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Volume 24, Issue 8; August 1, 2004
Editorials
Brief Reviews
Vascular Biology
Atherosclerosis and Lipoproteins
Thrombosis
Letters to the Editor
NCEP Report
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Editorials
A Summary of Implications of Recent Clinical Trials for the National Cholesterol Education Program Adult Treatment Panel III Guidelines
Scott M. Grundy, James I. Cleeman, C. Noel Bairey Merz, H. Bryan Brewer, Jr, Luther T. Clark, Donald B. Hunninghake, Richard C. Pasternak, Sidney C. Smith, Jr, Neil J. Stone for the Coordinating Committee of the National Cholesterol Education Program
Arterioscler Thromb Vasc Biol. 2004;24:1329-1330, doi:10.1161/01.ATV.0000139012.45265.e0.
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Aortic Valve: Turning Over a New Leaf(let) in Endothelial Phenotypic Heterogeneity
Peter F. Davies, Anthony G. Passerini, and Craig A. Simmons
Arterioscler Thromb Vasc Biol. 2004;24:1331-1333, doi:10.1161/01.ATV.0000130659.89433.c1.
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How Does Mutant Proprotein Convertase Neural Apoptosis-Regulated Convertase 1 Induce Autosomal Dominant Hypercholesterolemia?
Pernilla Jirholt, Martin Adiels, and Jan Borén
Arterioscler Thromb Vasc Biol. 2004;24:1334-1336, doi:10.1161/01.ATV.0000133682.97348.ff.
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The Mystery of PCSK9
Alan D. Attie
Arterioscler Thromb Vasc Biol. 2004;24:1337-1339, doi:10.1161/01.ATV.0000137288.82390.04.
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Brief Reviews
ATVB In Focus: Diabetic Vascular Disease: Pathophysiological Mechanisms in the Diabetic Milieu and Therapeutic Implications
Richard A. Cohen
Arterioscler Thromb Vasc Biol. 2004;24:1340-1341, doi:10.1161/01.ATV.0000137187.16206.79.
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RAGE Axis: Animal Models and Novel Insights Into the Vascular Complications of Diabetes
Yoshifumi Naka, Loredana G. Bucciarelli, Thoralf Wendt, Larisse K. Lee, Ling Ling Rong, Ravichandran Ramasamy, Shi Fang Yan, and Ann Marie Schmidt
Arterioscler Thromb Vasc Biol. 2004;24:1342-1349; published online before print May 20 2004, doi:10.1161/01.ATV.0000133191.71196.90.
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Ligand engagement of the receptor for advanced glycation end products (RAGE) evokes vascular inflammation and perturbation. In diabetes, when fueled by oxidation, hyperglycemia, and superimposed stresses, the ligand-RAGE axis accelerates atherosclerosis and neointimal expansion. Studies in rodent models of diabetes suggest that testing the impact of RAGE blockade in human subjects is logical.
Proteolysis of the Pericellular Matrix: A Novel Element Determining Cell Survival and Death in the Pathogenesis of Plaque Erosion and Rupture
Ken A. Lindstedt, Markus J. Leskinen, and Petri T. Kovanen
Arterioscler Thromb Vasc Biol. 2004;24:1350-1358; published online before print June 10 2004, doi:10.1161/01.ATV.0000135322.78008.55.
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Acute atherothrombotic events relate to erosion and rupture of unstable coronary plaques. Plaque stability critically depends on the integrity of the pericellular matrix (PCM) regulating plaque cell survival. By secreting PCM-degrading proteases, infiltrating macrophages, T-lymphocytes, and mast cells trigger plaque cell apoptosis, linking inflammation-dependent proteolysis with plaque erosion and rupture.
Lysosomal Cysteine Proteases in Atherosclerosis
Jian Liu, Galina K. Sukhova, Jiu-Song Sun, Wei-Hua Xu, Peter Libby, and Guo-Ping Shi
Arterioscler Thromb Vasc Biol. 2004;24:1359-1366; published online before print June 3 2004, doi:10.1161/01.ATV.0000134530.27208.41.
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Atherosclerosis is an inflammatory disease characterized by extensive remodeling of the extracellular matrix architecture of the arterial wall. Although matrix metalloproteinases and serine proteases participate in these pathologic events, recent data from atherosclerotic patients and animals suggest the participation of lysosomal cysteine proteases in atherogenesis.
Vascular Protection: Superoxide Dismutase Isoforms in the Vessel Wall
Frank M. Faraci and Sean P. Didion
Arterioscler Thromb Vasc Biol. 2004;24:1367-1373; published online before print May 27 2004, doi:10.1161/01.ATV.0000133604.20182.cf.
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Recent studies have begun to define the role of specific isoforms of superoxide dismutase (SOD) in vascular biology. This review focuses on the role of SODs in vessels in health and disease. This area is important because reactive oxygen species are thought to play a major role in vascular pathophysiology.
Thrombomodulin-Protein C-EPCR System: Integrated to Regulate Coagulation and Inflammation
Marlies Van de Wouwer, Désiré Collen, and Edward M. Conway
Arterioscler Thromb Vasc Biol. 2004;24:1374-1383; published online before print June 3 2004, doi:10.1161/01.ATV.0000134298.25489.92.
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Vascular Biology
Basic Fibroblast Growth Factor Antagonizes Transforming Growth Factor-ß1Induced Smooth Muscle Gene Expression Through Extracellular SignalRegulated Kinase 1/2 Signaling Pathway Activation
Keiko Kawai-Kowase, Hiroko Sato, Yuko Oyama, Hiroyoshi Kanai, Mahito Sato, Hiroshi Doi, and Masahiko Kurabayashi
Arterioscler Thromb Vasc Biol. 2004;24:1384-1390; published online before print June 24 2004, doi:10.1161/01.ATV.0000136548.17816.07.
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TGFß1 induces SMC gene expression through an increase in SRF gene expression, which activates CArG-dependent transcription, and Src-tyrosine kinase is required for such an induction in 10T1/2 cells and vascular SMC. bFGF antagonizes TGFß1-induced SMC gene expression, although MEK1 activation without interfering with SRF:DNA binding activity and SRF gene expression.
Smad Expression in Human Atherosclerotic Lesions: Evidence for Impaired TGF-ß/Smad Signaling in Smooth Muscle Cells of Fibrofatty Lesions
Natalia Kalinina, Alex Agrotis, Yulia Antropova, Olga Ilyinskaya, Vladimir Smirnov, Eduard Tararak, and Alex Bobik
Arterioscler Thromb Vasc Biol. 2004;24:1391-1396; published online before print May 27 2004, doi:10.1161/01.ATV.0000133605.89421.79.
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The actions of TGF-ß in human atherosclerotic lesions were defined by examining the expression of Smad proteins in relation to TGF-ß-mediated responses. Expression of Smad proteins was restricted to macrophages of fibrofatty lesions and SMCs of fibrous plaques. Smad-dependent TGF-ß signaling appeared to be impaired SMCs of fibrofatty lesions.
Rat Aortic MCP-1 and Its Receptor CCR2 Increase With Age and Alter Vascular Smooth Muscle Cell Function
Gaia Spinetti, Mingyi Wang, Robert Monticone, Jing Zhang, Di Zhao, and Edward G. Lakatta
Arterioscler Thromb Vasc Biol. 2004;24:1397-1402; published online before print June 3 2004, doi:10.1161/01.ATV.0000134529.65173.08.
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This study demonstrates that MCP-1 and CCR2 are increased within the thickened aortas of older rats. In early-passage VSMCs from young rats, MCP-1 increased migration and invasion, imparting to these cells the characteristics of VSMCs from older rat aorta. Thus, MCP-1/CCR2 may be implicated in age-associated vascular remodeling.
Vasodilator-Stimulated Phosphoprotein Regulates Proliferation and Growth Inhibition by Nitric Oxide in Vascular Smooth Muscle Cells
Lihua Chen, Günter Daum, Kanchan Chitaley, Scott A. Coats, Daniel F. Bowen-Pope, Martin Eigenthaler, Naresh R. Thumati, Ulrich Walter, and Alexander W. Clowes
Arterioscler Thromb Vasc Biol. 2004;24:1403-1408; published online before print June 3 2004, doi:10.1161/01.ATV.0000134705.39654.53.
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This study investigated the effects of VASP and VASP phosphorylation at serine157 and serine239 on smooth muscle cell proliferation and nitric oxide-mediated growth inhibition. Our data suggest that VASP is a modulator of smooth muscle cell growth by integrating positive and negative signals that target different phosphorylation sites of VASP.
Attenuation of Graft Arterial Disease by Manipulation of the LIGHT Pathway
Hisanori Kosuge, Jun-ichi Suzuki, Tsunekazu Kakuta, Go Haraguchi, Noritaka Koga, Hideki Futamatsu, Ryo Gotoh, Manabu Inobe, Mitsuaki Isobe, and Toshimitsu Uede
Arterioscler Thromb Vasc Biol. 2004;24:1409-1415; published online before print June 3 2004, doi:10.1161/01.ATV.0000134645.53285.02.
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The role of the LIGHT pathway in the progression of graft arterial disease (GAD) is not yet evaluated. We demonstrate that blockade of the LIGHT pathway plays important roles in the regulation not only of T cell activation but also of smooth muscle cell proliferation, resulting in prevention of GAD.
EGF-Like Domain of Tenascin-C Is Proapoptotic for Cultured Smooth Muscle Cells
Kurt Wallner, Chen Li, Prediman K. Shah, Kai-Jin Wu, Stephen M. Schwartz, and Behrooz G. Sharifi
Arterioscler Thromb Vasc Biol. 2004;24:1416-1421; published online before print June 3 2004, doi:10.1161/01.ATV.0000134299.89599.53.
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Tenascin-C was found to undergo fragmentation in cultured smooth muscle cells and in human atherosclerotic plaques generating a fragment that contains the epidermal growth factor-like domain of tenascin-C. Recombinant epidermal growth factor-like domain of tenascin-C induces apoptosis of cultured smooth muscle cells, an activity that was blocked by chymotrypsin inhibitor and MMP inhibitor.
LRP1B Attenuates the Migration of Smooth Muscle Cells by Reducing Membrane Localization of Urokinase and PDGF Receptors
Kousei Tanaga, Hideaki Bujo, Yanjuan Zhu, Tatsuro Kanaki, Satoshi Hirayama, Kazuo Takahashi, Masahiro Inoue, Keiji Mikami, Wolfgang J. Schneider, and Yasushi Saito
Arterioscler Thromb Vasc Biol. 2004;24:1422-1428; published online before print May 27 2004, doi:10.1161/01.ATV.0000133607.80554.09.
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LDL receptor relatives (LRs) in atherosclerosis have gained new focus because of the specific expression of these receptors in the thickened intima. LRP1B modulates the migration of SMCs by increasing the degradation of uPAR and PDGFR. This functional characterization of LRP1B elucidates the (patho)physiological significance of SMC migration in plaques.
Unique Morphology and Focal Adhesion Development of Valvular Endothelial Cells in Static and Fluid Flow Environments
Jonathan T. Butcher, Andrea M. Penrod, Andrés J. García, and Robert M. Nerem
Arterioscler Thromb Vasc Biol. 2004;24:1429-1434; published online before print April 29 2004, doi:10.1161/01.ATV.0000130462.50769.5a.
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Endothelial cells native to the aortic valve may play an important role in mediating tissue responses to the complex fluid environment, and may therefore respond to fluid flow in a different manner than more characterized vascular endothelial cells. These differences in response to mechanical forces suggest a unique phenotype of valvular endothelial cells not mimicked by vascular endothelial cells, and could have implications for cardiovascular cell biology and cell-source considerations for tissue-engineered valvular substitutes.
Heat Shock Protein 90 Transfection Reduces Ischemia-ReperfusionInduced Myocardial Dysfunction via Reciprocal Endothelial NO Synthase Serine 1177 Phosphorylation and Threonine 495 Dephosphorylation
Christian Kupatt, Chantal Dessy, Rabea Hinkel, Philip Raake, Géraldine Daneau, Caroline Bouzin, Peter Boekstegers, and Olivier Feron
Arterioscler Thromb Vasc Biol. 2004;24:1435-1441; published online before print June 3 2004, doi:10.1161/01.ATV.0000134300.87476.d1.
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Percutaneous liposome-based Hsp90 gene transfer in a pig cardiac infarct model was shown to preserve the myocardium from the deleterious effects of ischemia-reperfusion. The gain in cardiac function was dependent on Hsp90-driven regulation of eNOS phosphorylation by Akt and calcineurin, thereby establishing Hsp90 as a promising target for cardiac diseases.
Smoking Cessation Rapidly Increases Circulating Progenitor Cells in Peripheral Blood in Chronic Smokers
Takahisa Kondo, Mutsuharu Hayashi, Kyosuke Takeshita, Yasushi Numaguchi, Koichi Kobayashi, Shigeo Iino, Yasuya Inden, and Toyoaki Murohara
Arterioscler Thromb Vasc Biol. 2004;24:1442-1447; published online before print June 10 2004, doi:10.1161/01.ATV.0000135655.52088.c5.
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We examined the effects of smoking and smoking cessation on endothelial progenitor cell (EPC) levels. Circulating EPCs were quantified by flow cytometry using cell surface markers CD45lowCD34+CD133+VEGFR2+. The EPC levels decreased as the cigarette consumption increased. EPCs increased rapidly after cessation and decreased again after resumption of smoking.
Atherosclerosis and Lipoproteins
Apolipoprotein B100 Metabolism in Autosomal-Dominant Hypercholesterolemia Related to Mutations in
PCSK9
Khadija Ouguerram, Maud Chetiveaux, Yassine Zair, Philippe Costet, Marianne Abifadel, Mathilde Varret, Catherine Boileau, Thierry Magot, and Michel Krempf
Arterioscler Thromb Vasc Biol. 2004;24:1448-1453; published online before print May 27 2004, doi:10.1161/01.ATV.0000133684.77013.88.
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Kinetic study using [2H3] leucine was conducted in 2 subjects with PCSK9 mutation and in controls. Patients exhibited a dramatic increase in the production rate of apolipoprotein B100 in VLDL, IDL, and LDL, a decrease in VLDL and IDL conversion rate, and a slight decrease in LDL fractional catabolic rate.
Statins Upregulate
PCSK9
, the Gene Encoding the Proprotein Convertase Neural Apoptosis-Regulated Convertase-1 Implicated in Familial Hypercholesterolemia
Geneviève Dubuc, Ann Chamberland, Hanny Wassef, Jean Davignon, Nabil G. Seidah, Lise Bernier, and Annik Prat
Arterioscler Thromb Vasc Biol. 2004;24:1454-1459; published online before print June 3 2004, doi:10.1161/01.ATV.0000134621.14315.43.
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The gene PCSK9, encoding NARC-1, has been implicated recently in autosomal dominant hypercholesterolemia. Using real-time polymerase chain reaction, we showed that PCSK9 is regulated by cholesterol in HepG2 cells and in human primary hepatocytes. PCSK9 promoter contains the typical elements for sterol regulation.
Subphysiologic Apolipoprotein E (ApoE) Plasma Levels Inhibit Neointimal Formation After Arterial Injury in ApoE-Deficient Mice
Hilke Wientgen, Fayanne E. Thorngate, Sabina Omerhodzic, Linda Rolnitzky, John T. Fallon, David L. Williams, and Edward A. Fisher
Arterioscler Thromb Vasc Biol. 2004;24:1460-1465; published online before print June 3 2004, doi:10.1161/01.ATV.0000134297.61979.3c.
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Using transgenic mice expressing different levels of plasma apoE, we have shown that after arterial injury, subphysiological apoE levels were associated with reduced intima-to-media (I/M) ratios of lesions. Lipid levels were not associated with reduced I/M ratios, consistent with previous mouse studies of apoE and atherosclerosis progression.
Endothelial Overexpression of Fas Ligand Decreases Atherosclerosis in Apolipoprotein EDeficient Mice
Jiang Yang, Kaori Sato, Tamar Aprahamian, Nathaniel J. Brown, Jack Hutcheson, Ann Bialik, Harris Perlman, and Kenneth Walsh
Arterioscler Thromb Vasc Biol. 2004;24:1466-1473; published online before print June 3 2004, doi:10.1161/01.ATV.0000134402.94963.2f.
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Fas ligand (FasL) can induce apoptosis in cells bearing the Fas receptor. This study examined the function of endothelial FasL during atherosclerosis. Overexpression of endothelial FasL transgene significantly reduced atherosclerotic lesion areas in aortae. Overexpression of endothelial FasL is antiinflammatory and inhibits atherosclerosis under hypercholesterolemic conditions.
Leukocyte-Derived Interleukin 10 Is Required for Protection Against Atherosclerosis in Low-Density Lipoprotein Receptor Knockout Mice
Stéphane Potteaux, Bruno Esposito, Olivia van Oostrom, Valérie Brun, Patrice Ardouin, Hervé Groux, Alain Tedgui, and Ziad Mallat
Arterioscler Thromb Vasc Biol. 2004;24:1474-1478; published online before print June 3 2004, doi:10.1161/01.ATV.0000134378.86443.cd.
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Here we show that IL-10 deficiency in leukocytes induced 2-fold increase in lesion development in the thoracic aorta of LDLr -/- mice compared with controls. Furthermore, IL-10 deficiency led to a marked increase in the accumulation of both lymphocytes and macrophages, associated with a significant reduction in collagen accumulation. Finally, transfer of IL-10-/- splenocytes to LDLr-/- mice resulted in a 3-fold increase in lesion size in the aortic sinus in comparison with mice transplanted with IL-10+/+ splenocytes.
Matrix Metalloproteinase-9 Genotype Influences Large Artery Stiffness Through Effects on Aortic Gene and Protein Expression
Tanya L. Medley, Timothy J. Cole, Anthony M. Dart, Christoph D. Gatzka, and Bronwyn A. Kingwell
Arterioscler Thromb Vasc Biol. 2004;24:1479-1484; published online before print June 10 2004, doi:10.1161/01.ATV.0000135656.49158.95.
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Coronary artery disease patients that carry at least 1 copy of the MMP-9 T allele have stiffer large arteries compared with C/C homozygotes. This relationship may result from increased degradation of important elastic components of the extracellular matrix secondary to elevated MMP-9 gene expression and protein levels in the aorta.
Effects of Long-Term Daily Low-Dose Supplementation With Antioxidant Vitamins and Minerals on Structure and Function of Large Arteries
Mahmoud Zureik, Pilar Galan, Sandrine Bertrais, Louise Mennen, Sébastien Czernichow, Jacques Blacher, Pierre Ducimetière, and Serge Hercberg
Arterioscler Thromb Vasc Biol. 2004;24:1485-1491; published online before print June 24 2004, doi:10.1161/01.ATV.0000136648.62973.c8.
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Limited data exist from randomized trials evaluating, noninvasively, the impact of antioxidant supplementation on vascular structure and function. The results of this large-scale study suggest no beneficial effects of long-term supplementation of antioxidant vitamins and minerals on carotid atherosclerosis and arterial stiffness in 1162 apparently healthy individuals (at baseline) in France.
Circulating Oxidized Low-Density Lipoprotein and Its Association With Carotid Intima-Media Thickness in Asymptomatic Members of Familial Combined Hyperlipidemia Families
Ming-Lin Liu, Kati Ylitalo, Riitta Salonen, Jukka T. Salonen, and Marja-Riitta Taskinen
Arterioscler Thromb Vasc Biol. 2004;24:1492-1497; published online before print June 17 2004, doi:10.1161/01.ATV.0000135982.60383.48.
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Ox-LDL, susceptibility of LDL to oxidation in vitro, plasma 8-isoprostane, and antioxidants, lipids and lipoproteins, LDL particle size, and carotid IMT were measured to investigate the determinants of Ox-LDL and its association with carotid IMT in 150 asymptomatic FCHL family members. Serum LDL cholesterol, apoB, and 8-isoprostane levels were the most important determinants of Ox-LDL. Ox-LDL is independently associated with carotid IMT in asymptomatic FCHL family members and can be used as a marker of early atherosclerosis in FCHL.
Incidence of Obesity-Associated Cardiovascular Disease Is Related to Inflammation-Sensitive Plasma Proteins: A Population-Based Cohort Study
Gunnar Engström, Bo Hedblad, Lars Stavenow, Susanna Jonsson, Peter Lind, Lars Janzon, and Folke Lindgärde
Arterioscler Thromb Vasc Biol. 2004;24:1498-1502; published online before print June 3 2004, doi:10.1161/01.ATV.0000134293.31512.be.
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This population-based study explored whether inflammation-sensitive plasma proteins (ISPs) (ie, fibrinogen, orosomucoid, {alpha}1-antitrypsin, haptoglobin, ceruloplasmin) modify the obesity-associated risk of myocardial infarction and stroke in initially healthy men (n=6075) followed-up over 18 years. The cardiovascular risk varied widely between obese and overweight men with high and low ISPs.
IL-8 Plasma Concentrations and the Risk of Future Coronary Artery Disease in Apparently Healthy Men and Women: The EPIC-Norfolk Prospective Population Study
S. Matthijs Boekholdt, Ron J. G. Peters, C. Erik Hack, Nicholas E. Day, Robert Luben, Sheila A. Bingham, Nicholas J. Wareham, Pieter H. Reitsma, and Kay-Tee Khaw
Arterioscler Thromb Vasc Biol. 2004;24:1503-1508; published online before print June 3 2004, doi:10.1161/01.ATV.0000134294.54422.2e.
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Using a prospective nested case-control study among apparently healthy individuals, we found that high plasma levels of IL-8 were predictive for the risk of future coronary artery disease, independent of traditional risk factors and C-reactive protein levels.
C-Reactive Protein as a Screening Test for Cardiovascular Risk in a Multiethnic Population
Sonia S. Anand, Fahad Razak, Qilong Yi, Bonnie Davis, Ruby Jacobs, Vlad Vuksan, Eva Lonn, Koon Teo, Matthew McQueen, and Salim Yusuf
Arterioscler Thromb Vasc Biol. 2004;24:1509-1515; published online before print June 17 2004, doi:10.1161/01.ATV.0000135845.95890.4e.
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CRP varies substantially between people of different ethnic origin. Compared with Europeans, Aboriginals, South Asians, and Chinese have significantly different CRP distributions, which are influenced by metabolic factors including abdominal adiposity, body weight, and HbA1c. CRP is independently associated with CVD across all populations.
Effects of Conventional or Lower Doses of Hormone Replacement Therapy in Postmenopausal Women
Kwang Kon Koh, Mi-Seung Shin, Ichiro Sakuma, Jeong Yeal Ahn, Dong Kyu Jin, Hyung Sik Kim, Dae Sung Kim, Seung Hwan Han, Wook-Jin Chung, and Eak Kyun Shin
Arterioscler Thromb Vasc Biol. 2004;24:1516-1521; published online before print May 27 2004, doi:10.1161/01.ATV.0000133683.65877.bc.
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Fifty-seven women received micronized progesterone 100 mg with either conjugated equine estrogen 0.625 mg (C-HRT) or 0.3 mg (L-HRT) daily for 2 months. Compared with C-HRT, L-HRT has comparable effects on lipoproteins, flow-mediated dilation, and PAI-1 antigen levels. However, L-HRT did not increase hsCRP or F1+2 levels.
Cholesterol-Lowering Independent Regression and Stabilization of Atherosclerotic Lesions by Pravastatin and by Antimonocyte Chemoattractant Protein-1 Therapy in Nonhuman Primates
Shiro Kitamoto, Kaku Nakano, Yasuhiko Hirouchi, Yoshiro Kohjimoto, Shunichi Kitajima, Makoto Usui, Shujiro Inoue, and Kensuke Egashira
Arterioscler Thromb Vasc Biol. 2004;24:1522-1528; published online before print June 3 2004, doi:10.1161/01.ATV.0000134518.27241.da.
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Treatment with pravastatin reduced plaque size and changed characteristics of plaques to more stable phenotype in cynomolgus monkeys with established atherosclerotic lesion independent of cholesterol lowering. Equivalent inhibitory effects were observed in animals that received anti-MCP-1 therapy. An antiinflammatory mechanism might be involved in the pleiotropic chloesterol-lowering independent antiatherosclerotic effects of pravastatin.
Thrombosis
Interleukin-6, Fibrin D-Dimer, and Coagulation Factors VII and XIIa in Prediction of Coronary Heart Disease
Gordon D.O. Lowe, Ann Rumley, Alex D. McMahon, Ian Ford, Denis St. J. OReilly, Christopher J. Packard for the West of Scotland Coronary Prevention Study Group
Arterioscler Thromb Vasc Biol. 2004;24:1529-1534; published online before print June 17 2004, doi:10.1161/01.ATV.0000135995.39488.6c.
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We compared fibrin D-dimer, IL-6, coagulation factors VII and XIIa, and C-reactive protein in prediction of coronary risk in a case-control study from the West of Scotland Coronary Prevention Study. Although D-dimer correlated with IL-6 and C-reactive protein, only D-dimer showed a significant independent relationship with coronary risk.
Letters to the Editor
Common Polymorphism in the MTP Promoter Attenuates the Dyslipidemic and Proatherogenic Effects of Excess Body Weight
Andrei C. Sposito, Sophie Gonbert, Gerard Turpin, M. John Chapman, and Joëlle Thillet
Arterioscler Thromb Vasc Biol. 2004;24:e143, doi:10.1161/01.ATV.0000136549.23994.b8.
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Associations Among Plasma Lipoprotein Subfractions as Characterized by Analytical Capillary Isotachophoresis, Apolipoprotein E Phenotype, Alzheimer Disease, and Mild Cognitive Impairment
Bo Zhang, Akira Matsunaga, Keijiro Saku, Seigo Nakano, and Tatsuo Yamada
Arterioscler Thromb Vasc Biol. 2004;24:e144, doi:10.1161/01.ATV.0000134391.01498.b8.
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Is There Really a Power Shortage in Clinical Trials Testing the "Homocysteine Hypothesis?"
G.J. Hankey, J.W. Eikelboom, K. Loh, Q. Yi, J. Pizzi, M. Tang, S. Hickling, M. Le, C.J. M. Klijn, P. Dusitanond, F. van Bockxmeer, A. Gelavis, R. Baker, and K. Jamrozik
Arterioscler Thromb Vasc Biol. 2004;24:e147, doi:10.1161/01.ATV.0000136385.50973.68.
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NCEP Report
Implications of Recent Clinical Trials for the National Cholesterol Education Program Adult Treatment Panel III Guidelines
Scott M. Grundy, James I. Cleeman, C. Noel Bairey Merz, H. Bryan Brewer, Jr, Luther T. Clark, Donald B. Hunninghake, Richard C. Pasternak, Sidney C. Smith, Jr, Neil J. Stone, for the Coordinating Committee of the National Cholesterol Education Program Endorsed by the National Heart, Lung, and Blood Institute, American College of Cardiology Foundation, and American Heart Association
Arterioscler Thromb Vasc Biol. 2004;24:e149-e161, doi:10.1161/01.ATV.0000133317.49796.0E.
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