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Coronary Artery Disease: HELP
Articles from Boston University
Based on 158 articles published since 2008

These are the 158 published articles about Coronary Artery Disease that originated from Boston University during 2008-2019.
+ Citations + Abstracts
Pages: 1 · 2 · 3 · 4 · 5 · 6 · 7
126 Article Geographic differences in outcomes in outpatients with established atherothrombotic disease: results from the REACH Registry. 2014

Ducrocq, G / Bhatt, D L / Labreuche, J / Corbalan, R / Porath, A / Gao, R / Panchenko, E / Liau, C S / Ikeda, Y / Goto, S / Amarenco, P / Steg, P G. ·Université Paris-Diderot, Sorbonne Paris Cité, France; AP-HP, Hopital Bichat - Paris, France; INSERM U-698, France gregory.ducrocq@bch.aphp.fr. · VA Boston Healthcare System, Brigham and Women's Hospital, Harvard Medical School, USA. · Université Paris-Diderot, Sorbonne Paris Cité, France; AP-HP, Hopital Bichat - Paris, France; INSERM U-698, France. · Pontificia Universidad Católica de Chile, Chile. · Department of Epidemiology, Ben-Gurion University of the Negev, Israel. · Cardiovascular Institute & Fuwai Hospital, People's Republic of China. · Cardiology Research Center, Russian Federation, Russia. · National Taiwan University Hospital, Taiwan. · Kokura Memorial Hospital, Japan. · Tokai University, Japan. ·Eur J Prev Cardiol · Pubmed #23965467.

ABSTRACT: AIMS: There are major differences in the prevalence and management of patients with atherothrombotic disease including coronary artery disease (CAD), cerebrovascular disease (CVD) and peripheral artery disease (PAD) across different geographical regions. There is, however, little data allowing comparisons of management and outcomes across broad geographic regions. We aimed to describe geographical differences in baseline characteristics, management and outcomes in stable outpatients with established atherothrombotic disease. METHODS AND RESULTS: From the REACH Registry of atherothrombosis, patients with documented CAD, PAD or CVD and with 4-year follow-up were included. Baseline characteristics, treatments and 4-year outcomes were recorded. Event rates were compared between geographical regions and were adjusted for risk scores predicting ischemic and bleeding events. The analyses of baseline characteristics and medications according to geographical region showed marked differences. For the composite primary outcome (cardiovascular death, non-fatal myocardial infarction (MI) and non-fatal stroke), rates ranged from 12.1% in Japan to 18.2% in Eastern Europe. After adjustment, substantial variations remained: taking North America as a reference, patients from Western Europe and Japan had a lower risk of primary outcome event (hazard ratio (HR) 0.93; p = 0.045, and HR = 0.67; p < 0.001 respectively) whereas patients from Eastern Europe had a higher risk (HR = 1.24; p < 0.001). There were no obvious differences between patients from North America and those from Latin America, the Middle East and Asia. CONCLUSION: There are important variations in the outcomes of patients with atherothrombotic across geographic regions. These observations have important implications for public health and clinical research.

127 Article Three vs twelve months of dual antiplatelet therapy after zotarolimus-eluting stents: the OPTIMIZE randomized trial. 2013

Feres, Fausto / Costa, Ricardo A / Abizaid, Alexandre / Leon, Martin B / Marin-Neto, J Antônio / Botelho, Roberto V / King, Spencer B / Negoita, Manuela / Liu, Minglei / de Paula, J Eduardo T / Mangione, José A / Meireles, George X / Castello, Hélio J / Nicolela, Eduardo L / Perin, Marco A / Devito, Fernando S / Labrunie, André / Salvadori, Décio / Gusmão, Marcos / Staico, Rodolfo / Costa, J Ribamar / de Castro, Juliana P / Abizaid, Andrea S / Bhatt, Deepak L / Anonymous390774. ·Instituto Dante Pazzanese de Cardiologia, São Paulo, São Paulo, Brazil. · New York Presbyterian Medical Center, Columbia University Medical Center, and the Cardiovascular Research Foundation, New York, New York. · University of São Paulo, Ribeirão Preto, São Paulo, Brazil. · Instituto do Coração do Triângulo Mineiro, Uberlândia, Minas Gerais, Brazil. · Saint Joseph's Medical Group, Atlanta, Georgia. · Medtronic CardioVascular, Santa Rosa, California. · Unicor de Linhares, Linhares, Espírito Santo, Brazil. · Hospital Beneficência Portuguesa de São Paulo, São Paulo, São Paulo, Brazil. · Hospital Público Estadual de São Paulo, São Paulo, São Paulo, Brazil. · Hospital Bandeirantes, São Paulo, São Paulo, Brazil. · Emcor Emergências do Coração, Piracicaba, São Paulo, Brazil. · Hospital Santa Marcelina, São Paulo, Brazil. · Hospital Padre Albino-FIPA, Catanduva, São Paulo, Brazil. · Santa Casa de Misericórdia de Marilia, Marilia, São Paulo, Brazil. · Hospital Agamenon Magalhães, Recife, Pernambuco, Brazil. · Cardiovascular Research Center, São Paulo, São Paulo, Brazil. · VA Boston Healthcare System, Brigham and Women's Hospital, and Harvard Medical School, Boston, Massachusetts. ·JAMA · Pubmed #24177257.

ABSTRACT: IMPORTANCE: The current recommendation is for at least 12 months of dual antiplatelet therapy after implantation of a drug-eluting stent. However, the optimal duration of dual antiplatelet therapy with specific types of drug-eluting stents remains unknown. OBJECTIVE: To assess the clinical noninferiority of 3 months (short-term) vs 12 months (long-term) of dual antiplatelet therapy in patients undergoing percutaneous coronary intervention (PCI) with zotarolimus-eluting stents. DESIGN, SETTING, AND PATIENTS: The OPTIMIZE trial was an open-label, active-controlled, 1:1 randomized noninferiority study including 3119 patients in 33 sites in Brazil between April 2010 and March 2012. Clinical follow-up was performed at 1, 3, 6, and 12 months. Eligible patients were those with stable coronary artery disease or history of low-risk acute coronary syndrome (ACS) undergoing PCI with zotarolimus-eluting stents. INTERVENTIONS: After PCI with zotarolimus-eluting stents, patients were prescribed aspirin (100-200 mg daily) and clopidogrel (75 mg daily) for 3 months (n = 1563) or 12 months (n = 1556), unless contraindicated because of occurrence of an end point. MAIN OUTCOMES AND MEASURES: The primary end point was net adverse clinical and cerebral events (NACCE; a composite of all-cause death, myocardial infarction [MI], stroke, or major bleeding); the expected event rate at 1 year was 9%, with a noninferiority margin of 2.7%. Secondary end points were major adverse cardiac events (MACE; a composite of all-cause death, MI, emergent coronary artery bypass graft surgery, or target lesion revascularization) and Academic Research Consortium definite or probable stent thrombosis. RESULTS: NACCE occurred in 93 patients receiving short-term and 90 patients receiving long-term therapy (6.0% vs 5.8%, respectively; risk difference, 0.17 [95% CI, -1.52 to 1.86]; P = .002 for noninferiority). Kaplan-Meier estimates demonstrated MACE rates at 1 year of 8.3% (128) in the short-term group and 7.4% (114) in the long-term group (HR, 1.12 [95% CI, 0.87-1.45]). Between 91 and 360 days, no statistically significant association was observed for NACCE (39 [2.6%] vs 38 [2.6%] for the short- and long-term groups, respectively; HR, 1.03 [95% CI, 0.66-1.60]), MACE (78 [5.3%] vs 64 [4.3%]; HR, 1.22 [95% CI, 0.88-1.70]), or stent thrombosis (4 [0.3%] vs 1 [0.1%]; HR, 3.97 [95% CI, 0.44-35.49]). CONCLUSIONS AND RELEVANCE: In patients with stable coronary artery disease or low-risk ACS treated with zotarolimus-eluting stents, 3 months of dual antiplatelet therapy was noninferior to 12 months for NACCE, without significantly increasing the risk of stent thrombosis. TRIAL REGISTRATION: clinicaltrials.gov Identifier: NCT01113372.

128 Article Discovery and refinement of loci associated with lipid levels. 2013

Willer, Cristen J / Schmidt, Ellen M / Sengupta, Sebanti / Peloso, Gina M / Gustafsson, Stefan / Kanoni, Stavroula / Ganna, Andrea / Chen, Jin / Buchkovich, Martin L / Mora, Samia / Beckmann, Jacques S / Bragg-Gresham, Jennifer L / Chang, Hsing-Yi / Demirkan, Ayşe / Den Hertog, Heleen M / Do, Ron / Donnelly, Louise A / Ehret, Georg B / Esko, Tõnu / Feitosa, Mary F / Ferreira, Teresa / Fischer, Krista / Fontanillas, Pierre / Fraser, Ross M / Freitag, Daniel F / Gurdasani, Deepti / Heikkilä, Kauko / Hyppönen, Elina / Isaacs, Aaron / Jackson, Anne U / Johansson, Åsa / Johnson, Toby / Kaakinen, Marika / Kettunen, Johannes / Kleber, Marcus E / Li, Xiaohui / Luan, Jian'an / Lyytikäinen, Leo-Pekka / Magnusson, Patrik K E / Mangino, Massimo / Mihailov, Evelin / Montasser, May E / Müller-Nurasyid, Martina / Nolte, Ilja M / O'Connell, Jeffrey R / Palmer, Cameron D / Perola, Markus / Petersen, Ann-Kristin / Sanna, Serena / Saxena, Richa / Service, Susan K / Shah, Sonia / Shungin, Dmitry / Sidore, Carlo / Song, Ci / Strawbridge, Rona J / Surakka, Ida / Tanaka, Toshiko / Teslovich, Tanya M / Thorleifsson, Gudmar / Van den Herik, Evita G / Voight, Benjamin F / Volcik, Kelly A / Waite, Lindsay L / Wong, Andrew / Wu, Ying / Zhang, Weihua / Absher, Devin / Asiki, Gershim / Barroso, Inês / Been, Latonya F / Bolton, Jennifer L / Bonnycastle, Lori L / Brambilla, Paolo / Burnett, Mary S / Cesana, Giancarlo / Dimitriou, Maria / Doney, Alex S F / Döring, Angela / Elliott, Paul / Epstein, Stephen E / Ingi Eyjolfsson, Gudmundur / Gigante, Bruna / Goodarzi, Mark O / Grallert, Harald / Gravito, Martha L / Groves, Christopher J / Hallmans, Göran / Hartikainen, Anna-Liisa / Hayward, Caroline / Hernandez, Dena / Hicks, Andrew A / Holm, Hilma / Hung, Yi-Jen / Illig, Thomas / Jones, Michelle R / Kaleebu, Pontiano / Kastelein, John J P / Khaw, Kay-Tee / Kim, Eric / Klopp, Norman / Komulainen, Pirjo / Kumari, Meena / Langenberg, Claudia / Lehtimäki, Terho / Lin, Shih-Yi / Lindström, Jaana / Loos, Ruth J F / Mach, François / McArdle, Wendy L / Meisinger, Christa / Mitchell, Braxton D / Müller, Gabrielle / Nagaraja, Ramaiah / Narisu, Narisu / Nieminen, Tuomo V M / Nsubuga, Rebecca N / Olafsson, Isleifur / Ong, Ken K / Palotie, Aarno / Papamarkou, Theodore / Pomilla, Cristina / Pouta, Anneli / Rader, Daniel J / Reilly, Muredach P / Ridker, Paul M / Rivadeneira, Fernando / Rudan, Igor / Ruokonen, Aimo / Samani, Nilesh / Scharnagl, Hubert / Seeley, Janet / Silander, Kaisa / Stančáková, Alena / Stirrups, Kathleen / Swift, Amy J / Tiret, Laurence / Uitterlinden, Andre G / van Pelt, L Joost / Vedantam, Sailaja / Wainwright, Nicholas / Wijmenga, Cisca / Wild, Sarah H / Willemsen, Gonneke / Wilsgaard, Tom / Wilson, James F / Young, Elizabeth H / Zhao, Jing Hua / Adair, Linda S / Arveiler, Dominique / Assimes, Themistocles L / Bandinelli, Stefania / Bennett, Franklyn / Bochud, Murielle / Boehm, Bernhard O / Boomsma, Dorret I / Borecki, Ingrid B / Bornstein, Stefan R / Bovet, Pascal / Burnier, Michel / Campbell, Harry / Chakravarti, Aravinda / Chambers, John C / Chen, Yii-Der Ida / Collins, Francis S / Cooper, Richard S / Danesh, John / Dedoussis, George / de Faire, Ulf / Feranil, Alan B / Ferrières, Jean / Ferrucci, Luigi / Freimer, Nelson B / Gieger, Christian / Groop, Leif C / Gudnason, Vilmundur / Gyllensten, Ulf / Hamsten, Anders / Harris, Tamara B / Hingorani, Aroon / Hirschhorn, Joel N / Hofman, Albert / Hovingh, G Kees / Hsiung, Chao Agnes / Humphries, Steve E / Hunt, Steven C / Hveem, Kristian / Iribarren, Carlos / Järvelin, Marjo-Riitta / Jula, Antti / Kähönen, Mika / Kaprio, Jaakko / Kesäniemi, Antero / Kivimaki, Mika / Kooner, Jaspal S / Koudstaal, Peter J / Krauss, Ronald M / Kuh, Diana / Kuusisto, Johanna / Kyvik, Kirsten O / Laakso, Markku / Lakka, Timo A / Lind, Lars / Lindgren, Cecilia M / Martin, Nicholas G / März, Winfried / McCarthy, Mark I / McKenzie, Colin A / Meneton, Pierre / Metspalu, Andres / Moilanen, Leena / Morris, Andrew D / Munroe, Patricia B / Njølstad, Inger / Pedersen, Nancy L / Power, Chris / Pramstaller, Peter P / Price, Jackie F / Psaty, Bruce M / Quertermous, Thomas / Rauramaa, Rainer / Saleheen, Danish / Salomaa, Veikko / Sanghera, Dharambir K / Saramies, Jouko / Schwarz, Peter E H / Sheu, Wayne H-H / Shuldiner, Alan R / Siegbahn, Agneta / Spector, Tim D / Stefansson, Kari / Strachan, David P / Tayo, Bamidele O / Tremoli, Elena / Tuomilehto, Jaakko / Uusitupa, Matti / van Duijn, Cornelia M / Vollenweider, Peter / Wallentin, Lars / Wareham, Nicholas J / Whitfield, John B / Wolffenbuttel, Bruce H R / Ordovas, Jose M / Boerwinkle, Eric / Palmer, Colin N A / Thorsteinsdottir, Unnur / Chasman, Daniel I / Rotter, Jerome I / Franks, Paul W / Ripatti, Samuli / Cupples, L Adrienne / Sandhu, Manjinder S / Rich, Stephen S / Boehnke, Michael / Deloukas, Panos / Kathiresan, Sekar / Mohlke, Karen L / Ingelsson, Erik / Abecasis, Gonçalo R / Anonymous3140771. ·Department of Internal Medicine, Division of Cardiovascular Medicine, University of Michigan, Ann Arbor, Michigan 48109, USA. · Department of Computational Medicine and Bioinformatics, University of Michigan, Ann Arbor, Michigan 48109, USA. · Department of Human Genetics, University of Michigan, Ann Arbor, Michigan 48109, USA. · Center for Statistical Genetics, Department of Biostatistics, University of Michigan, Ann Arbor, Michigan 48109, USA. · Department of Biostatistics, Boston University School of Public Health, Boston, Massachusetts 02118, USA. · Center for Human Genetic Research, Massachusetts General Hospital, Boston, Massachusetts 02114, USA. · Broad Institute, Program in Medical and Population Genetics, Cambridge, Massachusetts 02142, USA. · Department of Medical Sciences, Molecular Epidemiology, Uppsala University, Uppsala, Sweden. · Science for Life Laboratory, Uppsala University, Uppsala, Sweden. · Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, CB10 1SA, Hinxton, United Kingdom. · Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden. · Department of Genetics, University of North Carolina, Chapel Hill, NC 27599 USA. · Division of Preventive Medicine, Brigham and Women's Hospital, 900 Commonwealth Ave., Boston MA 02215, USA. · Harvard Medical School, Boston MA 02115, USA. · Service of Medical Genetics, Lausanne University Hospital, Lausanne, Switzerland. · Department of Medical Genetics, University of Lausanne, Lausanne, Switzerland. · Division of Preventive Medicine and Health Services Research, Institute of Population Health Sciences, National Health Research Institutes, Zhunan, Taiwan. · Genetic Epidemiology Unit, Department of Epidemiology, Erasmus University Medical Center, Rotterdam, The Netherlands. · Department of Neurology, Erasmus Medical Center, Rotterdam, The Netherlands. · Medical Research Institute, University of Dundee, Ninewells Hospital and Medical School. Dundee, DD1 9SY, United Kingdom. · Cardiology, Department of Specialities of Medicine, Geneva University Hospital, Rue Gabrielle-Perret-Gentil 4, 1211 Geneva 14, Switzerland. · Center for Complex Disease Genomics, McKusick-Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA. · Estonian Genome Center of the University of Tartu, Tartu, Estonia. · Institute of Molecular and Cell Biology, University of Tartu, Tartu, Estonia. · Department of Genetics, Washington University School of Medicine, USA. · Wellcome Trust Centre for Human Genetics, University of Oxford, Oxford, OX3 7BN, United Kingdom. · Centre for Population Health Sciences, University of Edinburgh, Teviot Place, Edinburgh, EH8 9AG, Scotland, United Kingdom. · Department of Public Health and Primary Care, University of Cambridge, Cambridge, United Kingdom. · Hjelt Institute, Department of Public Health, University of Helsinki, Finland. · Centre For Paediatric Epidemiology and Biostatistics/MRC Centre of Epidemiology for Child Health, University College of London Institute of Child Health, London, United Kingdom. · Centre for Medical Systems Biology, Leiden, the Netherlands. · Department of Immunology, Genetics and Pathology, Uppsala University, Uppsala, Sweden. · Uppsala Clinical Research Center, Uppsala University, Uppsala, Sweden. · Genome Centre, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, UK. · Clinical Pharmacology, NIHR Cardiovascular Biomedical Research Unit, William Harvey Research Institute, Barts and The London School of Medicine and Dentistry Queen Mary University of London, London, UK. · Biocenter Oulu, University of Oulu, Oulu, Finland. · Institute of Health Sciences, University of Oulu, Finland. · Institute for Molecular Medicine Finland FIMM, University of Helsinki, Finland. · Public Health Genomics Unit, National Institute for Health and Welfare, Helsinki, Finland. · Department of Internal Medicine II - Cardiology, University of Ulm Medical Centre, Ulm, Germany. · Mannheim Institute of Public Health, Social and Preventive Medicine, Medical Faculty of Mannheim, University of Heidelberg, Ludolf-Krehl-Strasse 7-11, 68167 Mannheim, Germany. · Medical Genetics Institute, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA. · MRC Epidemiology Unit, Institute of Metabolic Science, Box 285, Addenbrooke's Hospital, Hills Road, Cambridge, CB2 0QQ, United Kingdom. · Department of Clinical Chemistry, Fimlab Laboratories, Tampere 33520, Finland. · Department of Clinical Chemistry, University of Tampere School of Medicine, Tampere 33014, Finland. · Department of Twin Research and Genetic Epidemiology, King's College London, London, United Kingdom. · Division of Endocrinology, Diabetes, and Nutrition, Department of Medicine, University of Maryland, School of Medicine, Baltimore, Maryland. · Institute of Genetic Epidemiology, Helmholtz Zentrum München, Neuherberg 85764, Germany. · Department of Medicine I, University Hospital Grosshadern, Ludwig-Maximilians University, Munich, Germany. · Institute of Medical Informatics, Biometry and Epidemiology, Ludwig-Maximilians-University of Munich, Munich, Germany. · Department of Epidemiology, University of Groningen, University Medical Center Groningen, The Netherlands. · Division of Endocrinology, Children's Hospital Boston, Massachusetts 02115, USA. · Division of Genetics, Program in Genomics, Children's Hospital, Boston, Massachusetts 02115, USA. · Istituto di Ricerca Genetica e Biomedica, CNR, Monserrato, 09042, Italy. · Massachusetts General Hospital/Broad Institute, Harvard University, Cambridge, MA, USA. · Center for Neurobehavioral Genetics, The Semel Institute for Neuroscience and Human Behavior, University of California, Los Angeles, USA. · Genetic Epidemiology Group, Deparment of Epidemiology and Public Health, UCL, London WC1E 6BT, United Kingdom. · Department of Clinical Sciences, Genetic & Molecular Epidemiology Unit, Lund University Diabetes Center, Scania University Hosptial, Malmö, Sweden. · Department of Odontology, Umeå University, Umeå, Sweden. · Department of Public Health and Primary Care, Unit of Medicine, Umeå University, Umeå, Sweden. · Dipartimento di Scienze Biomediche, Universita di Sassari, 07100 SS, Italy. · Atherosclerosis Research Unit, Department of Medicine Solna, Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden. · Center for Molecular Medicine, Karolinska University Hospital, Stockholm, Sweden. · Clinical Research Branch, National Institute Health, Baltimore, MD, USA. · deCODE Genetics/Amgen, 101 Reykjavik, Iceland. · Department of Genetics, University of Pennsylvania - School of Medicine, Philadelphia PA, 19104, USA. · Department of Systems Pharmacology and Translational Therapeutics, University of Pennsylvania - School of Medicine, Philadelphia PA, 19104, USA. · Human Genetics Center, University of Texas Health Science Center - School of Public Health, Houston, TX 77030, USA. · HudsonAlpha Institute for Biotechnology, Huntsville, AL, USA. · MRC Unit for Lifelong Health and Ageing, 33 Bedford Place, London, WC1B 5JU, United Kingdom. · Department of Epidemiology and Biostatistics, School of Public Health, Imperial College London, London, United Kingdom. · Ealing Hospital, Southall, Middlesex UB1 3HW, United Kingdom. · MRC/UVRI Uganda Research Unit on AIDS, Entebbe, Uganda. · University of Cambridge Metabolic Research Laboratories and NIHR Cambridge Biomedical Research Centre, Level 4, Institute of Metabolic Science Box 289 Addenbrooke's Hospital Cambridge CB2 OQQ, UK. · Department of Pediatrics, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA. · Genome Technology Branch, National Human Genome Research Institute, NIH, Bethesda, MD 20892, USA. · Department of Experimental Medicine, University of Milano Bicocca, Italy. · MedStar Health Research Institute, 6525 Belcrest Road, Suite 700, Hyattsville, MD 20782, USA. · Research Centre on Public Health, University of Milano Bicocca, Italy. · Department of Dietetics-Nutrition, Harokopio University, 70 El. Venizelou Str, Athens, Greece. · Institute of Epidemiology I, Helmholtz Zentrum München, Neuherberg 85764, Germany. · Institute of Epidemiology II, Helmholtz Zentrum München, Neuherberg 85764, Germany. · Department of Epidemiology and Biostatistics, MRC Health Protection Agency (HPA) Centre for Environment and Health, School of Public Health, Imperial College London, UK. · The Laboratory in Mjodd, 108 Reykjavik, Iceland. · Division of Cardiovascular Epidemiology, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden. · Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA. · Research Unit of Molecular Epidemiology, Helmholtz Zentrum München, Neuherberg 85764, Germany. · Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, OX3 7LJ, United Kingdom. · Department of Public Health and Clinical Medicine, Nutritional research, Umeå University, Umeå, Sweden. · Department of Clinical Sciences/Obstetrics and Gynecology, Oulu University Hospital, Oulu, Finland. · MRC Human Genetics Unit, Institute of Genetics and Molecular Medicine, Western General Hospital, Edinburgh, Scotland, United Kingdom. · Laboratory of Neurogenetics, National Institute on Aging, Bethesda, MD 20892, USA. · Center for Biomedicine, European Academy Bozen/Bolzano (EURAC), Bolzano, Italy - Affiliated Institute of the University of Lübeck, Lübeck, Germany. · Division of Endocrinology & Metabolism, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan. · Hannover Unified Biobank, Hannover Medical School, Hannover 30625, Germany. · Department of Vascular Medicine, Academic Medical Center, Amsterdam, The Netherlands. · Clinical Gerontology Unit, University of Cambridge, Cambridge, United Kingdom. · Kuopio Research Institute of Exercise Medicine, Kuopio, Finland. · Division of Endocrine and Metabolism, Department of Internal Medicine, Taichung Veterans General Hospital, School of Medicine, National Yang-Ming University, Taipei, Taiwan. · Diabetes Prevention Unit, National Institute for Health and Welfare, 00271 Helsinki, Finland. · The Genetics of Obesity and Related Metabolic Traits Program, The Icahn School of Medicine at Mount Sinai, New York, USA. · The Charles Bronfman Institute for Personalized Medicine, The Icahn School of Medicine at ount Sinai, New York, USA. · The Mindich Child Health and Development Institute, The Icahn School of Medicine at Mount Sinai, New York. · School of Social and Community Medicine, University of Bristol, Oakfield House, Oakfield Grove, Bristol BS8 2BN, United Kingdom. · Institute for Medical Informatics and Biometrics, University of Dresden, Medical Faculty Carl Gustav Carus, Fetscherstrasse 74, 01307 Dresden, Germany. · Laboratory of Genetics, National Institute on Aging, Baltimore, MD21224, USA. · Department of Clinical Pharmacology, University of Tampere School of Medicine, Tamperew 33014, Finland. · Department of Internal Medicine, Päijät-Häme Central Hospital, Lahti, Finland. · Division of Cardiology, Helsinki University Central Hospital, Helsinki, Finland. · Department of Clinical Biochemistry, Landspitali University Hospital, 101 Reykjavik, Iceland. · Department of Medical Genetics, Haartman Institute, University of Helsinki and Helsinki University Central Hospital, Helsinki, Finland. · Genetic Epidemiology Group, Wellcome Trust Sanger Institute, Hinxton, Cambridge, United ingdom. · Department of Statistical Sciences, University College of London, London, United Kingdom. · National Institute for Health and Welfare, Oulu, Finland. · Cardiovascular Institute, Perelman School of Medicine at the University of Pennsylvania, 3400 Civic Center Blvd, Building 421, Translational Research Center, Philadelphia, PA 19104-5158, USA. · Division of Translational Medicine and Human Genetics, Perelman School of Medicine at the University of Pennsylvania, 3400 Civic Center Blvd, Building 421, Translational Research Center, Philadelphia, PA 19104-5158, USA. · Department of Epidemiology, Erasmus University Medical Center, Rotterdam, the Netherlands. · Department of Internal Medicine, Erasmus University Medical Center, Rotterdam, the Netherlands. · Netherlands Genomics Initiative (NGI)-sponsored Netherlands Consortium for Healthy Aging NCHA), Leiden, The Netherlands. · Department of Clinical Sciences/Clinical Chemistry, University of Oulu, Oulu, Finland. · National Institute for Health Research Leicester Cardiovascular Biomedical Research Unit, Glenfield Hospital, Leicester LE3 9QP, UK. · Department of Cardiovascular Sciences, University of Leicester, Glenfield Hospital, Leicester, LE3 9QP, UK. · Clinical Institute of Medical and Chemical Laboratory Diagnostics, Medical University of Graz, Austria. · School of International Development, University of East Anglia, Norwich NR4 7TJ, United Kingdom. · University of Eastern Finland and Kuopio University Hospital, 70210 Kuopio, Finland. · INSERM UMRS 937, Pierre and Marie Curie University, Paris, France. · Department of Laboratory Medicine, University of Groningen, University Medical Center Groningen, The Netherlands. · LifeLines Cohort Study, University of Groningen, University Medical Center Groningen, The Netherlands. · Department of Genetics, University of Groningen, University Medical Center Groningen, The Netherlands. · Department of Biological Psychology, VU Univ, Amsterdam, The Netherlands. · Department of Community Medicine, Faculty of Health Sciences, University of Tromsø, Tromsø, Norway. · Department of Nutrition, University of North Carolina, Chapel Hill, NC, USA. · Department of Epidemiology and Public Health, EA 3430, University of Strasbourg, Faculty of Medicine, Strasbourg, France. · Department of Medicine, Stanford University School of Medicine, Stanford, CA, USA. · Geriatric Unit, Azienda Sanitaria Firenze (ASF), Florence, Italy. · Chemical Pathology, Department of Pathology, University of the West Indies, Mona, Kingston 7, Jamaica. · Institute of Social and Preventive Medicine (IUMSP), Lausanne University Hospital, Route de la Corniche 10, 1010 Lausanne, Switzerland. · Division of Endocrinology and Diabetes, Department of Internal Medicine, Ulm University Medical Centre, Ulm, Germany. · Lee Kong Chian School of Medicine, Nanyang Technological University, Singapore. · Department of Medicine III, University of Dresden, Medical Faculty Carl Gustav Carus, Fetscherstrasse 74, 01307 Dresden, Germany. · Ministry of Health, Victoria, Republic of Seychelles. · Service of Nephrology, Lausanne University Hospital, Lausanne, Switzerland. · Imperial College Healthcare NHS Trust, London, United Kingdom. · Division of Reproductive Endocrinology, Department of Obstetrics and Gynecology, Cedars-Sinai Medical Center, Los Angeles, California, USA. · Department of Medicine, University of California Los Angeles, Los Angeles, California, USA. · Department of Preventive Medicine and Epidemiology, Loyola University Medical School, Maywood, Illinois 60153, USA. · Office of Population Studies Foundation, University of San Carlos, Talamban, Cebu City, Philippines. · Department of Cardiology, Toulouse University School of Medicine, Rangueil Hospital, Toulouse, France. · Department of Psychiatry, University of California, Los Angeles, USA. · Department of Clinical Sciences, Lund University, SE-20502, Malmö, Sweden. · Department of Medicine, Helsinki University Hospital, FI-00029 Helsinki, Finland. · Icelandic Heart Association, Kopavogur, Iceland. · Department of Cardiology, Karolinska University Hospital, Stockholm, Sweden. · Laboratory of Epidemiology, Demography, and Biometry, National Institute on Ageing, Bethesda, MD, USA. · Institute of Population Health Sciences, National Health Research Institutes, Zhunan, Taiwan. · Cardiovascular Genetics, BHF Laboratories, Institute Cardiovascular Science, University College London, London, United Kingdom. · Cardiovascular Genetics, University of Utah School of Medicine, Salt Lake City, UT, USA. · HUNT Research Centre, Department of Public Health and General Practice, Norwegian University of Science and Technology, Levanger, Norway. · Kaiser Permanente, Division of Research, Oakland, CA, USA. · Unit of Primary Care, Oulu University Hospital, Oulu, Finland. · Department of Chronic Disease Prevention, National Institute for Health and Welfare, Turku, Finland. · Department of Clinical Physiology, University of Tampere School of Medicine, Tampere 33014, Finland. · Department of Mental Health and Substance Abuse Services, National Institute for Health and Welfare, Helsinki, Finland. · Institute of Clinical Medicine, Department of Medicine, University of Oulu and Clinical Research Center, Oulu University Hospital, Oulu, Finland. · National Heart & Lung Institute, Imperial College London, Hammersmith Hospital, London, United Kingdom. · Children's Hospital Oakland Research Institute, 5700 Martin Luther King Junior Way, Oakland, CA 94609, USA. · Department of Medicine, University of Eastern Finland and Kuopio University Hospital, 70210 Kuopio, Finland. · Institute of Regional Health Services Research, University of Southern Denmark, Odense, Denmark. · Odense Patient data Explorative Network (OPEN), Odense University Hospital, Odense, Denmark. · Institute of Biomedicine/Physiology, University of Eastern Finland, Kuopio Campus, Finland. · Department of Medical Sciences, Uppsala University, Uppsala, Sweden. · Queensland Institute of Medical Research, Locked Bag 2000, Royal Brisbane Hospital, Queensland 4029, Australia. · Synlab Academy, Synlab Services GmbH,Gottlieb-Daimler-Straße 25, 68165 Mannheim, Germany. · Tropical Metabolism Research Unit, Tropical Medicine Research Institute, University of the West Indies, Mona, Kingston 7, Jamaica. · U872 Institut National de la Santé et de la Recherche Médicale, Centre de Recherche des Cordeliers, 75006 Paris, France. · Department of Medicine, Kuopio University Hospital, Kuopio, Finland. · Department of Neurology, General Central Hospital, Bolzano, Italy. · Department of Neurology, University of Lübeck, Lübeck, Germany. · Cardiovascular Health Research Unit, Departments of Medicine, Epidemiology, and Health Services, University of Washington, Seattle, WA, USA. · Group Health Research Institute, Group Health Cooperative, Seattle, WA, USA. · Department of Clinical Physiology and Nuclear Medicine, Kuopio University Hospital, Kuopio, Finland. · Center for Non-Communicable Diseases, Karachi, Pakistan. · Department of Medicine, University of Pennsylvania, USA. · Unit of Chronic Disease Epidemiology and Prevention, National Institute for Health and Welfare, Helsinki, Finland. · South Karelia Central Hospital, Lappeenranta, Finland. · Paul Langerhans Institute Dresden, German Center for Diabetes Research (DZD), Dresden, Germany. · Division of Endocrine and Metabolism, Department of Internal Medicine, Taichung Veterans General Hospital, Taichung, Taiwan. · Geriatric Research and Education Clinical Center, Veterans Administration Medical Center, Baltimore, Maryland. · Faculty of Medicine, University of Iceland, 101 Reykjavík, Iceland. · Division of Population Health Sciences and Education, St George's, University of London, Cranmer Terrace, London SW17 0RE, United Kingdom. · Department of Pharmacological Sciences, University of Milan, Monzino Cardiology Center, IRCCS, Milan, Italy. · Centre for Vascular Prevention, Danube-University Krems, 3500 Krems, Austria. · King Abdulaziz University, Faculty of Medicine, Jeddah 21589, Saudi Arabia. · Red RECAVA Grupo RD06/0014/0015, Hospital Universitario La Paz, 28046. · Institute of Public Health and Clinical Nutrition, University of Eastern Finland, Finland. · Research Unit, Kuopio University Hospital, Kuopio, Finland. · Department of Medicine, Lausanne University Hospital, Switzerland. · Department of Endocrinology, University of Groningen, University Medical Center Groningen, The Netherlands. · Department of Cardiovascular Epidemiology and Population Genetics, National Center for rdiovascular Investigation, Madrid, Spain. · IMDEA-Alimentacion, Madrid, Spain. · Nutrition and Genomics Laboratory, Jean Mayer-USDA Human Nutrition Research Center on Aging at Tufts University, Boston, MA, USA. · Department of Nutrition, Harvard School of Public Health, Boston, MA, USA. · Framingham Heart Study, Framingham, MA, USA. · Center for Public Health Genomics, University of Virginia, Charlottesville, VA 22908, USA. · Cardiovascular Research Center, Massachusetts General Hospital, Boston, Massachusetts 02114, USA. · Department of Medicine, Harvard Medical School, Boston, Massachusetts 02115, USA. ·Nat Genet · Pubmed #24097068.

ABSTRACT: Levels of low-density lipoprotein (LDL) cholesterol, high-density lipoprotein (HDL) cholesterol, triglycerides and total cholesterol are heritable, modifiable risk factors for coronary artery disease. To identify new loci and refine known loci influencing these lipids, we examined 188,577 individuals using genome-wide and custom genotyping arrays. We identify and annotate 157 loci associated with lipid levels at P < 5 × 10(-8), including 62 loci not previously associated with lipid levels in humans. Using dense genotyping in individuals of European, East Asian, South Asian and African ancestry, we narrow association signals in 12 loci. We find that loci associated with blood lipid levels are often associated with cardiovascular and metabolic traits, including coronary artery disease, type 2 diabetes, blood pressure, waist-hip ratio and body mass index. Our results demonstrate the value of using genetic data from individuals of diverse ancestry and provide insights into the biological mechanisms regulating blood lipids to guide future genetic, biological and therapeutic research.

129 Article Consensus and update on the definition of on-treatment platelet reactivity to adenosine diphosphate associated with ischemia and bleeding. 2013

Tantry, Udaya S / Bonello, Laurent / Aradi, Daniel / Price, Matthew J / Jeong, Young-Hoon / Angiolillo, Dominick J / Stone, Gregg W / Curzen, Nick / Geisler, Tobias / Ten Berg, Jurrien / Kirtane, Ajay / Siller-Matula, Jolanta / Mahla, Elisabeth / Becker, Richard C / Bhatt, Deepak L / Waksman, Ron / Rao, Sunil V / Alexopoulos, Dimitrios / Marcucci, Rossella / Reny, Jean-Luc / Trenk, Dietmar / Sibbing, Dirk / Gurbel, Paul A / Anonymous50771. ·Sinai Center for Thrombosis Research, Sinai Hospital of Baltimore, Baltimore, Maryland. · Département de Cardiologie, Hôpital Universitaire Nord, Aix-Marseille University, Marseille, France. · Department of Cardiology, Heart Center Balatonfüred, Balatonfüred, Hungary. · Scripps Clinic and Scripps Translational Science Institute, La Jolla, California. · Department of Internal Medicine, Gyeongsang National University Hospital, Gyeongsang National University, Jinju, South Korea. · Cardiovascular Research Center, University of Florida College of Medicine, Jacksonville, Florida. · Cardiovascular Research and Education, Columbia University Medical Center/New York-Presbyterian Hospital, New York, New York. · Wessex Cardiothoracic Unit, University Hospital, Southampton National Health Service Foundation Trust, Southampton, United Kingdom. · Medizinische Klinik III, Kardiologie und Kreislauferkrankungen, Universitätsklinikum Tübingen, Tübingen, Germany. · Department of Cardiology, St. Antonius Hospital Nieuwegein, Nieuwegein, the Netherlands. · Department of Cardiology, Medical University of Vienna, Vienna, Austria. · Department of Anesthesiology and Intensive Care Medicine, Medical University of Graz, Graz, Austria. · Duke Clinical Research Institute, Duke University School of Medicine, Durham, North Carolina. · Veterans Affairs Boston Healthcare System, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts. · Interventional Cardiology, Medstar Washington Hospital Center, Washington, DC. · The Duke Clinical Research Institute, Durham, North Carolina. · Department of Cardiology, Patras University Hospital, Patras, Greece. · Department of Medical and Surgical Critical Care, University of Florence, Florence, Italy. · Department of Internal Medicine, Rehabilitation, and Geriatrics, Geneva Platelet Group, Geneva University Hospitals and School of Medicine, Geneva, Switzerland. · Universitaets-Herzzentrum Freiburg-Bad Krozingen, Bad Krozingen, Germany. · Department of Cardiology, Ludwig-Maximilians Universität München, Medizinische Klinik und Poliklinik I, Munich, Germany. · Sinai Center for Thrombosis Research, Sinai Hospital of Baltimore, Baltimore, Maryland. Electronic address: pgurbel@lifebridgehealth.org. ·J Am Coll Cardiol · Pubmed #24076493.

ABSTRACT: Dual antiplatelet therapy with aspirin and a P2Y12 receptor blocker is a key strategy to reduce platelet reactivity and to prevent thrombotic events in patients treated with percutaneous coronary intervention. In an earlier consensus document, we proposed cutoff values for high on-treatment platelet reactivity to adenosine diphosphate (ADP) associated with post-percutaneous coronary intervention ischemic events for various platelet function tests (PFTs). Updated American and European practice guidelines have issued a Class IIb recommendation for PFT to facilitate the choice of P2Y12 receptor inhibitor in selected high-risk patients treated with percutaneous coronary intervention, although routine testing is not recommended (Class III). Accumulated data from large studies underscore the importance of high on-treatment platelet reactivity to ADP as a prognostic risk factor. Recent prospective randomized trials of PFT did not demonstrate clinical benefit, thus questioning whether treatment modification based on the results of current PFT platforms can actually influence outcomes. However, there are major limitations associated with these randomized trials. In addition, recent data suggest that low on-treatment platelet reactivity to ADP is associated with a higher risk of bleeding. Therefore, a therapeutic window concept has been proposed for P2Y12 inhibitor therapy. In this updated consensus document, we review the available evidence addressing the relation of platelet reactivity to thrombotic and bleeding events. In addition, we propose cutoff values for high and low on-treatment platelet reactivity to ADP that might be used in future investigations of personalized antiplatelet therapy.

130 Article Activation of sterol regulatory element binding protein and NLRP3 inflammasome in atherosclerotic lesion development in diabetic pigs. 2013

Li, Yu / Xu, Shanqin / Jiang, Bingbing / Cohen, Richard A / Zang, Mengwei. ·Vascular Biology Section, Department of Medicine, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts, United States of America. ·PLoS One · Pubmed #23825667.

ABSTRACT: BACKGROUND: Aberrantly elevated sterol regulatory element binding protein (SREBP), the lipogenic transcription factor, contributes to the development of fatty liver and insulin resistance in animals. Our recent studies have discovered that AMP-activated protein kinase (AMPK) phosphorylates SREBP at Ser-327 and inhibits its activity, represses SREBP-dependent lipogenesis, and thereby ameliorates hepatic steatosis and atherosclerosis in insulin-resistant LDLR(-/-) mice. Chronic inflammation and activation of NLRP3 inflammasome have been implicated in atherosclerosis and fatty liver disease. However, whether SREBP is involved in vascular lipid accumulation and inflammation in atherosclerosis remains largely unknown. PRINCIPAL FINDINGS: The preclinical study with aortic pouch biopsy specimens from humans with atherosclerosis and diabetes shows intense immunostaining for SREBP-1 and the inflammatory marker VCAM-1 in atherosclerotic plaques. The cleavage processing of SREBP-1 and -2 and expression of their target genes are increased in the well-established porcine model of diabetes and atherosclerosis, which develops human-like, complex atherosclerotic plaques. Immunostaining analysis indicates an elevation in SREBP-1 that is primarily localized in endothelial cells and in infiltrated macrophages within fatty streaks, fibrous caps with necrotic cores, and cholesterol crystals in advanced lesions. Moreover, concomitant suppression of NAD-dependent deacetylase SIRT1 and AMPK is observed in atherosclerotic pigs, which leads to the proteolytic activation of SREBP-1 by diminishing the deacetylation and Ser-372 phosphorylation of SREBP-1. Aberrantly elevated NLRP3 inflammasome markers are evidenced by increased expression of inflammasome components including NLPR3, ASC, and IL-1β. The increase in SREBP-1 activity and IL-1β production in lesions is associated with vascular inflammation and endothelial dysfunction in atherosclerotic pig aorta, as demonstrated by the induction of NF-κB, VCAM-1, iNOS, and COX-2, as well as by the repression of eNOS. CONCLUSIONS: These translational studies provide in vivo evidence that the dysregulation of SIRT1-AMPK-SREBP and stimulation of NLRP3 inflammasome may contribute to vascular lipid deposition and inflammation in atherosclerosis.

131 Article Coronary intravascular ultrasound. 2013

Bangalore, Sripal / Bhatt, Deepak L. ·VA Boston Healthcare System and Women’s Hospital Boston, MA, USA. ·Circulation · Pubmed #23797744.

ABSTRACT: -- No abstract --

132 Article Removable dental prostheses and cardiovascular survival: a 15-year follow-up study. 2013

Janket, S J / Surakka, M / Jones, J A / Lam, A / Schnell, R A / Rose, L M / Walls, A W G / Meurman, J H. ·Boston University, Henry M. Goldman School of Dental Medicine, Boston, MA, USA. skjanket@bu.edu ·J Dent · Pubmed #23770385.

ABSTRACT: OBJECTIVES: In previous studies, increasing number of teeth predicted better survival and the acute needs for dental treatment predicted mortality. We sought to investigate whether restored dentitions by various removable dental prostheses impact cardiovascular (CVD) longevity. METHODS: Kuopio Oral Health and Heart study was initiated as a cross-sectional investigation with 256 subjects with diagnosed coronary artery disease [CAD] and 250 age- and sex-matched controls without CAD in 1995-1996. The mean age of both groups was 61, 30% were females. We appended mortality follow-up records to the baseline data and formulated this 15-year follow-up study. We examined the relationship between various types of dental prostheses and cardiovascular mortality by proportional hazard regression analyses. We also explored their correlation to oral and systemic inflammatory markers such as asymptotic dental score and C-reactive protein. RESULTS: In a model adjusted for age, sex and smoking, groups having only natural teeth (NT), removable partial denture(s) [PD] and NT, a PD and a full denture [FD], and FD/FD or FD/NT demonstrated the following hazard ratios for mortality (95% confidence interval). NT both arches: 1.00 [reference]; PD and NT: 0.75 [0.22-2.56]; PD and FD: 1.99 [1.05-3.81]; and FD opposed by FD or NT: 1.71 [0.93-3.13], respectively [p for trend=0.05]. Although statistically not significant, those with PD and NT with mean a number of teeth [Nteeth] of 15.4 had better survival compared with those who had all NT [Nteeth=22.5]; while those who had FD and PD [Nteeth=6.5] had shorter longevity than those with FD/FD or FD/NT [Nteeth=3.5]. CONCLUSIONS: Although not all subgroups of dental prostheses reached significant relationship with CVD mortality, our study suggests that not only the number [quantity] of remaining teeth but their maintenance [quality] removing potential inflammatory foci, such as pericoronitis or retained root tips, may positively impact on cardiovascular survival.

133 Article Peripheral artery disease is associated with severe impairment of vascular function. 2013

Kiani, Soroosh / Aasen, Jonathan G / Holbrook, Monika / Khemka, Abhishek / Sharmeen, Farhana / LeLeiko, Rebecca M / Tabit, Corey E / Farber, Alik / Eberhardt, Robert T / Gokce, Noyan / Vita, Joseph A / Hamburg, Naomi M. ·Evans Department of Medicine and Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, MA, USA. ·Vasc Med · Pubmed #23509089.

ABSTRACT: Patients with peripheral artery disease (PAD) have higher cardiovascular event rates than patients with established coronary artery disease (CAD) and abnormal endothelial function predicts cardiovascular risk in PAD and CAD. We investigated the hypothesis that PAD is associated with a greater degree of impairment in vascular function than CAD. We used several non-invasive tests to evaluate endothelial function in 1320 men and women with combined PAD and CAD (n = 198), PAD alone (n = 179), CAD alone (n = 466), or controls aged > 45 years without CAD or PAD (n = 477). Patients with PAD had lower brachial artery flow-mediated dilation (5.1 ± 3.9% PAD and CAD, 5.9 ± 4.4% PAD alone) compared to patients with CAD alone (7.0 ± 4.5%) and no PAD or CAD (8.1 ± 5.1%, p < 0.0001). In multivariable models adjusting for clinical covariates and the presence of CAD, PAD remained associated with lower flow-mediated dilation (p < 0.0001). PAD was associated also with lower nitroglycerin-mediated dilation and reactive hyperemia. Patients with both PAD and CAD had a lower digital pulse amplitude tonometry (PAT) ratio in unadjusted models but not in adjusted models. Flow-mediated dilation was modestly associated with PAT ratio in patients with atherosclerotic disease (r = 0.23, p < 0.0001) but not among control participants (r = 0.008, p = 0.93). Our findings indicate that patients with PAD have greater impairment of vasodilator function and are consistent with the possibility that endothelial dysfunction may contribute to adverse cardiovascular prognosis in PAD.

134 Article Nonemergency PCI at hospitals with or without on-site cardiac surgery. 2013

Jacobs, Alice K / Normand, Sharon-Lise T / Massaro, Joseph M / Cutlip, Donald E / Carrozza, Joseph P / Marks, Anthony D / Murphy, Nancy / Romm, Iyah K / Biondolillo, Madeleine / Mauri, Laura / Anonymous3080752. ·Boston University School of Medicine, Cardiovascular Medicine, Department of Medicine, Boston Medical Center, Boston, MA 02118, USA. alice.jacobs@bmc.org ·N Engl J Med · Pubmed #23477625.

ABSTRACT: BACKGROUND: Emergency surgery has become a rare event after percutaneous coronary intervention (PCI). Whether having cardiac-surgery services available on-site is essential for ensuring the best possible outcomes during and after PCI remains uncertain. METHODS: We enrolled patients with indications for nonemergency PCI who presented at hospitals in Massachusetts without on-site cardiac surgery and randomly assigned these patients, in a 3:1 ratio, to undergo PCI at that hospital or at a partner hospital that had cardiac surgery services available. A total of 10 hospitals without on-site cardiac surgery and 7 with on-site cardiac surgery participated. The coprimary end points were the rates of major adverse cardiac events--a composite of death, myocardial infarction, repeat revascularization, or stroke--at 30 days (safety end point) and at 12 months (effectiveness end point). The primary end points were analyzed according to the intention-to-treat principle and were tested with the use of multiplicative noninferiority margins of 1.5 (for safety) and 1.3 (for effectiveness). RESULTS: A total of 3691 patients were randomly assigned to undergo PCI at a hospital without on-site cardiac surgery (2774 patients) or at a hospital with on-site cardiac surgery (917 patients). The rates of major adverse cardiac events were 9.5% in hospitals without on-site cardiac surgery and 9.4% in hospitals with on-site cardiac surgery at 30 days (relative risk, 1.00; 95% one-sided upper confidence limit, 1.22; P<0.001 for noninferiority) and 17.3% and 17.8%, respectively, at 12 months (relative risk, 0.98; 95% one-sided upper confidence limit, 1.13; P<0.001 for noninferiority). The rates of death, myocardial infarction, repeat revascularization, and stroke (the components of the primary end point) did not differ significantly between the groups at either time point. CONCLUSIONS: Nonemergency PCI procedures performed at hospitals in Massachusetts without on-site surgical services were noninferior to procedures performed at hospitals with on-site surgical services with respect to the 30-day and 1-year rates of clinical events. (Funded by the participating hospitals without on-site cardiac surgery; MASS COM ClinicalTrials.gov number, NCT01116882.).

135 Article Body height and late-life cognition among patients with atherothrombotic disease. 2013

Weinstein, Galit / Goldbourt, Uri / Tanne, David. ·Department of Epidemiology and Preventive Medicine, School of Public Health, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel. galitwai@bu.edu ·Alzheimer Dis Assoc Disord · Pubmed #22683666.

ABSTRACT: BACKGROUND/AIMS: Height is associated with a lower risk of stroke and dementia. We tested the hypothesis that higher stature is also associated with better cognitive performance, and examined whether these associations were mediated through the extent of vascular disease. METHODS: A subgroup of patients (mean age at baseline 57.9±6.6 y; 94.6% males) with coronary heart disease who previously participated in a clinical trial (1990 to 1997) was assessed for cognitive function and measures of atherosclerosis 15±3 years later. Cognitive performance was assessed using the Mindstreams computerized battery. Measures of overall battery performance and in specific cognitive domains were obtained, and a score of ≤85 (1 SD below the mean) was defined as cognitive impairment overall and in a specific domain. We compared the risk of cognitive impairment and means of cognitive scores by quartiles of height. RESULTS: Among 536 patients, 23.2% were cognitively impaired. After controlling for potential risk factors and correcting for multiple comparisons, odds ratios for impairment in the visual-spatial domain decreased with increasing height quartiles (P for trend =0.018), and odds ratio (95% confidence interval) associated with being at the top versus the bottom quartile was 0.40 (0.18-0.88). An increment of 1 SD of height was associated with a higher global score (β=1.98; 95% confidence interval, 0.73-4.49; P=0.004) and with higher executive function, attention, and visual-spatial scores. CONCLUSIONS: Among our sample of coronary heart disease patients, a higher stature is associated with a lower risk of impairment in the visual-spatial function and with better cognitive performance.

136 Article Effect of sulfasalazine on inflammation and endothelial function in patients with established coronary artery disease. 2012

Tabit, Corey E / Holbrook, Monica / Shenouda, Sherene M / Dohadwala, Mustali M / Widlansky, Michael E / Frame, Alissa A / Kim, Brian H / Duess, Mai-Ann / Kluge, Matthew A / Levit, Aaron / Keaney, John F / Vita, Joseph A / Hamburg, Naomi M. ·Evans Department of Medicine and Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, MA, USA. ·Vasc Med · Pubmed #22496207.

ABSTRACT: Inflammation is critical for atherosclerosis development and may be a target for risk-reduction therapy. In experimental studies, activation of the inflammatory regulator, nuclear factor kappa B (NFlB), contributes to endothelial activation and reduced nitric oxide production. We treated patients with coronary artery disease with sulfasalazine, an inhibitor of NFκB, and placebo in a randomized, double-blind, crossover study design. Brachial artery flow-mediated dilation (FMD) and digital vascular function were measured at baseline and after each 6-week treatment period. Of the 53 patients enrolled in the crossover study, 32 (age 60 ± 10, 22% female) completed all the visits, with a high rate of study withdrawal due to gastrointestinal side effects. In a subset of 10 participants, we compared the effects of 4 days of sulfasalazine treatment (n = 5) to no treatment (n = 5) on NFκB-regulated gene expression in peripheral blood mononuclear cells. Tumor necrosis factor α-stimulated expression of CD69 and NFlB subunit p50 was significantly blunted after 4 days of sulfasalazine treatment but not after no treatment. However, FMD and digital vasodilator response did not significantly change from baseline with long-term sulfasalazine treatment. Short-term sulfasalazine inhibited NFlB activity; however, long-term treatment was poorly tolerated and did not improve endothelial function. Our findings suggest that sulfasalazine therapy is not the optimal anti-inflammatory treatment for reversing endothelial dysfunction in cardiovascular disease. Further studies are warranted to investigate the potential for NFlB inhibition to reduce cardiovascular risk.

137 Article Effects of aggressive versus moderate glycemic control on clinical outcomes in diabetic coronary artery bypass graft patients. 2011

Lazar, Harold L / McDonnell, Marie M / Chipkin, Stuart / Fitzgerald, Carmel / Bliss, Caleb / Cabral, Howard. ·Department of Cardiothoracic Surgery, Boston University School of Medicine, Boston, MA 02118, USA. Harold.lazar@bmc.org ·Ann Surg · Pubmed #21865944.

ABSTRACT: OBJECTIVE: This study sought to determine whether aggressive glycemic control (90-120 mg/dL) would result in more optimal clinical outcomes and less morbidity than moderate glycemic control (120-180 mg/dL) in diabetic patients undergoing coronary artery bypass graft (CABG) surgery. SUMMARY OF BACKGROUND DATA: Maintaining serum glucose levels between 120 and 180 mg/dL with continuous insulin infusions decreases morbidity in diabetic patients undergoing CABG surgery. Studies in surgical patients requiring prolonged ventilation suggest that aggressive glycemic control (<120 mg/dL) may improve survival; however, its effect in diabetic CABG patients is unknown. METHODS: Eighty-two diabetic patients undergoing CABG were prospectively randomized to aggressive glycemic control (90-120 mg/dL) or moderate glycemic control (120-180 mg/dL) using continuous intravenous insulin solutions (100 units regular insulin in 100 mL: normal saline) beginning at the induction of anesthesia and continuing for 18 hours after CABG. Primary end points were the incidence of major adverse events (major adverse events = 30-day mortality, myocardial infarction, neurologic events, deep sternal infections, and atrial fibrillation), the level of serum glucose, and the incidence of hypoglycemic events. RESULTS: There were no differences in the incidence of major adverse events between the groups (17 moderate vs 15 aggressive; P = 0.91). Patients with aggressive control had a lower mean glucose at the end of 18 hours of insulin infusion (135 ± 12 mg/dL moderate vs 103 ± 17 mg/dL aggressive; P < 0.0001). Patients with aggressive control had a higher incidence of hypoglycemic events (4 vs 30; P < 0.0001). CONCLUSIONS: In diabetic patients undergoing CABG surgery, aggressive glycemic control increases the incidence of hypoglycemic events and does not result in any significant improvement in clinical outcomes that can be achieved with moderate control. Clinical Trials.gov (ID #NCT00460499).

138 Article Transcriptional profiling of human liver identifies sex-biased genes associated with polygenic dyslipidemia and coronary artery disease. 2011

Zhang, Yijing / Klein, Kathrin / Sugathan, Aarathi / Nassery, Najlla / Dombkowski, Alan / Zanger, Ulrich M / Waxman, David J. ·Division of Cell and Molecular Biology, Department of Biology, Boston University, Boston, Massachusetts, United States of America. ·PLoS One · Pubmed #21858147.

ABSTRACT: Sex-differences in human liver gene expression were characterized on a genome-wide scale using a large liver sample collection, allowing for detection of small expression differences with high statistical power. 1,249 sex-biased genes were identified, 70% showing higher expression in females. Chromosomal bias was apparent, with female-biased genes enriched on chrX and male-biased genes enriched on chrY and chr19, where 11 male-biased zinc-finger KRAB-repressor domain genes are distributed in six clusters. Top biological functions and diseases significantly enriched in sex-biased genes include transcription, chromatin organization and modification, sexual reproduction, lipid metabolism and cardiovascular disease. Notably, sex-biased genes are enriched at loci associated with polygenic dyslipidemia and coronary artery disease in genome-wide association studies. Moreover, of the 8 sex-biased genes at these loci, 4 have been directly linked to monogenic disorders of lipid metabolism and show an expression profile in females (elevated expression of ABCA1, APOA5 and LDLR; reduced expression of LIPC) that is consistent with the lower female risk of coronary artery disease. Female-biased expression was also observed for CYP7A1, which is activated by drugs used to treat hypercholesterolemia. Several sex-biased drug-metabolizing enzyme genes were identified, including members of the CYP, UGT, GPX and ALDH families. Half of 879 mouse orthologs, including many genes of lipid metabolism and homeostasis, show growth hormone-regulated sex-biased expression in mouse liver, suggesting growth hormone might play a similar regulatory role in human liver. Finally, the evolutionary rate of protein coding regions for human-mouse orthologs, revealed by dN/dS ratio, is significantly higher for genes showing the same sex-bias in both species than for non-sex-biased genes. These findings establish that human hepatic sex differences are widespread and affect diverse cell metabolic processes, and may help explain sex differences in lipid profiles associated with sex differential risk of coronary artery disease.

139 Article Regional variation in patient risk factors and mortality after coronary artery bypass grafting. 2011

Quin, Jacquelyn A / Sheng, Shubin / O'Brien, Sean M / Welke, Karl F / Grover, Frederick L / Shroyer, A Laurie. ·VA Boston Healthcare System, West Roxbury, MA, USA. jacquelyn.quin@va.gov ·Ann Thorac Surg · Pubmed #21855853.

ABSTRACT: BACKGROUND: Geographic variations in patient risk factors and operative mortality after coronary artery bypass graft surgery have not been well studied. METHODS: Using The Society of Thoracic Surgeons National Cardiac Database, a retrospective cohort study was performed of patients undergoing isolated coronary artery bypass graft surgery from 2004 to 2007 (n = 504,608). Records were sorted into four major geographic regions (Northeast, Midwest, South, and West) and compared with respect to patient risk profiles and outcomes. Using marginal and hierarchical logistic regression, risk-adjusted operative mortality rates were compared across regions and variation assessed within regions, states and hospital referral regions. RESULTS: Patient risk profiles in the Northeast and West appeared similar, as did profiles in the Midwest and South. Risk-adjusted mortality rates were as follows: Northeast 1.63%, Midwest 2.01%, South 2.25%, and West 1.82%. Compared with the Northeast, mortality rates in the Midwest and South were higher, with the following odds ratios (95% confidence intervals): Midwest 1.26 (1.12 to 1.42), South 1.44 (1.27 to 1.62), and West 1.12 (0.98 to 1.28). Major geographic regions accounted for 16.5% of the variation observed in mortality rates; states and hospital referral regions accounted for 17.8% and 65.7%, respectively. CONCLUSIONS: Variations in absolute coronary artery bypass graft surgery mortality rates across large regions were subtle, although rates within the Northeast were comparatively lower. Most of the variation was seen at the hospital referral region level. Given that geographic location has not been routinely incorporated into statistical risk model predictions, additional research appears warranted to identify regional "best care" practices and to advance nationwide improvements in cardiac surgical patient outcomes.

140 Article Evaluation of endoscopic vein extraction on structural and functional viability of saphenous vein endothelium. 2011

Hussaini, Bader E / Lu, Xiu-Gui / Wolfe, J Alan / Thatte, Hemant S. ·Cardiothoracic Surgery Division, Veterans Affairs Boston Healthcare System, Boston, MA, USA. ·J Cardiothorac Surg · Pubmed #21663646.

ABSTRACT: OBJECTIVES: Endothelial injury during harvest influences graft patency post CABG. We have previously shown that endoscopic harvest causes structural and functional damage to the saphenous vein (SV) endothelium. However, causes of such injury may depend on the extraction technique. In order to assess this supposition, we evaluated the effect of VirtuoSaph endoscopic SV harvesting technique (VsEVH) on structural and functional viability of SV endothelium using multiphoton imaging, biochemical and immunofluorescence assays. METHODS: Nineteen patients scheduled for CABG were prospectively identified. Each underwent VsEVH for one portion and "No-touch" open SV harvesting (OSVH) for another portion of the SV. A two cm segment from each portion was immersed in GALA conduit preservation solution and transported overnight to our lab for processing. The segments were labeled with fluorescent markers to quantify cell viability, calcium mobilization and generation of nitric oxide. Morphology, expression, localization and stability of endothelial caveolin, eNOS, von Willebrand factor and cadherin were evaluated using immunofluorescence, Western blot and multiphoton microscopy (MPM). RESULTS: Morphological, biochemical and immunofluorescence parameters of viability, structure and function were well preserved in VsEVH group as in OSVH group. However, tonic eNOS activity, agonist-dependent calcium mobilization and nitric oxide production were partially attenuated in the VsEVH group. CONCLUSIONS: This study indicates that VirtuoSaph endoscopic SV harvesting technique preserves the structural and functional viability of SV endothelium, but may differentially attenuate the vasomotor function of the saphenous vein graft.

141 Article Increased adverse events after percutaneous coronary intervention in patients with COPD: insights from the National Heart, Lung, and Blood Institute dynamic registry. 2011

Enriquez, Jonathan R / Parikh, Shailja V / Selzer, Faith / Jacobs, Alice K / Marroquin, Oscar / Mulukutla, Suresh / Srinivas, Vankeepuram / Holper, Elizabeth M. ·Division of Cardiology, University of Texas Southwestern Medical Center, Dallas, TX. · Department of Epidemiology, University of Pittsburgh, Pittsburgh, PA. · Division of Cardiology, Boston University Medical Center, Boston, MA. · Division of Cardiology, University of Pittsburgh, Pittsburgh, PA. · Division of Cardiology, Jack D. Weiler/Montefiore Medical Center, Bronx, NY. · Division of Cardiology, University of Texas Southwestern Medical Center, Dallas, TX. Electronic address: Elizabeth.Holper@UTSouthwestern.edu. ·Chest · Pubmed #21527507.

ABSTRACT: BACKGROUND: Previous studies have demonstrated that patients with COPD are at higher risk for death after percutaneous coronary intervention (PCI), but other clinical outcomes and possible associations with adverse events have not been described. METHODS: Using waves 1 through 5 (1999-2006) of the National Heart, Lung, and Blood Institute Dynamic Registry, patients with COPD (n = 860) and without COPD (n = 10,048) were compared. Baseline demographics, angiographic characteristics, and in-hospital and 1-year adverse events were compared. RESULTS: Patients with COPD were older (mean age 66.8 vs 63.2 years, P < .001), more likely to be women, and more likely to have a history of diabetes, prior myocardial infarction, peripheral arterial disease, renal disease, and smoking. Patients with COPD also had a lower mean ejection fraction (49.1% vs 53.0%, P < .001) and a greater mean number of significant lesions (3.2 vs 3.0, P = .006). Rates of in-hospital death (2.2% vs 1.1%, P = .003) and major entry site complications (6.6% vs 4.2%, P < .001) were higher in pulmonary patients. At discharge, pulmonary patients were significantly less likely to be prescribed aspirin (92.4% vs 95.3%, P < .001), β-blockers (55.7% vs 76.2%, P < .001), and statins (60.0% vs 66.8%, P < .001). After adjustment, patients with COPD had significantly increased risk of death (hazard ratio [HR] = 1.30, 95% CI = 1.01-1.67) and repeat revascularization (HR = 1.22, 95% CI = 1.02-1.46) at 1 year, compared with patients without COPD. CONCLUSIONS: COPD is associated with higher mortality rates and repeat revascularization within 1 year after PCI. These higher rates of adverse outcomes may be associated with lower rates of guideline-recommended class 1 medications prescribed at discharge.

142 Article Impact of endoscopic versus open saphenous vein harvest technique on late coronary artery bypass grafting patient outcomes in the ROOBY (Randomized On/Off Bypass) Trial. 2011

Zenati, Marco A / Shroyer, A Laurie / Collins, Joseph F / Hattler, Brack / Ota, Takeyoshi / Almassi, G Hossein / Amidi, Morteza / Novitzky, Dimitri / Grover, Frederick L / Sonel, Ali F. ·Veterans Affairs Boston Healthcare System, West Roxbury, MA 02132, USA. Marco_Zenati@hms.harvard.edu ·J Thorac Cardiovasc Surg · Pubmed #21130476.

ABSTRACT: OBJECTIVE: In the Randomized On/Off Bypass (ROOBY) Trial, the efficacy of on-pump versus off-pump coronary artery bypass grafting was evaluated. This ROOBY Trial planned subanalysis compared the effects on postbypass patient clinical outcomes and graft patency of endoscopic vein harvesting and open vein harvesting. METHODS: From April 2003 to April 2007, the technique used for saphenous vein graft harvesting was recorded in 1471 cases. Of these, 894 patients (341 endoscopic harvest and 553 open harvest) also underwent coronary angiography 1 year after coronary artery bypass grafting. Univariate and multivariable analyses were used to compare patient outcomes in the endoscopic and open groups. RESULTS: Preoperative patient characteristics were statistically similar between the endoscopic and open groups. Endoscopic vein harvest was used in 38% of the cases. There were no significant differences in both short-term and 1-year composite outcomes between the endoscopic and open groups. For patients with 1-year catheterization follow-up (n=894), the saphenous vein graft patency rate for the endoscopic group was lower than that in the open harvest group (74.5% vs 85.2%, P<.0001), and the repeat revascularization rate was significantly higher (6.7% vs 3.4%, P<.05). Multivariable regression documented no interaction effect between endoscopic approach and off-pump treatment. CONCLUSIONS: In the ROOBY Trial, endoscopic vein harvest was associated with lower 1-year saphenous vein graft patency and higher 1-year revascularization rates, independent of the use of off-pump or on-pump cardiac surgical approach.

143 Article Serum urate is not associated with coronary artery calcification: the NHLBI Family Heart Study. 2011

Neogi, Tuhina / Terkeltaub, Robert / Ellison, R Curtis / Hunt, Steven / Zhang, Yuqing. ·Boston University School of Medicine, 650 Albany Street, Clin Epi Unit, Suite X-200, Boston, MA 02118, USA. tneogi@bu.edu ·J Rheumatol · Pubmed #20889594.

ABSTRACT: OBJECTIVE: urate may have effects on vascular remodeling and atherosclerosis. We had shown an association between serum uric acid (SUA) and carotid atherosclerotic plaques. Inflammation and vascular remodeling in atherosclerosis promote coronary artery calcification (CAC), a preclinical marker for atherosclerosis. Here, we examined whether SUA is associated with CAC, using the same study sample and methods as for our previous carotid atherosclerosis study. METHODS: the national Heart, Lung, and Blood Institute Family Heart Study is a multicenter study designed to assess risk factors for heart disease. Participants were recruited from population-based cohorts in the US states of Massachusetts, North Carolina, Minnesota, Utah, and Alabama. CAC was assessed with helical computed tomography (CT). We conducted sex-specific and family-cluster analyses, as well as additional analyses among persons without risk factors related to both cardiovascular disease and hyperuricemia, adjusting for potential confounders as we had in the previous study of carotid atherosclerosis. RESULTS: for the CAC study, 2412 subjects had both SUA and helical CT results available (55% women, age 58 ± 13 yrs, body mass index 27.6 ± 5.3). We found no association of SUA with CAC in men or women [OR in men: 1.0, 1.11, 0.86, 0.90; women: 1.0, 0.83, 1.00, 0.87 for increasing categories of SUA: < 5 (referent group), 5 to < 6, 6 to < 6.8, ≥ 6.8 mg/dl, respectively], nor in subgroup analyses. CONCLUSION: replicating the methods used to demonstrate an association of SUA with carotid atherosclerosis did not reveal any association between SUA and CAC, suggesting that SUA likely does not contribute to atherosclerosis through effects on arterial calcification. The possibility that urate has divergent pathophysiologic effects on atherosclerosis and artery calcification merits further study.

144 Article A planar elliptical model of cardio-vagal hysteresis. 2010

Ler, A S H / Cohen, M A / Taylor, J A. ·Department of Cognitive and Neural Systems, Boston University, Boston, MA, USA. ·Physiol Meas · Pubmed #20489240.

ABSTRACT: The state-dependent portion of cardio-vagal baroreflex control is called baroreflex hyteresis: we observe hysteresis when RR interval and carotid diameter depend on both the direction and value of arterial pressure. The elasticity of arterial walls, as well as the responsiveness of central command reset controls the real-time pattern of neural outflow, which is indirectly measured by RR interval in humans. We model the state-dependent relationship among pressure, vessel diameter and heart rate as a three-dimensional planar ellipse. Two-dimensional projections of this ellipse provide motion direction and quantify hysteresis between mechanical (pressure-diameter), neural (diameter-heart rate), and integrated baroreflex (pressure-heart rate) components. A convenient measure for the magnitude of hysteresis is the ratio of the semi-minor and semi-major axes of the best fitting ellipse. This ratio is given a sign according to the direction of its motion. The signed sum of the hysteresis ratio for vessel mechanics and central neural control reliably predicts cardio-vagal hysteresis. Using this relationship, we can quantify the relative importance of neural versus mechanical contributions to integrated baroreflex responses.

145 Article Acute anterolateral papillary muscle rupture in the absence of coronary artery disease. 2010

Lazar, Harold L / Bernard, Sheilah A. ·Department of Cardiothoracic Surgery, Boston Medical Center and Boston University School of Medicine, Boston, Massachusetts 02118, USA. harold.lazar@bmc.org ·J Card Surg · Pubmed #20459454.

ABSTRACT: Acute papillary muscle rupture is usually associated with a myocardial infarction and involves the posteromedial muscle. We present a case of spontaneous rupture of the anterolateral papillary muscle due to an isolated infarct of the papillary muscle in the absence of epicardial coronary artery disease.

146 Article In vivo detection of vulnerable atherosclerotic plaque by MRI in a rabbit model. 2010

Phinikaridou, Alkystis / Ruberg, Frederick L / Hallock, Kevin J / Qiao, Ye / Hua, Ning / Viereck, Jason / Hamilton, James A. ·Department of Physiology and Biophysics, Boston University School of Medicine, Boston, MA 02118, USA. ·Circ Cardiovasc Imaging · Pubmed #20194634.

ABSTRACT: BACKGROUND: The ability to identify atherosclerotic plaques with a high risk for sudden disruption before stroke or myocardial infarction would be of great utility. We used a rabbit model of controlled atherothrombosis to test whether in vivo MRI can noninvasively distinguish between plaques that disrupt after pharmacological triggering (vulnerable) and those that do not (stable). METHODS AND RESULTS: Atherosclerosis was induced in male New Zealand White (n=17) rabbits by cholesterol diet and endothelial denudation of the abdominal aorta. After baseline (pretrigger) MRI with and without gadolinium contrast, the rabbits underwent 2 pharmacological triggerings to induce atherothrombosis, followed by another MRI 48 hours later (post-triggering). Atherosclerosis was identified by the pretriggered images in all rabbits, and thrombosis was identified in 9 of 17 animals (53%) by post-trigger MRI. After the animals were euthanized, 95 plaques were analyzed; 28 (29.5%) had thrombi (vulnerable) and 67 did not (stable) (70.5%). Pretriggered MRI revealed comparable stenosis in stable and vulnerable plaques, but vulnerable plaques had a larger plaque area (4.8+/-1.6 versus 3.0+/-1.0 mm(2); P=0.01), vessel area (9.2+/-3.0 versus. 15.8+/-4.9 mm(2); P=0.01), and higher remodeling ratio (1.16+/-0.2 versus 0.93+/-0.2; P=0.01) compared with stable plaques. Furthermore, vulnerable plaques more frequently exhibited (1) positive remodeling (67.8% versus 22.3%; P=0.01), in which the plaque is hidden within the vessel wall instead of occluding the lumen; and (2) enhanced gadolinium uptake (78.6% versus 20.9%; P=0.01) associated with histological findings of neovascularization, inflammation, and tissue necrosis. CONCLUSIONS: We demonstrate that in vivo MRI at 3.0 T detects features of vulnerable plaques in an animal model of controlled atherothrombosis. These findings suggest that MRI may be used as a noninvasive modality for localization of plaques that are prone to disruption.

147 Article Diagnostic accuracy of 64-slice multidetector CT for detection of in-stent restenosis in an unselected, consecutive patient population. 2010

Haraldsdottir, Sigurdis / Gudnason, Thorarinn / Sigurdsson, Axel F / Gudjonsdottir, Jonina / Lehman, Sam J / Eyjolfsson, Kristjan / Scheving, Sigurpall S / Gibson, C Michael / Hoffmann, Udo / Jonsdottir, Birna / Andersen, Karl. ·Boston Medical Center, Boston, MA 02118, USA. sigurdisha@gmail.com ·Eur J Radiol · Pubmed #19570632.

ABSTRACT: OBJECTIVES: To investigate the diagnostic accuracy of 64-slice multidetector computed tomography (64-CT) for detection of in-stent restenosis (ISR) in an unselected, consecutive patient population. BACKGROUND: Detection of in-stent restenosis by cardiac CT would be a major advance for the evaluation of patients suspected of having ISR. However, the diagnostic accuracy of current generation 64-CT in this context is not fully established. METHODS: We conducted a prospective study on patients with stable angina or acute coronary syndrome with no prior history of coronary artery disease. Six months after percutaneous coronary intervention (PCI) with stent placement they underwent a 64-CT scan (Toshiba Multi-Slice Aquilion 64) and consequently a repeat coronary angiography for comparison. Cardiac CT data sets were analyzed for the presence of in-stent restenosis by two independent expert readers blinded to the coronary angiographic data. RESULTS: Ninety-three patients with a total of 140 stents were evaluated. Males comprised 82% of the study group and the mean age was 63±10 years. The mean time from PCI to the repeat coronary angiography was 208±37 days and the mean time from 64-CT to repeat coronary angiography was 3.7±4.9 days. The restenosis rate according to coronary angiography was 26%. Stent diameter, strut thickness, heart rate and body mass index (BMI) significantly affected image quality. The sensitivity, specificity, positive and negative predictive values of 64-CT for detection of in-stent restenosis were 27%, 95%, 67% and 78%, respectively. CONCLUSIONS: Current generation, 64-slice CT, remains limited in its ability to accurately detect in-stent restenosis.

148 Article The effect of L-arginine and creatine on vascular function and homocysteine metabolism. 2009

Jahangir, Eiman / Vita, Joseph A / Handy, Diane / Holbrook, Monica / Palmisano, Joseph / Beal, Ryan / Loscalzo, Joseph / Eberhardt, Robert T. ·Boston University School of Medicine, Boston, MA 02118, USA. ·Vasc Med · Pubmed #19651674.

ABSTRACT: Studies with L-arginine supplementation have shown inconsistent effects on endothelial function. The generation of guanidinoacetate (GAA) from L-arginine with subsequent formation of creatine and homocysteine and consumption of methionine may reduce the pool of L-arginine available for nitric oxide generation. Experimental studies suggest that creatine supplementation might block this pathway. We sought to determine the effects of L-arginine, creatine, or the combination on endothelium-dependent vasodilation and homocysteine metabolism in patients with coronary artery disease. Patients with coronary artery disease were randomized to L-arginine (9 g/day), creatine (21 g/day), L-arginine plus creatine, or placebo for 4 days (n = 26-29/group). Brachial artery flow-mediated dilation and plasma levels of L-arginine, creatine, homocysteine, methionine, and GAA were measured at baseline and follow-up. L-arginine and creatine supplementation had no effects on vascular function. L-arginine alone increased GAA (p < 0.01) and the ratio of homocysteine to methionine (p < 0.01), suggesting increased methylation demand. The combination of creatinine and L-arginine did not suppress GAA production or prevent the increase in homocysteine-to-methionine ratio. Unexpectedly, creatine supplementation (alone or in combination with L-arginine) was associated with an 11-20% increase in homocysteine concentration (p < 0.05), which was not attributable to worsened renal function, providing evidence against an effect of creatine on decreasing methylation demand. In conclusion, the present study provides no evidence that L-arginine supplementation improves endothelial function and suggests that l-arginine may increase methylation demand. Creatine supplementation failed to alter the actions of L-arginine on vascular function or suppress methylation demand. The unexpected increase in homocysteine levels following creatine supplementation could have adverse effects and merits further study, since creatine is a commonly used dietary supplement.

149 Article Prior polyvascular disease: risk factor for adverse ischaemic outcomes in acute coronary syndromes. 2009

Bhatt, Deepak L / Peterson, Eric D / Harrington, Robert A / Ou, Fang-Shu / Cannon, Christopher P / Gibson, C Michael / Kleiman, Neal S / Brindis, Ralph G / Peacock, W Frank / Brener, Sorin J / Menon, Venu / Smith, Sidney C / Pollack, Charles V / Gibler, W Brian / Ohman, E Magnus / Roe, Matthew T / Anonymous40630625. ·VA Boston Healthcare System and Brigham and Women's Hospital, Boston, MA, USA. dlbhattmd@alum.mit.edu ·Eur Heart J · Pubmed #19339264.

ABSTRACT: AIMS: The presence of peripheral arterial disease (PAD) or cerebrovascular disease (CVD) is associated with higher likelihood of significant coronary artery disease (CAD). We sought to assess the prevalence of PAD, CVD, prior CAD, or pre-existent disease in multiple arterial territories ('polyvascular' disease) in patients presenting with non-ST-segment elevation acute coronary syndrome and its impact on adverse events. METHODS AND RESULTS: Data from 95 749 patients enrolled from February 2003 to September 2006 at 484 sites in the CRUSADE registry were analysed. Patients were categorized as having prior 0, 1, 2, or 3 affected arterial beds. The rates of in-hospital mortality, myocardial infarction, stroke, and congestive heart failure were analysed, as were the rates of non-bypass surgery-related red blood cell transfusion and major bleeding. On presentation, 11,345 (11.9%) patients had established PAD, 9973 (10.4%) had documented CVD, and 41,404 (43.2%) had prior CAD. In this cohort, 0, 1, 2, and 3 arterial bed disease before presentation was present in 46 814 (48.9%, 95% CI 48.6-49.2%), 36 704 (38.3%, 95% CI 37.8-39.0%), 10 675 (11.2%, 95% CI 10.9-11.9%), and 1556 (1.6%, 95% CI 1.5-1.8%) patients, respectively. The rates of ischaemic events increased with the number of affected vascular beds. The adjusted odds ratio for the composite of in-hospital ischaemic events for pre-existent disease in 1, 2, or 3 arterial beds (compared with 0 arterial bed involvement) increased from 1.07 to 1.26 to 1.31 (P < 0.001). Similarly, the adjusted odds ratio for transfusion increased with greater disease burden from 1.11 to 1.28 to 1.30 (P < 0.001), although the adjusted rates of protocol-defined non-bypass surgery-related major bleeding did not. CONCLUSION: Prior polyvascular disease increases the risk of in-hospital adverse events, including mortality. Identification of these patients in clinical trial and real world populations may provide an opportunity to reduce their excess risk with intensive secondary prevention efforts.

150 Article The brachial artery remodels to maintain local shear stress despite the presence of cardiovascular risk factors. 2009

Chung, William B / Hamburg, Naomi M / Holbrook, Monika / Shenouda, Sherene M / Dohadwala, Mustali M / Terry, Dellara F / Gokce, Noyan / Vita, Joseph A. ·Evans Department of Medicine, Boston University School of Medicine, Boston, MA 02118, USA. ·Arterioscler Thromb Vasc Biol · Pubmed #19164807.

ABSTRACT: OBJECTIVE: Under physiological conditions, arteries remodel in response to changes in blood flow to maintain local shear stress. Risk factors and developing atherosclerosis may be associated with maladaptive remodeling that produces relatively large arteries with low levels of shear stress. Recent studies have shown that the brachial artery and other peripheral arteries are enlarged in patients with risk factors and cardiovascular disease, and we tested the hypothesis that this finding represents maladaptive remodeling. METHODS AND RESULTS: We measured brachial artery diameter and flow by ultrasound and calculated shear stress in a diverse cohort of 1583 subjects (age 53+/-17 years, 62% male, and 51% with coronary artery disease and/or peripheral arterial disease). In a stepwise linear regression model, age (P<0.001), gender (P<0.001), body mass index (P<0.001), hypertension (P=0.005), and hypercholesterolemia (P=0.02) were associated with larger brachial diameter. Older age was associated with lower shear stress (P<0.01), consistent with maladaptive remodeling. However, body mass index, hypertension, hypercholesterolemia, and prevalent atherosclerosis were associated with proportionate changes in blood flow and no difference in shear stress compared to reference groups, suggesting adaptive remodeling. CONCLUSIONS: These findings suggest that enlargement of the brachial artery in the setting of obesity, hypertension, hypercholesterolemia, and atherosclerosis reflects adaptive remodeling. The results provide further support for the concept that arterial remodeling is an important homeostatic response that is maintained despite the presence of risk factors and developing atherosclerosis.

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