITER 2 studies suggests that continued evaluation of niacin is worthwhile.


CETP inhibitors:
CETP is a plasma glycoprotein important in regulating lipid homeostasis. It facilitates transfer of cholestryl ester (CE) from antiatherogenic HDL to atherogenic LDL and VLDL. Theoretically, inhibition of CETP breaks the bridge between the antiatherogenic and atherogenic pathways. This leads to a greater redirection of cholesterol back to the liver for clearance and away from the atherogenic pathway. Further support to this theory came from studies showing that CETP gene mutations were associated with elevated HDL levels and decreased CHD  ADDIN EN.CITE  ADDIN EN.CITE.DATA 44, 45. This encouraged the development of synthetic CETP inhibitors namely, JTT-705 and torcetrapib. Initial study results were encouraging. A Phase II trial of JTT-705 demonstrated a 34% increase in HDL levels and a 7% decrease in LDL levels  ADDIN EN.CITE  ADDIN EN.CITE.DATA 46. Torcetrapib increased HDL by 91% and decreased LDL-C by 42% at high doses, with no apparent significant adverse effects  ADDIN EN.CITE <EndNote><Cite><Author>Clark</Author><Year>2004</Year><RecNum>944</RecNum><DisplayText><style face="superscript">47</style></DisplayText><record><rec-number>944</rec-number><foreign-keys><key app="EN" db-id="90dsvsxdjxwazqe0xdmpzaxsdea20t2fdvvt" timestamp="0">944</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Clark, Ronald W.</author><author>Sutfin, Tamara A.</author><author>Ruggeri, Roger B.</author><author>Willauer, Ann T.</author><author>Sugarman, Eliot D.</author><author>Magnus-Aryitey, George</author><author>Cosgrove, Patricia G.</author><author>Sand, Thomas M.</author><author>Wester, Ronald T.</author><author>Williams, John A.</author><author>Perlman, Michael E.</author><author>Bamberger, Mark J.</author></authors></contributors><titles><title>Raising High-Density Lipoprotein in Humans Through Inhibition of Cholesteryl Ester Transfer Protein: An Initial Multidose Study of Torcetrapib</title><secondary-title>Arterioscler Thromb Vasc Biol</secondary-title></titles><pages>490-497</pages><volume>24</volume><number>3</number><dates><year>2004</year><pub-dates><date>March 1, 2004</date></pub-dates></dates><urls><related-urls><url>http://atvb.ahajournals.org/cgi/content/abstract/24/3/490</url></related-urls></urls><electronic-resource-num>10.1161/01.atv.0000118278.21719.17</electronic-resource-num></record></Cite></EndNote>47. 
In Phase II studies, torcetrapib came under more scrutiny due to an increase of 1.3�2.2 mmHg in mean systolic blood pressure and 0.9�1.1 mmHg in mean diastolic blood pressure at doses of 60 or 90 mg/day. Approximately 4% of individuals demonstrated an increase in blood pressure of greater than 15 mmHg. As a result, doses were restricted to 60mg/day in Phase III trials.
Phase III trials had to be stopped abruptly, due to the interim findings of the ILLUMINATE (Investigation of Lipid Level Management to Understand Its Impact in Atherosclerotic Events) trial. This study randomised patients at high risk of CVD to either atorvastatin + placebo or atorvastatin + torcetrapib. Patients in the torcetrapib arm demonstrated an increased risk of cardiovascular events (hazard ratio, 1.25; 95% confidence interval, 1.09 to 2.19, p=0.006) despite a 72.1% increase in HDL and 24.9% decrease in LDL levels. Additionally, torcetrapib had negligible to no effect on rates of coronary and carotid atherosclerosis disease progression as shown in the ILLUSTRATE (Investigation of Lipid Level Management Using Coronary Atherosclerosis by CETP Inhibition and HDL Elevation), RADIANCE-1 (Rating Atherosclerosis Disease Change with a New CETP Inhibitor) and RADIANCE-2 trials. 
Post hoc analysis of patients� plasma electrolytes in the torcetrapib trials provided clues into its harmful effects. Torcetrapib treatment was associated with a significant reduction in plasma potassium levels and elevation of plasma bicarbonate, both of which were associated with increased mortality. This is suggestive of an off-target effect of torcetrapib related to the activation of the renin-angiotensin-aldosterone system  ADDIN EN.CITE  ADDIN EN.CITE.DATA 48, 49.
There is also considerable speculation about the HDL that is produced by torcetrapib, suggesting that it is dysfunctional or proatherogenic. Analysing HDL related mortality in the torcetrapib group refuted this theory. It has been shown that within the torcetrapib group HDL levels were inversely related to the rate of CHD death and non-fatal MI. 
Despite the discouraging results from torcetrapib, the concept of CETP inhibition should not be completely discarded. Other CETP inhibitors, such as dalcetrapib (JJT-705) and anacetrapib, do not posses the biochemical and toxic features of torcetrapib. Initial studies have demonstrated that dalcetrapib at a dose of 900mg/day can result in a 34% increase in plasma HDL and a 7% decrease in LDL  ADDIN EN.CITE  ADDIN EN.CITE.DATA 46. More recently, anacetrapib has been shown to be well tolerated with no significant adverse effects. Additionally, it has had desirable effects on plasma HDL and LDL (HDL increased by 140% and LDL decreased by 40%)  ADDIN EN.CITE  ADDIN EN.CITE.DATA 50.

Emerging HDL based therapies
HDL therapy can be defined as the administration of reconstituted HDL particles, whether they contain purified, authentic apo-A1, recombinant apo-A1 variants or small apo-A1 mimetic peptides for the acute or subacute treatment of atherosclerotic lesions  ADDIN EN.CITE <EndNote><Cite><Author>Newton</Author><Year>2002</Year><RecNum>191</RecNum><DisplayText><style face="superscript">51</style></DisplayText><record><rec-number>191</rec-number><foreign-keys><key app="EN" db-id="90dsvsxdjxwazqe0xdmpzaxsdea20t2fdvvt" timestamp="0">191</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Newton, R. S.</author><author>Krause, B. R.</author></authors></contributors><auth-address>Esperion Therapeutics, Inc, 3621 South State Street, 695 KMS Place, Ann Arbor, MI 48108, USA. rnewton@esperion.com</auth-address><titles><title>HDL therapy for the acute treatment of atherosclerosis</title><secondary-title>Atheroscler Suppl</secondary-title></titles><pages>31-8</pages><volume>3</volume><number>4</number><edition>2003/02/08</edition><keywords><keyword>Animals</keyword><keyword>Apolipoprotein A-I/physiology/therapeutic use</keyword><keyword>Arteriosclerosis/*drug therapy/*physiopathology</keyword><keyword>Humans</keyword><keyword>Lipoproteins, HDL/*physiology/*therapeutic use</keyword></keywords><dates><year>2002</year><pub-dates><date>Dec</date></pub-dates></dates><isbn>1567-5688 (Print)</isbn><accession-num>12573361</accession-num><urls><related-urls><url>http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&amp;db=PubMed&amp;dopt=Citation&amp;list_uids=12573361</url></related-urls></urls><electronic-resource-num>S1567568802000442 [pii]</electronic-resource-num><language>eng</language></record></Cite></EndNote>51. Although the mechanisms by which HDL acutely alters the atherosclerotic disease process are not well understood, it is believed that HDL could have a therapeutic application in CVD treatment. More clinical studies are being conducted to test the potential use of HDL therapy for acute cardiovascular (CV) events. 

Apo-A1 mimetic peptides:
Apo-A1 is the main constituent of HDL that gives it its antiatherogenic properties. In animal models, administration of Apo-A1 mimetic peptides reduced atherosclerotic lesions by up to 79%, improved endothelial dysfunction, depressed monocyte recruitment and decreased proinflammatory HDL levels  ADDIN EN.CITE  ADDIN EN.CITE.DATA 52, 53. It has to be noted that all these effects were independent of increasing plasma HDL levels  ADDIN EN.CITE  ADDIN EN.CITE.DATA 54. This could be due to antioxidant properties of HDL that are retained in the apo-A1 mimetic peptides, such as the ability to modulate the activity of PON1  ADDIN EN.CITE <EndNote><Cite><Author>Navab</Author><Year>2006</Year><RecNum>953</RecNum><DisplayText><style face="superscript">55</style></DisplayText><record><rec-number>953</rec-number><foreign-keys><key app="EN" db-id="90dsvsxdjxwazqe0xdmpzaxsdea20t2fdvvt" timestamp="0">953</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Navab, M.</author><author>Anantharamaiah, G. M.</author><author>Reddy, S. T.</author><author>Van Lenten, B. J.</author><author>Datta, G.</author><author>Garber, D.</author><author>Fogelman, A. M.</author></authors></contributors><auth-address>David Geffen School of Medicine at UCLA, Los Angeles, California, USA. mnavab@mednet.ucla.edu</auth-address><titles><title>Potential clinical utility of high-density lipoprotein-mimetic peptides</title><secondary-title>Curr Opin Lipidol</secondary-title></titles><pages>440-4</pages><volume>17</volume><number>4</number><edition>2006/07/13</edition><keywords><keyword>Animals</keyword><keyword>Anti-Inflammatory Agents/chemistry/*pharmacology</keyword><keyword>Apolipoproteins/genetics</keyword><keyword>Atherosclerosis/*drug therapy</keyword><keyword>Biomimetic Materials/chemistry/*pharmacology</keyword><keyword>Lipoproteins, HDL/*chemistry/genetics</keyword><keyword>Peptides/chemistry/genetics/*pharmacology</keyword></keywords><dates><year>2006</year><pub-dates><date>Aug</date></pub-dates></dates><isbn>0957-9672 (Print)</isbn><accession-num>16832169</accession-num><urls><related-urls><url>http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&amp;db=PubMed&amp;dopt=Citation&amp;list_uids=16832169</url></related-urls></urls><electronic-resource-num>10.1097/01.mol.0000236371.27508.d4&#xD;00041433-200608000-00011 [pii]</electronic-resource-num><language>eng</language></record></Cite></EndNote>55.
Apo-A1 mimetics are more easily produced than the reconstituted forms of HDL. They can also be orally administered. This makes them attractive candidates for therapy. However, considerable mystery and uncertainty still surrounds the underlying mechanisms and potential toxicity of Apo-A1 peptides.
Phospholipids:
Phospholipid liposomes mediate RCT and promote cholesterol efflux  ADDIN EN.CITE  ADDIN EN.CITE.DATA 56. In animal models, phospholipids increased HDL levels and decreased atheroma formation  ADDIN EN.CITE  ADDIN EN.CITE.DATA 57. In humans, phospholipid based therapy increased HDL and Apo-A1 by 18% and 6% respectively, without apparent significant side effects  ADDIN EN.CITE <EndNote><Cite><Author>Burgess</Author><Year>2005</Year><RecNum>947</RecNum><DisplayText><style face="superscript">58</style></DisplayText><record><rec-number>947</rec-number><foreign-keys><key app="EN" db-id="90dsvsxdjxwazqe0xdmpzaxsdea20t2fdvvt" timestamp="0">947</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Burgess, J. W.</author><author>Neville, T. A.</author><author>Rouillard, P.</author><author>Harder, Z.</author><author>Beanlands, D. S.</author><author>Sparks, D. L.</author></authors></contributors><auth-address>Liponex, Inc., Ottawa, Ontario, Canada, K2G 3R8.</auth-address><titles><title>Phosphatidylinositol increases HDL-C levels in humans</title><secondary-title>J Lipid Res</secondary-title></titles><pages>350-5</pages><volume>46</volume><number>2</number><edition>2004/12/04</edition><keywords><keyword>Adult</keyword><keyword>Apolipoprotein A-I/metabolism</keyword><keyword>Bile/metabolism</keyword><keyword>Cholesterol/metabolism</keyword><keyword>Cholesterol, HDL/*blood</keyword><keyword>Cohort Studies</keyword><keyword>Fasting</keyword><keyword>Female</keyword><keyword>Humans</keyword><keyword>Liver/metabolism</keyword><keyword>Male</keyword><keyword>Niacin/pharmacology</keyword><keyword>Phosphatidylinositols/*pharmacology</keyword><keyword>Time Factors</keyword><keyword>Triglycerides/blood/metabolism</keyword></keywords><dates><year>2005</year><pub-dates><date>Feb</date></pub-dates></dates><isbn>0022-2275 (Print)</isbn><accession-num>15576836</accession-num><urls><related-urls><url>http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&amp;db=PubMed&amp;dopt=Citation&amp;list_uids=15576836</url></related-urls></urls><electronic-resource-num>M400438-JLR200 [pii]&#xD;10.1194/jlr.M400438-JLR200</electronic-resource-num><language>eng</language></record></Cite></EndNote>58. Further assessment of phospholipid therapy, particularly examining atherosclerotic disease end-points (mortality, morbidity, disease progression) will help determine its utility in clinical practice. 

PPAR agonists: 
The PPAR family are a group of nuclear receptor proteins that regulate lipid metabolism. PPAR-( agonism increases Apo-A1 and Apo-A2 production while stimulating VLDL catabolism, whereas PPAR-( agonism enhances adipocyte differentiation and induces lipid efflux from macrophages  ADDIN EN.CITE <EndNote><Cite><Author>Berger</Author><Year>2005</Year><RecNum>960</RecNum><DisplayText><style face="superscript">59</style></DisplayText><record><rec-number>960</rec-number><foreign-keys><key app="EN" db-id="90dsvsxdjxwazqe0xdmpzaxsdea20t2fdvvt" timestamp="0">960</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Berger, J. P.</author><author>Akiyama, T. E.</author><author>Meinke, P. T.</author></authors></contributors><auth-address>Department of Metabolic Disorders, Merck Research Laboratories, Rahway, NJ 07065, USA. joel_berger@merck.com</auth-address><titles><title>PPARs: therapeutic targets for metabolic disease</title><secondary-title>Trends Pharmacol Sci</secondary-title></titles><pages>244-51</pages><volume>26</volume><number>5</number><edition>2005/04/30</edition><keywords><keyword>Animals</keyword><keyword>Humans</keyword><keyword>Ligands</keyword><keyword>Lipid Metabolism</keyword><keyword>Metabolic Diseases/*drug therapy/metabolism</keyword><keyword>Peroxisome Proliferator-Activated Receptors/genetics/*metabolism</keyword></keywords><dates><year>2005</year><pub-dates><date>May</date></pub-dates></dates><isbn>0165-6147 (Print)</isbn><accession-num>15860371</accession-num><urls><related-urls><url>http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&amp;db=PubMed&amp;dopt=Citation&amp;list_uids=15860371</url></related-urls></urls><electronic-resource-num>S0165-6147(05)00075-1 [pii]&#xD;10.1016/j.tips.2005.03.003</electronic-resource-num><language>eng</language></record></Cite></EndNote>59. Thus, dual PPAR ((( agonism was an obvious and attractive therapeutic option. The first such agent, muraglitazar raised HDL levels by 19%  ADDIN EN.CITE  ADDIN EN.CITE.DATA 60. Despite this seemingly beneficial effect on HDL levels, muraglitazar was found to be associated with increased mortality rates, major cardiovascular events and congestive heart failure and was therefore taken off the market and further research was suspended  ADDIN EN.CITE  ADDIN EN.CITE.DATA 61. The enthusiasm for dual PPAR agonism was further curbed by later results from trials with tesaglitizar (another dual PPAR agonist)  ADDIN EN.CITE <EndNote><Cite><Author>AstraZeneca</Author><Year>2006</Year><RecNum>963</RecNum><DisplayText><style face="superscript">62</style></DisplayText><record><rec-number>963</rec-number><foreign-keys><key app="EN" db-id="90dsvsxdjxwazqe0xdmpzaxsdea20t2fdvvt" timestamp="0">963</key></foreign-keys><ref-type name="Newspaper Article">23</ref-type><contributors><authors><author>AstraZeneca</author></authors></contributors><titles><title>AstraZeneca Discontinues Development of GALIDA TM (tesaglitazar)</title><secondary-title>online</secondary-title></titles><dates><year>2006</year></dates><urls></urls></record></Cite></EndNote>62. 
More research is being conducted focusing on the effect of pioglitazone (PPAR-( agonist) on HDL metabolism and its potential effects in recent ischemic stroke patients. ADDIN EN.CITE <EndNote><Cite><Author>IRIS</Author><RecNum>964</RecNum><DisplayText><style face="superscript">63</style></DisplayText><record><rec-number>964</rec-number><foreign-keys><key app="EN" db-id="90dsvsxdjxwazqe0xdmpzaxsdea20t2fdvvt" timestamp="0">964</key></foreign-keys><ref-type name="Web Page">12</ref-type><contributors><authors><author>IRIS, </author></authors></contributors><titles><title>Insulin resistance intervention after stroke trial</title></titles><number>12/05/2008</number><dates></dates><urls><related-urls><url><style face="underline" font="default" size="100%">http://www.Iristrial.org/</style></url></related-urls></urls></record></Cite></EndNote>63

Apo-A1Milano  (Apo-A1M):
Apo-A1M differs from Apo-A1 by an arginine to cysteine substitution at position 173. Individuals with Apo-A1M mutation have lower HDL levels without increased CVD risk  ADDIN EN.CITE  ADDIN EN.CITE.DATA 64. The vascular protective effect of Apo-A1M may arise from its ability to increase HDL meditated cholesterol efflux. 
The infusion of Apo-A1M containing phospholipid vesicles has been shown to beneficially affect atheromatous plaque volume in animal models  ADDIN EN.CITE  ADDIN EN.CITE.DATA 65. In addition, vector-based gene transfer of Apo-A1M into LDL-receptor deficient mice showed significant delays in atherosclerosis progression  ADDIN EN.CITE <EndNote><Cite><Author>Lebherz</Author><Year>2007</Year><RecNum>959</RecNum><DisplayText><style face="superscript">66</style></DisplayText><record><rec-number>959</rec-number><foreign-keys><key app="EN" db-id="90dsvsxdjxwazqe0xdmpzaxsdea20t2fdvvt" timestamp="0">959</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Lebherz, C.</author><author>Sanmiguel, J.</author><author>Wilson, J. M.</author><author>Rader, D. J.</author></authors></contributors><auth-address>Department of Pathology and Laboratory Medicine, Gene Therapy Program, University of Pennsylvania School of Medicine, Philadelphia, PA, USA. corinna.lebherz@med.uni-muenchen.de</auth-address><titles><title>Gene transfer of wild-type apoA-I and apoA-I Milano reduce atherosclerosis to a similar extent</title><secondary-title>Cardiovasc Diabetol</secondary-title></titles><pages>15</pages><volume>6</volume><edition>2007/05/04</edition><keywords><keyword>Animals</keyword><keyword>Apolipoprotein A-I/*genetics</keyword><keyword>Atherosclerosis/*genetics/*metabolism/prevention &amp; control</keyword><keyword>Genetic Vectors/administration &amp; dosage/genetics</keyword><keyword>Humans</keyword><keyword>Hypercholesterolemia/genetics/metabolism</keyword><keyword>Male</keyword><keyword>Mice</keyword><keyword>Mice, Inbred C57BL</keyword><keyword>Mice, Knockout</keyword><keyword>Mice, Transgenic</keyword><keyword>Mutation</keyword><keyword>Receptors, LDL/deficiency/genetics</keyword><keyword>*Transduction, Genetic/methods</keyword></keywords><dates><year>2007</year></dates><isbn>1475-2840 (Electronic)</isbn><accession-num>17475009</accession-num><urls><related-urls><url>http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&amp;db=PubMed&amp;dopt=Citation&amp;list_uids=17475009</url></related-urls></urls><electronic-resource-num>1475-2840-6-15 [pii]&#xD;10.1186/1475-2840-6-15</electronic-resource-num><language>eng</language></record></Cite></EndNote>66.
Nissen and colleagues tested the concept that Apo-A1M infusion may have the ability to acutely stabilize vulnerable atherosclerotic plaque. In this study patients suffering from ACS received weekly infusions of either a placebo or recombinant Apo-A1M complexes over a period of 5 weeks  ADDIN EN.CITE  ADDIN EN.CITE.DATA 67. Atherosclerosis progression was measured at baseline and 2 weeks after treatment using IVUS. In the Apo-A1M infusions arm, a significant reduction of atheroma volume of 4.2% (P <0.001) was observed. No change in atheroma volume was detected in the placebo group.
To date, there are no large studies assessing clinical endpoints with Apo-A1M therapy. Hence, additional studies are needed to further evaluate its clinical utility.

Reconstituted HDL (rHDL):
Reconstituted HDL consists of Apo-A1 (purified from pooled human plasma) combined with soybean phosphatidylcholine (PC).The reconstituted particle generated resembles discoidal nascent native HDL, both chemically and biologically. 
Intravenous administration of rHDL has been shown to be safe and effective in raising plasma HDL levels  ADDIN EN.CITE  ADDIN EN.CITE.DATA 69, 70. rHDL has been shown to effectively induce cholesterol reflux and inhibit proinflammatory changes and platelet aggregation  ADDIN EN.CITE  ADDIN EN.CITE.DATA 51, 71, 72.  In the ERASE (Effect of Reconstituted HDL on Atherosclerosis and Efficacy) trial, it was shown that short term rHDL infusions can induce plaque regression within 4 weeks of treatment in acute coronary syndrome patients  ADDIN EN.CITE  ADDIN EN.CITE.DATA 70. Additionally, rHDL therapy was associated with significant improvement in plaque characterisation indices. More recently, Shaw et al  ADDIN EN.CITE <EndNote><Cite><Author>Shaw</Author><Year>2008</Year><RecNum>1002</RecNum><DisplayText><style face="superscript">69</style></DisplayText><record><rec-number>1002</rec-number><foreign-keys><key app="EN" db-id="90dsvsxdjxwazqe0xdmpzaxsdea20t2fdvvt" timestamp="0">1002</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Shaw, J. A.</author><author>Bobik, A.</author><author>Murphy, A.</author><author>Kanellakis, P.</author><author>Blombery, P.</author><author>Mukhamedova, N.</author><author>Woollard, K.</author><author>Lyon, S.</author><author>Sviridov, D.</author><author>Dart, A. M.</author></authors></contributors><auth-address>Departments of Cardiology, and Radiology, Alfred Hospital; and Baker IDI Heart and Diabetes Institute, Melbourne, Australia.</auth-address><titles><title>Infusion of Reconstituted High-Density Lipoprotein Leads to Acute Changes in Human Atherosclerotic Plaque</title><secondary-title>Circ Res</secondary-title></titles><edition>2008/10/04</edition><dates><year>2008</year><pub-dates><date>Oct 2</date></pub-dates></dates><isbn>1524-4571 (Electronic)</isbn><accession-num>18832751</accession-num><urls><related-urls><url>http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&amp;db=PubMed&amp;dopt=Citation&amp;list_uids=18832751</url></related-urls></urls><electronic-resource-num>CIRCRESAHA.108.182063 [pii]&#xD;10.1161/CIRCRESAHA.108.182063</electronic-resource-num><language>Eng</language></record></Cite></EndNote>69 tested the effects of a single high dose rHDL (80mg/kg) infusion on plaques from claudicants undergoing superficial femoral artery atherectomy. They have demonstrated that rHDL infusion could lead to acute reduction in plaque lipid content and both local and systemic measures of inflammation. Theoretically, this suggests that rHDL may represent a useful agent for patients with acute ischaemic cardiovascular events, but more work is needed to evaluate the acute effects on other parameters and markers of disease activity. 

Conclusion
It is well established that low HDL dyslipidaemia is an important risk factor that is highly modifiable in relation to atherosclerosis. The combination of statins and extended release niacin may be the best means of raising serum HDL at present. Because of the biological complexity associated with HDL�s structure and function, HDL elevation alone may not translate into clinical benefit. Future studies will need to focus on identifying different subclasses of HDL, and their independent response to pharmacotherapy and subsequent association with atherosclerotic disease progression and complication. 
Despite the disappointment with torcetrapib, other HDL based therapies such as rHDL, Apo-A1M and phospholipids have shown promising results. This highlights the need for more research to determine which agents are safest and most efficacious in halting atherosclerotic disease progression and reducing the risk of CV events.

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FIGURE LEGENDS
Figure 1. Schematic model of reverse cholesterol transport (RCT), mediated by HDL
Figure 2. Antiatherogenic properties of HDL
Figure 1

	
Figure 2

































PAGE  


PAGE  1



HDL = High density lipoprotein
nHDL = Nascent native HDL
sHDL = Spherical HDL
VLDL = Very low density lipoprotein
LDL = Low density lipoprotein


LCAT = Lecithin�cholesterol acyltransferase
CETP = Cholesteryl ester transfer protein
ABCA-1 = ATP-binding cassette A-1
SR-B1 = Scavenger receptor class-B type-1
CE = Cholesteryl ester 





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