PMID- 30322267 OWN - NLM STAT- In-Data-Review LR - 20181109 IS - 2047-4881 (Electronic) IS - 2047-4873 (Linking) VI - 25 IP - 17 DP - 2018 Nov TI - Coronary disease prevention: towards a more personalised approach. PG - 1884-1886 LID - 10.1177/2047487318805578 [doi] FAU - Landmesser, Ulf AU - Landmesser U AD - 1 Department of Cardiology, Charite - Universitatsmedizin Berlin, Germany. AD - 2 Berlin Institute of Health, Germany. AD - 3 German Center for Cardiovascular Research (DZHK), Germany. FAU - Catapano, Alberico AU - Catapano A AD - 4 IRCCS MultiMedica, Sesto S Giovanni, Italy. AD - 5 Department of Pharmacological and Biomolecular Sciences, University of Milan, Italy. LA - eng PT - Journal Article DEP - 20181015 PL - England TA - Eur J Prev Cardiol JT - European journal of preventive cardiology JID - 101564430 EDAT- 2018/10/17 06:00 MHDA- 2018/10/17 06:00 CRDT- 2018/10/17 06:00 PHST- 2018/10/17 06:00 [pubmed] PHST- 2018/10/17 06:00 [medline] PHST- 2018/10/17 06:00 [entrez] AID - 10.1177/2047487318805578 [doi] PST - ppublish SO - Eur J Prev Cardiol. 2018 Nov;25(17):1884-1886. doi: 10.1177/2047487318805578. Epub 2018 Oct 15. PMID- 30235339 OWN - NLM STAT- PubMed-not-MEDLINE LR - 20190225 IS - 1932-6203 (Electronic) IS - 1932-6203 (Linking) VI - 13 IP - 9 DP - 2018 TI - Correction: Predictive value for cardiovascular events of common carotid intima media thickness and its rate of change in individuals at high cardiovascular risk - Results from the PROG-IMT collaboration. PG - e0204633 LID - 10.1371/journal.pone.0204633 [doi] AB - [This corrects the article DOI: 10.1371/journal.pone.0191172.]. FAU - Lorenz, Matthias W AU - Lorenz MW FAU - Gao, Lu AU - Gao L FAU - Ziegelbauer, Kathrin AU - Ziegelbauer K FAU - Norata, Giuseppe Danilo AU - Norata GD FAU - Empana, Jean Philippe AU - Empana JP FAU - Schmidtmann, Irene AU - Schmidtmann I FAU - Lin, Hung-Ju AU - Lin HJ FAU - McLachlan, Stela AU - McLachlan S FAU - Bokemark, Lena AU - Bokemark L FAU - Ronkainen, Kimmo AU - Ronkainen K FAU - Amato, Mauro AU - Amato M FAU - Schminke, Ulf AU - Schminke U FAU - Srinivasan, Sathanur R AU - Srinivasan SR FAU - Lind, Lars AU - Lind L FAU - Okazaki, Shuhei AU - Okazaki S FAU - Stehouwer, Coen D A AU - Stehouwer CDA FAU - Willeit, Peter AU - Willeit P FAU - Polak, Joseph F AU - Polak JF FAU - Steinmetz, Helmuth AU - Steinmetz H FAU - Sander, Dirk AU - Sander D FAU - Poppert, Holger AU - Poppert H FAU - Desvarieux, Moise AU - Desvarieux M FAU - Ikram, M Arfan AU - Ikram MA FAU - Johnsen, Stein Harald AU - Johnsen SH FAU - Staub, Daniel AU - Staub D FAU - Sirtori, Cesare R AU - Sirtori CR FAU - Iglseder, Bernhard AU - Iglseder B FAU - Beloqui, Oscar AU - Beloqui O FAU - Engstrom, Gunnar AU - Engstrom G FAU - Friera, Alfonso AU - Friera A FAU - Rozza, Francesco AU - Rozza F FAU - Xie, Wuxiang AU - Xie W FAU - Parraga, Grace AU - Parraga G FAU - Grigore, Liliana AU - Grigore L FAU - Plichart, Matthieu AU - Plichart M FAU - Blankenberg, Stefan AU - Blankenberg S FAU - Su, Ta-Chen AU - Su TC FAU - Schmidt, Caroline AU - Schmidt C FAU - Tuomainen, Tomi-Pekka AU - Tuomainen TP FAU - Veglia, Fabrizio AU - Veglia F FAU - Volzke, Henry AU - Volzke H FAU - Nijpels, Giel AU - Nijpels G FAU - Willeit, Johann AU - Willeit J FAU - Sacco, Ralph L AU - Sacco RL FAU - Franco, Oscar H AU - Franco OH FAU - Uthoff, Heiko AU - Uthoff H FAU - Hedblad, Bo AU - Hedblad B FAU - Suarez, Carmen AU - Suarez C FAU - Izzo, Raffaele AU - Izzo R FAU - Zhao, Dong AU - Zhao D FAU - Wannarong, Thapat AU - Wannarong T FAU - Catapano, Alberico AU - Catapano A FAU - Ducimetiere, Pierre AU - Ducimetiere P FAU - Espinola-Klein, Christine AU - Espinola-Klein C FAU - Chien, Kuo-Liong AU - Chien KL FAU - Price, Jackie F AU - Price JF FAU - Bergstrom, Goran AU - Bergstrom G FAU - Kauhanen, Jussi AU - Kauhanen J FAU - Tremoli, Elena AU - Tremoli E FAU - Dorr, Marcus AU - Dorr M FAU - Berenson, Gerald AU - Berenson G FAU - Kitagawa, Kazuo AU - Kitagawa K FAU - Dekker, Jacqueline M AU - Dekker JM FAU - Kiechl, Stefan AU - Kiechl S FAU - Sitzer, Matthias AU - Sitzer M FAU - Bickel, Horst AU - Bickel H FAU - Rundek, Tatjana AU - Rundek T FAU - Hofman, Albert AU - Hofman A FAU - Mathiesen, Ellisiv B AU - Mathiesen EB FAU - Castelnuovo, Samuela AU - Castelnuovo S FAU - Landecho, Manuel F AU - Landecho MF FAU - Rosvall, Maria AU - Rosvall M FAU - Gabriel, Rafael AU - Gabriel R FAU - de Luca, Nicola AU - de Luca N FAU - Liu, Jing AU - Liu J FAU - Baldassarre, Damiano AU - Baldassarre D FAU - Kavousi, Maryam AU - Kavousi M FAU - de Groot, Eric AU - de Groot E FAU - Bots, Michiel L AU - Bots ML FAU - Yanez, David N AU - Yanez DN FAU - Thompson, Simon G AU - Thompson SG CN - PROG-IMT study group LA - eng PT - Journal Article PT - Published Erratum DEP - 20180920 PL - United States TA - PLoS One JT - PloS one JID - 101285081 EFR - PLoS One. 2018 Apr 12;13(4):e0191172. PMID: 29649236 PMC - PMC6147579 EDAT- 2018/09/21 06:00 MHDA- 2018/09/21 06:01 CRDT- 2018/09/21 06:00 PHST- 2018/09/21 06:00 [entrez] PHST- 2018/09/21 06:00 [pubmed] PHST- 2018/09/21 06:01 [medline] AID - 10.1371/journal.pone.0204633 [doi] AID - PONE-D-18-26761 [pii] PST - epublish SO - PLoS One. 2018 Sep 20;13(9):e0204633. doi: 10.1371/journal.pone.0204633. eCollection 2018. PMID- 29760220 OWN - NLM STAT- In-Data-Review LR - 20180629 IS - 1530-8561 (Electronic) IS - 0009-9147 (Linking) VI - 64 IP - 7 DP - 2018 Jul TI - Quantifying Atherogenic Lipoproteins: Current and Future Challenges in the Era of Personalized Medicine and Very Low Concentrations of LDL Cholesterol. A Consensus Statement from EAS and EFLM. PG - 1006-1033 LID - 10.1373/clinchem.2018.287037 [doi] AB - BACKGROUND: The European Atherosclerosis Society-European Federation of Clinical Chemistry and Laboratory Medicine Consensus Panel aims to provide recommendations to optimize atherogenic lipoprotein quantification for cardiovascular risk management. CONTENT: We critically examined LDL cholesterol, non-HDL cholesterol, apolipoprotein B (apoB), and LDL particle number assays based on key criteria for medical application of biomarkers. (a) Analytical performance: Discordant LDL cholesterol quantification occurs when LDL cholesterol is measured or calculated with different assays, especially in patients with hypertriglyceridemia >175 mg/dL (2 mmol/L) and low LDL cholesterol concentrations <70 mg/dL (1.8 mmol/L). Increased lipoprotein(a) should be excluded in patients not achieving LDL cholesterol goals with treatment. Non-HDL cholesterol includes the atherogenic risk component of remnant cholesterol and can be calculated in a standard nonfasting lipid panel without additional expense. ApoB more accurately reflects LDL particle number. (b) Clinical performance: LDL cholesterol, non-HDL cholesterol, and apoB are comparable predictors of cardiovascular events in prospective population studies and clinical trials; however, discordance analysis of the markers improves risk prediction by adding remnant cholesterol (included in non-HDL cholesterol) and LDL particle number (with apoB) risk components to LDL cholesterol testing. (c) Clinical and cost-effectiveness: There is no consistent evidence yet that non-HDL cholesterol-, apoB-, or LDL particle-targeted treatment reduces the number of cardiovascular events and healthcare-related costs than treatment targeted to LDL cholesterol. SUMMARY: Follow-up of pre- and on-treatment (measured or calculated) LDL cholesterol concentration in a patient should ideally be performed with the same documented test method. Non-HDL cholesterol (or apoB) should be the secondary treatment target in patients with mild to moderate hypertriglyceridemia, in whom LDL cholesterol measurement or calculation is less accurate and often less predictive of cardiovascular risk. Laboratories should report non-HDL cholesterol in all standard lipid panels. CI - (c) 2018 American Association for Clinical Chemistry. FAU - Langlois, Michel R AU - Langlois MR AD - Department of Laboratory Medicine, AZ St-Jan, Brugge, and University of Ghent, Belgium; michel.langlois@azsintjan.be. FAU - Chapman, M John AU - Chapman MJ AD - National Institute for Health and Medical Research (INSERM), and Endocrinology-Metabolism Service, Pitie-Salpetriere University Hospital, Paris, France. FAU - Cobbaert, Christa AU - Cobbaert C AD - Department of Clinical Chemistry and Laboratory Medicine, Leiden University Medical Center, Leiden, the Netherlands. FAU - Mora, Samia AU - Mora S AD - Divisions of Preventive and Cardiovascular Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA. FAU - Remaley, Alan T AU - Remaley AT AD - Lipoprotein Metabolism Section, Cardiovascular-Pulmonary Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD. FAU - Ros, Emilio AU - Ros E AD - Lipid Clinic, Department of Endocrinology and Nutrition, Institut d'Investigacions Biomediques August Pi Sunyer, Hospital Clinic, Barcelona and Ciber Fisiopatologia de la Obesidad y Nutricion (CIBEROBN), Instituto de Salud Carlos III (ISCIII), Spain. FAU - Watts, Gerald F AU - Watts GF AD - Lipid Disorders Clinic, Department of Cardiology, Royal Perth Hospital, University of Western Australia, Perth, Australia. FAU - Boren, Jan AU - Boren J AD - Sahlgrenska University Hospital, Gothenburg, Sweden. FAU - Baum, Hannsjorg AU - Baum H AD - Institute for Laboratory Medicine, Blutdepot und Krankenhaushygiene, Regionale Kliniken Holding RKH GmbH, Ludwigsburg, Germany. FAU - Bruckert, Eric AU - Bruckert E AD - Pitie-Salpetriere University Hospital, Paris, France. FAU - Catapano, Alberico AU - Catapano A AD - Department of Pharmacological and Biomolecular Sciences, University of Milan, Italy. FAU - Descamps, Olivier S AU - Descamps OS AD - Hopital de Jolimont, Haine-Saint-Paul, Belgium. FAU - von Eckardstein, Arnold AU - von Eckardstein A AD - Institute for Clinical Chemistry, University Hospital Zurich, Zurich, Switzerland. FAU - Kamstrup, Pia R AU - Kamstrup PR AD - Herlev and Gentofte Hospital, Copenhagen University Hospital, University of Copenhagen, Copenhagen, Denmark. FAU - Kolovou, Genovefa AU - Kolovou G AD - Cardiology Department, Onassis Cardiac Surgery Center, Athens, Greece. FAU - Kronenberg, Florian AU - Kronenberg F AD - Department of Medical Genetics, Molecular and Clinical Pharmacology, Division of Genetic Epidemiology, Medical University of Innsbruck, Innsbruck, Austria. FAU - Langsted, Anne AU - Langsted A AD - Herlev and Gentofte Hospital, Copenhagen University Hospital, University of Copenhagen, Copenhagen, Denmark. FAU - Pulkki, Kari AU - Pulkki K AD - Department of Clinical Chemistry, University of Turku and Turku University Hospital, Turku, Finland. FAU - Rifai, Nader AU - Rifai N AD - Boston Children's Hospital, Harvard Medical School, Boston, MA. FAU - Sypniewska, Grazyna AU - Sypniewska G AD - Department of Laboratory Medicine, Collegium Medicum, NC University, Bydgoszcz, Poland. FAU - Wiklund, Olov AU - Wiklund O AD - Sahlgrenska University Hospital, Gothenburg, Sweden. FAU - Nordestgaard, Borge G AU - Nordestgaard BG AD - Herlev and Gentofte Hospital, Copenhagen University Hospital, University of Copenhagen, Copenhagen, Denmark. CN - European Atherosclerosis Society (EAS) and the European Federation of Clinical Chemistry and Laboratory Medicine (EFLM) Joint Consensus Initiative LA - eng PT - Journal Article DEP - 20180514 PL - United States TA - Clin Chem JT - Clinical chemistry JID - 9421549 EDAT- 2018/05/16 06:00 MHDA- 2018/05/16 06:00 CRDT- 2018/05/16 06:00 PHST- 2018/01/22 00:00 [received] PHST- 2018/04/09 00:00 [accepted] PHST- 2018/05/16 06:00 [pubmed] PHST- 2018/05/16 06:00 [medline] PHST- 2018/05/16 06:00 [entrez] AID - clinchem.2018.287037 [pii] AID - 10.1373/clinchem.2018.287037 [doi] PST - ppublish SO - Clin Chem. 2018 Jul;64(7):1006-1033. doi: 10.1373/clinchem.2018.287037. Epub 2018 May 14. PMID- 29649236 OWN - NLM STAT- MEDLINE DCOM- 20180709 LR - 20190329 IS - 1932-6203 (Electronic) IS - 1932-6203 (Linking) VI - 13 IP - 4 DP - 2018 TI - Predictive value for cardiovascular events of common carotid intima media thickness and its rate of change in individuals at high cardiovascular risk - Results from the PROG-IMT collaboration. PG - e0191172 LID - 10.1371/journal.pone.0191172 [doi] AB - AIMS: Carotid intima media thickness (CIMT) predicts cardiovascular (CVD) events, but the predictive value of CIMT change is debated. We assessed the relation between CIMT change and events in individuals at high cardiovascular risk. METHODS AND RESULTS: From 31 cohorts with two CIMT scans (total n = 89070) on average 3.6 years apart and clinical follow-up, subcohorts were drawn: (A) individuals with at least 3 cardiovascular risk factors without previous CVD events, (B) individuals with carotid plaques without previous CVD events, and (C) individuals with previous CVD events. Cox regression models were fit to estimate the hazard ratio (HR) of the combined endpoint (myocardial infarction, stroke or vascular death) per standard deviation (SD) of CIMT change, adjusted for CVD risk factors. These HRs were pooled across studies. In groups A, B and C we observed 3483, 2845 and 1165 endpoint events, respectively. Average common CIMT was 0.79mm (SD 0.16mm), and annual common CIMT change was 0.01mm (SD 0.07mm), both in group A. The pooled HR per SD of annual common CIMT change (0.02 to 0.43mm) was 0.99 (95% confidence interval: 0.95-1.02) in group A, 0.98 (0.93-1.04) in group B, and 0.95 (0.89-1.04) in group C. The HR per SD of common CIMT (average of the first and the second CIMT scan, 0.09 to 0.75mm) was 1.15 (1.07-1.23) in group A, 1.13 (1.05-1.22) in group B, and 1.12 (1.05-1.20) in group C. CONCLUSIONS: We confirm that common CIMT is associated with future CVD events in individuals at high risk. CIMT change does not relate to future event risk in high-risk individuals. FAU - Lorenz, Matthias W AU - Lorenz MW AUID- ORCID: 0000-0002-7565-1751 AD - Department of Neurology, Goethe University, Frankfurt am Main, Germany. FAU - Gao, Lu AU - Gao L AD - MRC Biostatistics Unit, Institute of Public Health, University Forvie Site, Cambridge, United Kingdom. FAU - Ziegelbauer, Kathrin AU - Ziegelbauer K AD - Department of Neurology, Goethe University, Frankfurt am Main, Germany. FAU - Norata, Giuseppe Danilo AU - Norata GD AD - Department of Medical Biotechnology and Translational Medicine, Universita degli Studi di Milano, Milano, Italy. AD - SISA Center for the Study of Atherosclerosis, Bassini Hospital, Cinisello Balsamo, Italy. FAU - Empana, Jean Philippe AU - Empana JP AD - Paris Cardiovascular Research Centre (PARCC), University Paris Descartes, Sorbonne Paris Cite, UMR, Paris, France. FAU - Schmidtmann, Irene AU - Schmidtmann I AD - Institut fuer Medizinische Biometrie, Epidemiologie und Informatik (IMBEI), Universitaetsmedizin Mainz, Mainz, Germany. FAU - Lin, Hung-Ju AU - Lin HJ AD - Department of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan. FAU - McLachlan, Stela AU - McLachlan S AD - Usher Institute of Population Health Sciences and Informatics, University of Edinburgh, Edinburgh, United Kingdom. FAU - Bokemark, Lena AU - Bokemark L AD - Wallenberg Laboratory for Cardiovascular Research, Institution for Medicin, Department for Molecular and Clinical Medicine, Sahlgrenska Academy, Gothenburg University, Gothenburg, Sweden. FAU - Ronkainen, Kimmo AU - Ronkainen K AD - Institute of Public Health and Clinical Nutrition, University of Eastern Finland, Kuopio Campus, Kuopio, Finland. FAU - Amato, Mauro AU - Amato M AD - Centro Cardiologico Monzino, IRCCS, Milano, Italy. FAU - Schminke, Ulf AU - Schminke U AD - Department of Neurology, Greifswald University Clinic, Greifswald, Germany. FAU - Srinivasan, Sathanur R AU - Srinivasan SR AD - Center for Cardiovascular Health, Department of Epidemiology, Biochemistry, Tulane University School of Public Health and Tropical Medicine, New Orleans, Louisiana, United States of America. FAU - Lind, Lars AU - Lind L AD - Department of Medicine, Uppsala University, Uppsala, Sweden. FAU - Okazaki, Shuhei AU - Okazaki S AD - Department of Neurology, Osaka University Graduate School of Medicine, Osaka, Japan. FAU - Stehouwer, Coen D A AU - Stehouwer CDA AD - Department of Internal Medicine and Cardiovascular Research Institute Maastricht (CARIM), Maastricht University Medical Centre, Maastricht, the Netherlands. FAU - Willeit, Peter AU - Willeit P AD - Department of Neurology, Medical University Innsbruck, Innsbruck, Austria. AD - Department of Public Health and Primary Care, School of Clinical Medicine, University of Cambridge, Cambridge, United Kingdom. FAU - Polak, Joseph F AU - Polak JF AD - Tufts University School of Medicine, Tufts Medical Center, Boston, Massachusetts, United States of America. FAU - Steinmetz, Helmuth AU - Steinmetz H AD - Department of Neurology, Goethe University, Frankfurt am Main, Germany. FAU - Sander, Dirk AU - Sander D AD - Department of Neurology, Benedictus Hospital Tutzing & Feldafing, Feldafing, Germany. FAU - Poppert, Holger AU - Poppert H AD - Department of Neurology, Technische Universitat Munchen, Munich, Germany. FAU - Desvarieux, Moise AU - Desvarieux M AD - Department of Epidemiology,Mailman School of Public Health,Columbia University, New York, United States of America. FAU - Ikram, M Arfan AU - Ikram MA AD - Department of Epidemiology, Erasmus University Medical Center, Rotterdam, the Netherlands. AD - Department of Neurology, Erasmus University Medical Center, Rotterdam, the Netherlands. AD - Department of Radiology, Erasmus University Medical Center, Rotterdam, the Netherlands. FAU - Johnsen, Stein Harald AU - Johnsen SH AD - Department of Clinical Medicine, Uit The Arctic University of Norway, Tromso, Norway. AD - Department of Neurology, University Hospital of Northern Norway, Tromso, Norway. FAU - Staub, Daniel AU - Staub D AD - Department of Angiology, University Hospital Basel, Basel, Switzerland. FAU - Sirtori, Cesare R AU - Sirtori CR AD - Center of Dyslipidemias, Niguarda Ca' Granda Hospital, Milano, Italy. FAU - Iglseder, Bernhard AU - Iglseder B AD - Parcelsus Medical University, Salzburg, Austria. AD - Department of Geriatric Medicine, Gemeinnutzige Salzburger Landeskliniken Betriebsgesellschaft GmbH Christian-Doppler-Klinik, Salzburg, Austria. FAU - Beloqui, Oscar AU - Beloqui O AD - Department of Internal Medicine, University Clinic of Navarra, Navarra, Spain. FAU - Engstrom, Gunnar AU - Engstrom G AD - Department of Clinical Sciences in Malmo, Lund University, Malmo, Sweden. FAU - Friera, Alfonso AU - Friera A AD - Radiology Department, Hospital Universitario de la Princesa, Universidad Autonoma de Madrid, Madrid, Spain. FAU - Rozza, Francesco AU - Rozza F AD - School of Medicine, Federico II University, Naples, Italy. FAU - Xie, Wuxiang AU - Xie W AD - Department of Epidemiology, Beijing Institute of Heart, Lung and Blood Vessel Diseases,Beijing Anzhen Hospital, Capital Medical University, Beijing, China. FAU - Parraga, Grace AU - Parraga G AD - Robarts Research Institute, Western University, London, Ontario, Canada. FAU - Grigore, Liliana AU - Grigore L AD - Centro Sisa per lo Studio della Aterosclerosi, Bassini Hospital, Cinisello Balsamo, Italy. FAU - Plichart, Matthieu AU - Plichart M AD - Assistance Publique, Hopitaux de Paris, Hopital Broca, Paris, France. FAU - Blankenberg, Stefan AU - Blankenberg S AD - 2nd Department of Medicine, Johannes Gutenberg-Universitat, Mainz, Germany. AD - Department of Cardiology, University Hospital Hamburg-Eppendorf, Hamburg, Germany. FAU - Su, Ta-Chen AU - Su TC AD - Department of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan. FAU - Schmidt, Caroline AU - Schmidt C AD - Wallenberg Laboratory for Cardiovascular Research, University of Gothenburg, Gothenburg, Sweden. FAU - Tuomainen, Tomi-Pekka AU - Tuomainen TP AD - Institute of Public Health and Clinical Nutrition, University of Eastern Finland, Kuopio Campus, Kuopio, Finland. FAU - Veglia, Fabrizio AU - Veglia F AD - Centro Cardiologico Monzino, IRCCS, Milano, Italy. FAU - Volzke, Henry AU - Volzke H AD - German Center for Cardiovascular Research (DZHK),partner site Greifswald, Greifswald, Germany. AD - Institute for Community Medicine, SHIP/Clinical-Epidemiological Research, Greifswald, Germany. FAU - Nijpels, Giel AU - Nijpels G AD - Department of General Practice, VU University Medical Center, Amsterdam, the Netherlands. AD - EMGO Institute for Health and Care Research, VU University Medical Center, Amsterdam, the Netherlands. FAU - Willeit, Johann AU - Willeit J AD - Department of Neurology, Medical University Innsbruck, Innsbruck, Austria. FAU - Sacco, Ralph L AU - Sacco RL AD - Department of Neurology, Miller School of Medicine, University of Miami, Miami, Florida, United States of America. FAU - Franco, Oscar H AU - Franco OH AD - Department of Epidemiology, Erasmus MC, University Medical Center Rotterdam, Rotterdam, the Netherlands. FAU - Uthoff, Heiko AU - Uthoff H AD - Department of Angiology, University Hospital Basel, Basel, Switzerland. FAU - Hedblad, Bo AU - Hedblad B AD - Department of Clinical Sciences in Malmo, Lund University, Malmo, Sweden. FAU - Suarez, Carmen AU - Suarez C AD - Internal Medicine Department, Hospital Universitario de la Princesa, Universidad Autonoma de Madrid, Madrid, Spain. FAU - Izzo, Raffaele AU - Izzo R AD - School of Medicine, Federico II University, Naples, Italy. FAU - Zhao, Dong AU - Zhao D AD - Department of Epidemiology, Beijing Institute of Heart, Lung and Blood Vessel Diseases,Beijing Anzhen Hospital, Capital Medical University, Beijing, China. FAU - Wannarong, Thapat AU - Wannarong T AD - Stroke Prevention & Atherosclerosis Research Centre, Robarts Research Institute, Western University, London, Ontario, Canada. AD - Department of Internal Medicine, Faculty of Medicine, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok, Thailand. FAU - Catapano, Alberico AU - Catapano A AD - IRCSS Multimedica, Milan, Italy. AD - Department of Pharmacological and Biomolecular Sciences, University of Milan, Milan, Italy. FAU - Ducimetiere, Pierre AU - Ducimetiere P AD - University Paris_Sud Xi, Kremlin-Bicetre, Le Kremlin-Bicetre, France. FAU - Espinola-Klein, Christine AU - Espinola-Klein C AD - 2nd Department of Medicine, Johannes-Gutenberg University, Mainz, Germany. FAU - Chien, Kuo-Liong AU - Chien KL AD - Institute of Epidemiology and Preventive Medicine, College of Public Health,National Taiwan University, Taipei, Taiwan. FAU - Price, Jackie F AU - Price JF AD - Usher Institute of Population Health Sciences and Informatics, University of Edinburgh, Edinburgh, United Kingdom. FAU - Bergstrom, Goran AU - Bergstrom G AD - Wallenberg Laboratory for Cardiovascular Research, Sahlgrenska Academy, Gothenburg University, Gotheborg, Sweden. FAU - Kauhanen, Jussi AU - Kauhanen J AD - Institute of Public Health and Clinical Nutrition, University of Eastern Finland, Kuopio Campus, Kuopio, Finland. FAU - Tremoli, Elena AU - Tremoli E AD - Department of Medical Biotechnology and Translational Medicine, Universita degli Studi di Milano, Milano, Italy. AD - Centro Cardiologico Monzino, IRCCS, Milano, Italy. FAU - Dorr, Marcus AU - Dorr M AD - Department B for Internal Medicine, University Medicine Greifswald, Greifswald, Germany. FAU - Berenson, Gerald AU - Berenson G AD - Department of Medicine, Pediatrics, Biochemistry, Epidemiology, Tulane University School of Medicine and School of Public Health and Tropical Medicine, New Orleans, Louisiana, United States of America. FAU - Kitagawa, Kazuo AU - Kitagawa K AD - Department of Neurology, Tokyo Women's Medical University, Tokyo, Japan. FAU - Dekker, Jacqueline M AU - Dekker JM AD - Department of Epidemiology and Biostatistics, EMGO Institute for Health and Care Research, VU University Medical Center, Amsterdam, the Netherlands. FAU - Kiechl, Stefan AU - Kiechl S AD - Department of Neurology, Medical University Innsbruck, Innsbruck, Austria. FAU - Sitzer, Matthias AU - Sitzer M AD - Department of Neuology, Klinikum Herford, Herford, Germany. FAU - Bickel, Horst AU - Bickel H AD - Department of Psychiatry and Psychotherapy, Technische Universitat Munchen, Munich, Germany. FAU - Rundek, Tatjana AU - Rundek T AD - Department of Neurology, Miller School of Medicine, University of Miami, Miami, Florida, United States of America. FAU - Hofman, Albert AU - Hofman A AD - Department of Epidemiology, Erasmus University Medical Center, Rotterdam, the Netherlands. FAU - Mathiesen, Ellisiv B AU - Mathiesen EB AD - Department of Clinical Medicine, Uit The Arctic University of Norway, Tromso, Norway. FAU - Castelnuovo, Samuela AU - Castelnuovo S AD - Center of Dyslipidemias, Niguarda Ca' Granda Hospital, Milano, Italy. FAU - Landecho, Manuel F AU - Landecho MF AD - Department of Internal Medicine, University Clinic of Navarra, Navarra, Spain. FAU - Rosvall, Maria AU - Rosvall M AD - Department of Clinical Sciences in Malmo, Lund University, Malmo, Sweden. FAU - Gabriel, Rafael AU - Gabriel R AD - Escuela National de Sanidad, Instituto de Salud Carlos III, Madrid, Spain. FAU - de Luca, Nicola AU - de Luca N AD - School of Medicine, Federico II University, Naples, Italy. FAU - Liu, Jing AU - Liu J AD - Department of Epidemiology, Beijing Institute of Heart, Lung and Blood Vessel Diseases,Beijing Anzhen Hospital, Capital Medical University, Beijing, China. FAU - Baldassarre, Damiano AU - Baldassarre D AD - Department of Medical Biotechnology and Translational Medicine, Universita degli Studi di Milano, Milano, Italy. AD - Centro Cardiologico Monzino, IRCCS, Milano, Italy. FAU - Kavousi, Maryam AU - Kavousi M AD - Department of Epidemiology and Biostatistics, Erasmus Medical Center, Rotterdam, the Netherlands. FAU - de Groot, Eric AU - de Groot E AD - Imagelabonline & Cardiovascular, Eindhoven and Lunteren, the Netherlands. AD - Department of Clinical Epidemiology, Biostatistics and Bioinformatics, Academic Medical Centre, Amsterdam, the Netherlands. FAU - Bots, Michiel L AU - Bots ML AD - Julius Center for Health Sciences and Primary Care, University Medical Center Utrecht, Utrecht, the Netherlands. FAU - Yanez, David N AU - Yanez DN AD - Department of Biostatistics, University of Washington, Seattle, Washington, United States of America. FAU - Thompson, Simon G AU - Thompson SG AD - Department of Public Health and Primary Care, School of Clinical Medicine, University of Cambridge, Cambridge, United Kingdom. CN - PROG-IMT study group LA - eng GR - RG/13/13/30194/British Heart Foundation/United Kingdom GR - R01 AG015928/AG/NIA NIH HHS/United States GR - U01 HL080295/HL/NHLBI NIH HHS/United States GR - R01 DE013094/DE/NIDCR NIH HHS/United States GR - N01 HC015103/HC/NHLBI NIH HHS/United States GR - R56 AG020098/AG/NIA NIH HHS/United States GR - N01HC55222/HL/NHLBI NIH HHS/United States GR - MR/L003120/1/Medical Research Council/United Kingdom GR - N01HC85086/HL/NHLBI NIH HHS/United States GR - R37 NS029993/NS/NINDS NIH HHS/United States GR - HHSN268201200036C/HL/NHLBI NIH HHS/United States GR - R01 HL080295/HL/NHLBI NIH HHS/United States GR - R01 AG020098/AG/NIA NIH HHS/United States GR - N01HC75150/HL/NHLBI NIH HHS/United States GR - N01HC85079/HL/NHLBI NIH HHS/United States GR - R01 AG023629/AG/NIA NIH HHS/United States GR - R01 AG027058/AG/NIA NIH HHS/United States GR - N01 HC045133/HC/NHLBI NIH HHS/United States GR - N01 HC035129/HC/NHLBI NIH HHS/United States GR - R56 AG023629/AG/NIA NIH HHS/United States PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20180412 PL - United States TA - PLoS One JT - PloS one JID - 101285081 SB - IM EIN - PLoS One. 2018 Sep 20;13(9):e0204633. PMID: 30235339 MH - Aged MH - Cardiovascular Diseases/*diagnosis/diagnostic imaging/epidemiology MH - *Carotid Intima-Media Thickness MH - Female MH - Humans MH - *Intersectoral Collaboration MH - Male MH - Middle Aged MH - Prognosis MH - Risk Factors PMC - PMC5896895 EDAT- 2018/04/13 06:00 MHDA- 2018/07/10 06:00 CRDT- 2018/04/13 06:00 PHST- 2017/09/29 00:00 [received] PHST- 2017/11/29 00:00 [accepted] PHST- 2018/04/13 06:00 [entrez] PHST- 2018/04/13 06:00 [pubmed] PHST- 2018/07/10 06:00 [medline] AID - 10.1371/journal.pone.0191172 [doi] AID - PONE-D-17-35265 [pii] PST - epublish SO - PLoS One. 2018 Apr 12;13(4):e0191172. doi: 10.1371/journal.pone.0191172. eCollection 2018. PMID- 28765036 OWN - NLM STAT- MEDLINE DCOM- 20180611 LR - 20180714 IS - 2211-8179 (Electronic) VI - 12 IP - 3 DP - 2017 Sep TI - World Heart Federation Cholesterol Roadmap. PG - 179-197.e5 LID - S2211-8160(17)30020-0 [pii] LID - 10.1016/j.gheart.2017.03.002 [doi] AB - BACKGROUND: The World Heart Federation has undertaken an initiative to develop a series of Roadmaps. OBJECTIVES: The aim of these is to promote development of national policies and health systems approaches and identify potential roadblocks on the road to effective prevention, detection and management of cardiovascular disease (CVD) in low-and middle-income countries (LMIC), and strategies for overcoming these. This Roadmap focuses on elevated blood cholesterol, a leading risk factor for myocardial infarction, stroke, and peripheral arterial disease. METHODS: Through a review of published guidelines and research papers, and consultation with a committee composed of experts in clinical management of cholesterol and health systems research in LMIC, this Roadmap identifies (1) key interventions for primordial, primary and secondary prevention of CVD through detection, treatment, and management of elevated cholesterol and familial hypercholesterolemia (FH); (2) gaps in implementation of these interventions (knowledge-practice gaps); (3) health system roadblocks to treatment of elevated cholesterol in LMIC; and (4) potential strategies for overcoming these. RESULTS: Despite strong evidence of the importance of cholesterol levels in primary or secondary prevention of CVD, and the effectiveness of statin therapy for cholesterol lowering and reduction of CVD risk, gaps exist in the detection, treatment, and management of high cholesterol globally. Some potential roadblocks include poor access to laboratory facilities or trained professionals for cholesterol management, low awareness of FH among the general population and health professionals, unaffordability of statins for patient households, and low awareness of the importance of persistent adherence to lipid-lowering medication. Potential solutions include point-of-care testing, provision of free or subsidized lipid-lowering medication, and treatment adherence support using text message reminders. CONCLUSIONS: Known effective strategies for detection, treatment, and management of elevated cholesterol and FH exist, but there are barriers to their implementation in many low-resource settings. Priorities for health system intervention should be identified at the national level, and the feasibility and effectiveness of proposed solutions should be assessed in specific contexts. Many solutions proposed in this Roadmap may apply to other cardiovascular conditions and present opportunities for integration of CVD care in LMIC. CI - Copyright (c) 2017 World Heart Federation (Geneva). Published by Elsevier B.V. All rights reserved. FAU - Murphy, Adrianna AU - Murphy A AD - Centre for Health and Social Change, Department of Health Services Research and Policy, London School of Hygiene and Tropical Medicine, London, United Kingdom. FAU - Faria-Neto, Jose R AU - Faria-Neto JR AD - School of Medicine, Pontificia Universidade Catolica do Parana, Curitiba, Brazil. FAU - Al-Rasadi, Khalid AU - Al-Rasadi K AD - Department of Biochemistry, Sultan Qaboos University Hospital, Muscat, Oman. FAU - Blom, Dirk AU - Blom D AD - Division of Lipidology, Department of Medicine, University of Cape Town, Cape Town, South Africa. FAU - Catapano, Alberico AU - Catapano A AD - Department of Pharmacology, Center of Epidemiology and Preventive Pharmacology, University of Milan, Milan, Italy; Laboratory of Lipoproteins, Immunity and Atherosclerosis, Department of Pharmacological and Biomolecular Sciences, University of Milan, Milan, Italy; Center for the Study of Atherosclerosis at Bassini Hospital, University of Milan, Milan, Italy. FAU - Cuevas, Ada AU - Cuevas A AD - Nutrition Department, Clinica Las Condes, Santiago, Chile. FAU - Lopez-Jimenez, Francisco AU - Lopez-Jimenez F AD - Department of Medicine, Mayo Medical School, Division of Preventive Cardiology, Mayo Clinic, Rochester, Minnesota, USA; Department of Research, Dan Abraham Healthy Living Center, Rochester, Minnesota, USA. FAU - Perel, Pablo AU - Perel P AD - World Heart Federation, Geneva, Switzerland; London School of Hygiene and Tropical Medicine, London, United Kingdom. FAU - Santos, Raul AU - Santos R AD - Lipid Clinic Heart Institute, University of Sao Paulo Medical School Hospital, Sao Paulo, Brazil; Preventive Medicine Center and Cardiology Program, Hospital Israelita Albert Einstein, Sao Paulo, Brazil. FAU - Sniderman, Allan AU - Sniderman A AD - Division of Cardiology, McGill University Health Centre, Montreal, Quebec, Canada. FAU - Sy, Rody AU - Sy R AD - Section of Cardiology, Department of Medicine, University of the Phillipines College of Medicine, Manila, Philippines; Cardiovascular Institute, Cardinal Santos Medical Center, San Juan, Philippines. FAU - Watts, Gerald F AU - Watts GF AD - Cardiometabolic Service, Department of Cardiology, Royal Perth Hospital, Perth, Western Australia, Australia; School of Medicine, Faculty of Health and Medical Sciences, University of Western Australia, Perth, Western Australia, Australia. FAU - Zhao, Dong AU - Zhao D AD - Beijing Institute of Heart, Lung and Blood Vessel Diseases, Capital Medical University, Beijing Anzhen Hospital, Beijing, China. FAU - Yusuf, Salim AU - Yusuf S AD - World Heart Federation, Geneva, Switzerland; Department of Medicine, McMaster University, Hamilton, Ontario, Canada; Population Health Research Institute, Hamilton, Ontario, Canada; Hamilton Health Sciences, McMaster University, Hamilton, Ontario, Canada. FAU - Wood, David AU - Wood D AD - World Heart Federation, Geneva, Switzerland; Department of Cardiovascular Medicine, Imperial College London, London, United Kingdom; National Heart and Lung Institute, Bethesda, MD, USA. LA - eng PT - Journal Article PT - Review PT - Research Support, Non-U.S. Gov't DEP - 20170729 PL - England TA - Glob Heart JT - Global heart JID - 101584391 RN - 97C5T2UQ7J (Cholesterol) SB - IM MH - *Cardiovascular Diseases/blood/epidemiology/prevention & control MH - Cholesterol/*blood MH - Global Health MH - Humans MH - Morbidity MH - *Practice Guidelines as Topic MH - Secondary Prevention/*methods EDAT- 2017/08/03 06:00 MHDA- 2018/06/12 06:00 CRDT- 2017/08/03 06:00 PHST- 2017/08/03 06:00 [pubmed] PHST- 2018/06/12 06:00 [medline] PHST- 2017/08/03 06:00 [entrez] AID - S2211-8160(17)30020-0 [pii] AID - 10.1016/j.gheart.2017.03.002 [doi] PST - ppublish SO - Glob Heart. 2017 Sep;12(3):179-197.e5. doi: 10.1016/j.gheart.2017.03.002. Epub 2017 Jul 29. PMID- 28751833 OWN - NLM STAT- PubMed-not-MEDLINE LR - 20190115 IS - 1520-765X (Print) IS - 1520-765X (Linking) VI - 19 IP - Suppl D DP - 2017 May TI - ANMCO/ISS/AMD/ANCE/ARCA/FADOI/GICR-IACPR/SICI-GISE/SIBioC/SIC/SICOA/SID/SIF/SIMEU /SIMG/SIMI/SISA Joint Consensus Document on cholesterol and cardiovascular risk: diagnostic-therapeutic pathway in Italy. PG - D3-D54 LID - 10.1093/eurheartj/sux029 [doi] AB - Atherosclerotic cardiovascular disease still represents the leading cause of death in Western countries. A wealth of scientific evidence demonstrates that increased blood cholesterol levels have a major impact on the outbreak and progression of atherosclerotic plaques. Moreover, several cholesterol-lowering pharmacological agents, including statins and ezetimibe, have proved effective in improving clinical outcomes. This document focuses on the clinical management of hypercholesterolaemia and has been conceived by 16 Italian medical associations with the support of the Italian National Institute of Health. The authors discuss in detail the role of hypercholesterolaemia in the genesis of atherosclerotic cardiovascular disease. In addition, the implications for high cholesterol levels in the definition of the individual cardiovascular risk profile have been carefully analysed, while all available therapeutic options for blood cholesterol reduction and cardiovascular risk mitigation have been explored. Finally, this document outlines the diagnostic and therapeutic pathways for the clinical management of patients with hypercholesterolaemia. FAU - Gulizia, Michele Massimo AU - Gulizia MM AD - Italian Association of Hospital Cardiologists (ANMCO). AD - Cardiology Department, Ospedale Garibaldi-Nesima, Azienda di Rilievo Nazionale e Alta Specializzazione 'Garibaldi', Via Palermo 636, 95122 Catania, Italy. FAU - Colivicchi, Furio AU - Colivicchi F AD - Italian Association of Hospital Cardiologists (ANMCO). FAU - Ricciardi, Gualtiero AU - Ricciardi G AD - Italian Institute of Health (ISS). FAU - Giampaoli, Simona AU - Giampaoli S AD - Italian Institute of Health (ISS). FAU - Maggioni, Aldo Pietro AU - Maggioni AP AD - ANMCO Research Centre. FAU - Averna, Maurizio AU - Averna M AD - Italian Society for the Study of Arteriosclerosis (SISA). FAU - Graziani, Maria Stella AU - Graziani MS AD - Italian Society of Clinical Biochemistry and Clinical Molecular Biology (SIBioC). FAU - Ceriotti, Ferruccio AU - Ceriotti F AD - Italian Society of Clinical Biochemistry and Clinical Molecular Biology (SIBioC). FAU - Mugelli, Alessandro AU - Mugelli A AD - Italian Society of Pharmacology (SIF). FAU - Rossi, Francesco AU - Rossi F AD - Italian Society of Pharmacology (SIF). FAU - Medea, Gerardo AU - Medea G AD - Italian Society of General Medicine (SIMG). FAU - Parretti, Damiano AU - Parretti D AD - Italian Society of General Medicine (SIMG). FAU - Abrignani, Maurizio Giuseppe AU - Abrignani MG AD - Italian Association of Hospital Cardiologists (ANMCO). FAU - Arca, Marcello AU - Arca M AD - Italian Society for the Study of Arteriosclerosis (SISA). FAU - Perrone Filardi, Pasquale AU - Perrone Filardi P AD - Italian Society of Cardiology (SIC). FAU - Perticone, Francesco AU - Perticone F AD - Italian Society of Internal Medicine (SIMI). FAU - Catapano, Alberico AU - Catapano A AD - Italian Society for the Study of Arteriosclerosis (SISA). FAU - Griffo, Raffaele AU - Griffo R AD - Italian Group of Rehabilitation and Preventative Cardiology (GICR-IACPR). FAU - Nardi, Federico AU - Nardi F AD - Italian Association of Hospital Cardiologists (ANMCO). FAU - Riccio, Carmine AU - Riccio C AD - Italian Association of Hospital Cardiologists (ANMCO). FAU - Di Lenarda, Andrea AU - Di Lenarda A AD - Italian Association of Hospital Cardiologists (ANMCO). FAU - Scherillo, Marino AU - Scherillo M AD - Italian Association of Hospital Cardiologists (ANMCO). FAU - Musacchio, Nicoletta AU - Musacchio N AD - Association of Medical Diabetologists (AMD). FAU - Panno, Antonio Vittorio AU - Panno AV AD - National Association of Out of Hospital Cardiologists (ANCE). FAU - Zito, Giovanni Battista AU - Zito GB AD - Regional Ambulatory Cardiologists Associations (ARCA). FAU - Campanini, Mauro AU - Campanini M AD - Federation of Internal Medicine Hospital Directors. FAU - Bolognese, Leonardo AU - Bolognese L AD - Italian Federation of Cardiology (FIC). FAU - Faggiano, Pompilio Massimo AU - Faggiano PM AD - Italian Society of Interventional Cardiology (SICI-GISE). FAU - Musumeci, Giuseppe AU - Musumeci G AD - Italian Society of Interventional Cardiology (SICI-GISE). FAU - Pusineri, Enrico AU - Pusineri E AD - Italian Society of Accredited Cardiology Hospital Care (SICOA). FAU - Ciaccio, Marcello AU - Ciaccio M AD - Italian Society of Clinical Biochemistry and Clinical Molecular Biology (SIBioC). FAU - Bonora, Enzo AU - Bonora E AD - Italian Society of Diabetology (SID). FAU - Cantelli Forti, Giorgio AU - Cantelli Forti G AD - Italian Society of Pharmacology (SIF). FAU - Ruggieri, Maria Pia AU - Ruggieri MP AD - Italian Society of Emergency and Urgent Medicine (SIMEU). FAU - Cricelli, Claudio AU - Cricelli C AD - Italian Society of General Medicine (SIMG). FAU - Romeo, Francesco AU - Romeo F AD - Italian Society of Cardiology (SIC). FAU - Ferrari, Roberto AU - Ferrari R AD - Italian Society of Cardiology (SIC). FAU - Maseri, Attilio AU - Maseri A AD - Fondazione 'per il Tuo cuore' Heart Care Foundation Onlus. LA - eng PT - Journal Article DEP - 20170502 PL - England TA - Eur Heart J Suppl JT - European heart journal supplements : journal of the European Society of Cardiology JID - 100886647 PMC - PMC5526476 OTO - NOTNLM OT - Atherosclerosis OT - Diagnostic and therapeutic pathways OT - Hypercholesterolaemia OT - PCSK9 inhibitors OT - Statins OT - Sustainable health care EDAT- 2017/07/29 06:00 MHDA- 2017/07/29 06:01 CRDT- 2017/07/29 06:00 PHST- 2017/07/29 06:00 [entrez] PHST- 2017/07/29 06:00 [pubmed] PHST- 2017/07/29 06:01 [medline] AID - 10.1093/eurheartj/sux029 [doi] AID - sux029 [pii] PST - ppublish SO - Eur Heart J Suppl. 2017 May;19(Suppl D):D3-D54. doi: 10.1093/eurheartj/sux029. Epub 2017 May 2. PMID- 27627804 OWN - NLM STAT- MEDLINE DCOM- 20170802 LR - 20181113 IS - 1932-6203 (Electronic) IS - 1932-6203 (Linking) VI - 11 IP - 9 DP - 2016 TI - Epicardial Adipose Tissue (EAT) Thickness Is Associated with Cardiovascular and Liver Damage in Nonalcoholic Fatty Liver Disease. PG - e0162473 LID - 10.1371/journal.pone.0162473 [doi] AB - BACKGROUND AND AIMS: Epicardial adipose tissue (EAT) has been proposed as a cardiometabolic and hepatic fibrosis risk factor in patients with non alcoholic fatty liver disease (NAFLD). Aim of this study was to evaluate the role of EAT in NAFLD by analyzing 1) the association between EAT, the other metabolic parameters and the severity of steatosis 2) the relationship between cardiovascular (cIMT, cplaques, E/A), liver (presence of NASH and significant fibrosis) damage and metabolic risk factors including EAT 3) the relationship between EAT and genetic factors strongly influencing liver steatosis. METHODS: In a cross-sectional study, we considered 512 consecutive patients with NAFLD (confirmed by biopsy in 100). EAT, severity of steatosis, carotid intima-media thickness (cIMT) and plaques were evaluated by ultrasonography and results analysed by multiple linear and logistic regression models. Variables independently associated with EAT (mm) were female gender (p = 0.003), age (p = 0.001), BMI (p = 0.01), diastolic blood pressure (p = 0.009), steatosis grade 2 (p = 0.01) and 3 (p = 0.04), fatty liver index (p = 0.001) and statin use (p = 0.03). Variables independently associated with carotid IMT were age (p = 0.0001), hypertension (p = 0.009), diabetes (p = 0.04), smoking habits (p = 0.04) and fatty liver index (p = 0.02), with carotid plaques age (p = 0.0001), BMI (p = 0.03), EAT (p = 0.02),) and hypertension (p = 0.02), and with E/A age (p = 0.0001), diabetes (p = 0.005), hypertension (p = 0.04) and fatty liver index (p = 0.004). In the 100 patients with available liver histology non alcoholic steatohepatitis (NASH) was independently associated with EAT (p = 0.04) and diabetes (p = 0.054) while significant fibrosis with EAT (p = 0.02), diabetes (p = 0.01) and waist circumference (p = 0.05). No association between EAT and PNPLA3 and TM6SF2 polymorphisms was found. CONCLUSION: In patients with NAFLD, EAT is associated with the severity of liver and vascular damage besides with the known metabolic risk factors. FAU - Fracanzani, Anna Ludovica AU - Fracanzani AL AUID- ORCID: http://orcid.org/0000-0001-5918-0171 AD - Department of Pathophysiology and Transplantation, Ca' Granda Foundation IRCCS Maggiore Policlinico Hospital, University of Milan, Milan, Italy. FAU - Pisano, Giuseppina AU - Pisano G AD - Department of Pathophysiology and Transplantation, Ca' Granda Foundation IRCCS Maggiore Policlinico Hospital, University of Milan, Milan, Italy. FAU - Consonni, Dario AU - Consonni D AD - Epidemiology Unit, Ca' Granda Foundation IRCCS Maggiore Policlinico Hospital, University of Milan, Milan, Italy. FAU - Tiraboschi, Silvia AU - Tiraboschi S AD - Department of Pathophysiology and Transplantation, Ca' Granda Foundation IRCCS Maggiore Policlinico Hospital, University of Milan, Milan, Italy. FAU - Baragetti, Andrea AU - Baragetti A AD - Department of Pharmacological and Biomolecular Sciences, University of Milan and Centro Studi Aterosclerosi Milan, Milan, Italy. FAU - Bertelli, Cristina AU - Bertelli C AD - Department of Pathophysiology and Transplantation, Ca' Granda Foundation IRCCS Maggiore Policlinico Hospital, University of Milan, Milan, Italy. FAU - Norata, Giuseppe Danilo AU - Norata GD AD - Department of Pharmacological and Biomolecular Sciences, University of Milan and Centro Studi Aterosclerosi Milan, Milan, Italy. FAU - Dongiovanni, Paola AU - Dongiovanni P AD - Department of Pathophysiology and Transplantation, Ca' Granda Foundation IRCCS Maggiore Policlinico Hospital, University of Milan, Milan, Italy. FAU - Valenti, Luca AU - Valenti L AD - Department of Pathophysiology and Transplantation, Ca' Granda Foundation IRCCS Maggiore Policlinico Hospital, University of Milan, Milan, Italy. FAU - Grigore, Liliana AU - Grigore L AD - Centro Studi Aterosclerosi, Bassini Hospital, Milan, Italy. FAU - Tonella, Tatiana AU - Tonella T AD - Cardiovascular Medicine Unit, Ca' Granda Foundation IRCCS Maggiore Policlinico Hospital, Milan, Italy. FAU - Catapano, Alberico AU - Catapano A AD - Department of Pharmacological and Biomolecular Sciences, University of Milano, and Multimedica IRCCS, Milan, Italy. FAU - Fargion, Silvia AU - Fargion S AD - Department of Pathophysiology and Transplantation, Ca' Granda Foundation IRCCS Maggiore Policlinico Hospital, University of Milan, Milan, Italy. LA - eng PT - Journal Article DEP - 20160914 PL - United States TA - PLoS One JT - PloS one JID - 101285081 SB - IM MH - Adipose Tissue/*pathology MH - Aged MH - Cardiovascular Diseases/*pathology MH - Cross-Sectional Studies MH - Female MH - Humans MH - Liver/*pathology MH - Male MH - Middle Aged MH - Non-alcoholic Fatty Liver Disease/*pathology MH - Pericardium/*pathology PMC - PMC5023162 COIS- The authors have declared that no competing interests exist. EDAT- 2016/09/15 06:00 MHDA- 2017/08/03 06:00 CRDT- 2016/09/15 06:00 PHST- 2016/06/03 00:00 [received] PHST- 2016/08/23 00:00 [accepted] PHST- 2016/09/15 06:00 [entrez] PHST- 2016/09/15 06:00 [pubmed] PHST- 2017/08/03 06:00 [medline] AID - 10.1371/journal.pone.0162473 [doi] AID - PONE-D-16-20141 [pii] PST - epublish SO - PLoS One. 2016 Sep 14;11(9):e0162473. doi: 10.1371/journal.pone.0162473. eCollection 2016. PMID- 26746227 OWN - NLM STAT- MEDLINE DCOM- 20171226 LR - 20181002 IS - 2047-4881 (Electronic) IS - 2047-4873 (Linking) VI - 23 IP - 11 DP - 2016 Jul TI - Normative values for carotid intima media thickness and its progression: Are they transferrable outside of their cohort of origin? PG - 1165-73 LID - 10.1177/2047487315625543 [doi] AB - BACKGROUND: The clinical use of carotid intima media thickness (cIMT) requires normal values, which may be subject to variation of geographical factors, ethnicity or measurement details. The influence of these factors has rarely been studied. The aim of this study was to determine whether normative cIMT values and their association with event risk are generalizable across populations. DESIGN: Meta-analysis of individual participant data. METHOD: From 22 general population cohorts from Europe, North America and Asia we selected subjects free of cardiovascular disease. Percentiles of cIMT and cIMT progression were assessed separately for every cohort. Cox proportional hazards models for vascular events were used to estimate hazard ratios for cIMT in each cohort. The estimates were pooled across Europe, North America and Asia, with random effects meta-analysis. The influence of geography, ethnicity and ultrasound protocols on cIMT values and on the hazard ratios was examined by meta-regression. RESULTS: Geographical factors, ethnicity and the ultrasound protocol had influence neither on the percentiles of cIMT and its progression, nor on the hazard ratios of cIMT for vascular events. Heterogeneity for percentiles of cIMT and cIMT progression was too large to create meaningful normative values. CONCLUSIONS: The distribution of cIMT values is too heterogeneous to define universal or regional population reference values. CIMT values vary widely between different studies regardless of ethnicity, geographic location and ultrasound protocol. Prediction of vascular events with cIMT values was more consistent across all cohorts, ethnicities and regions. CI - (c) The European Society of Cardiology 2016. FAU - Liao, Ximing AU - Liao X AD - Department of Neurology, Goethe University, Frankfurt am Main, Germany. FAU - Norata, Giuseppe D AU - Norata GD AD - Dipartimento di Scienze Farmacologiche e Biomolecolari, Universita degli Studi di Milano, Italy SISA Centre for the Study of Atherosclerosis, Bassini Hospital, Cinisello Balsamo, Italy. FAU - Polak, Joseph F AU - Polak JF AD - Tufts University School of Medicine, Tufts Medical Center, Boston, USA. FAU - Stehouwer, Coen DA AU - Stehouwer CD AD - Department of Internal Medicine and Cardiovascular Research Institute Maastricht (CARIM), Maastricht University Medical Centre, The Netherlands. FAU - Catapano, Alberico AU - Catapano A AD - IRCSS Multimedica, Milan, Italy Department of Pharmacological and Biomolecular Sciences, University of Milan, Italy. FAU - Rundek, Tatjana AU - Rundek T AD - Department of Neurology, Miller School of Medicine, University of Miami, USA. FAU - Ezhov, Marat AU - Ezhov M AD - Atherosclerosis Department, Cardiology Research Centre, Moscow, Russia. FAU - Sander, Dirk AU - Sander D AD - Department of Neurology, Benedictus Hospital Tutzing & Feldafing, Feldafing, Germany Department of Neurology, Technische Universitat Munchen, Germany. FAU - Thompson, Simon G AU - Thompson SG AD - Department of Public Health and Primary Care, School of Clinical Medicine, University of Cambridge, UK. FAU - Lorenz, Matthias W AU - Lorenz MW AD - Department of Neurology, Goethe University, Frankfurt am Main, Germany matthias.lorenz@em.uni-frankfurt.de. CN - PROG-IMT study group FAU - Balakhonova, Tatyana AU - Balakhonova T AD - Ultrasound Vascular Laboratory, Cardiology Research Centre2, Moscow, Russia. FAU - Safarova, Maya AU - Safarova M AD - Atherosclerosis Department, Cardiology Research Centre, Moscow, Russia. FAU - Grigore, Liliana AU - Grigore L AD - SISA Centre for the Study of Atherosclerosis, Bassini Hospital, Cinisello Balsamo, Italy. FAU - Empana, Jean-Philippe AU - Empana JP AD - Paris Cardiovascular Research Centre (PARCC), University Paris Descartes, Sorbonne Paris Cite, France. FAU - Lin, Hung-Ju AU - Lin HJ AD - Department of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan. FAU - McLachlan, Stela AU - McLachlan S AD - Centre for Population Health Sciences, University of Edinburgh, UK. FAU - Bokemark, Lena AU - Bokemark L AD - Wallenberg Laboratory for Cardiovascular Research, Institution for Medicin, Department for Molecular and Clinical Medicine, Sahlgrenska Academy, Gothenburg University, Sweden. FAU - Ronkainen, Kimmo AU - Ronkainen K AD - Institute of Public Health and Clinical Nutrition, University of Eastern Finland, Kuopio, Finland. FAU - Schminke, Ulf AU - Schminke U AD - Department of Neurology, Greifswald University Clinic, Germany. FAU - Lind, Lars AU - Lind L AD - Department of Medicine, Uppsala University, Sweden. FAU - Willeit, Peter AU - Willeit P AD - Department of Public Health and Primary Care, School of Clinical Medicine, University of Cambridge, UK Department of Neurology, Medical University Innsbruck, Austria. FAU - Yanez, David N AU - Yanez DN AD - Department of Biostatistics, University of Washington, Seattle, USA. FAU - Steinmetz, Helmuth AU - Steinmetz H AD - Department of Neurology, Goethe University, Frankfurt am Main, Germany. FAU - Poppert, Holger AU - Poppert H AD - Department of Neurology, Technische Universitat Munchen, Germany. FAU - Desvarieux, Moise AU - Desvarieux M AD - Department of Epidemiology, Mailman School of Public Health, Columbia University, New York, USA. FAU - Ikram, M Arfan AU - Ikram MA AD - Department of Epidemiology, Erasmus University Medical Centre, Rotterdam, The Netherlands Department of Neurology, Erasmus University Medical Centre, Rotterdam, The Netherlands Department of Radiology, Erasmus University Medical Centre, Rotterdam, The Netherlands. FAU - Johnsen, Stein Harald AU - Johnsen SH AD - Department of Clinical Medicine, University of Tromso, Norway Department of Neurology, University Hospital of Northern Norway, Tromso, Norway. FAU - Iglseder, Bernhard AU - Iglseder B AD - Parcelsus Medical University, Salzburg, Austria Department of Geriatric Medicine, Gemeinnutzige Salzburger Landeskliniken Betriebsgesellschaft GmbH Christian-Doppler-Klinik, Salzburg, Austria. FAU - Friera, Alfonsa AU - Friera A AD - Radiology Department, Hospital Universitario de la Princesa, Universidad Autonoma de Madrid, Spain. FAU - Xie, Wuxiang AU - Xie W AD - Department of Epidemiology, Beijing Institute of Heart, Lung and Blood Vessel Diseases, Beijing Anzhen Hospital, Capital Medical University, China. FAU - Plichart, Matthieu AU - Plichart M AD - Assistance Publique, Hopitaux de Paris, Hopital Broca, Paris, France. FAU - Su, Ta-Chen AU - Su TC AD - Department of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan. FAU - Srinivasan, Sathanur R AU - Srinivasan SR AD - Center for Cardiovascular Health, Department of Epidemiology, Biochemistry, Tulane University School of Public Health and Tropical Medicine, New Orleans, USA. FAU - Schmidt, Caroline AU - Schmidt C AD - Wallenberg Laboratory for Cardiovascular Research, Institution for Medicin, Department for Molecular and Clinical Medicine, Sahlgrenska Academy, Gothenburg University, Sweden. FAU - Tuomainen, Tomi-Pekka AU - Tuomainen TP AD - Institute of Public Health and Clinical Nutrition, University of Eastern Finland, Kuopio, Finland. FAU - Volzke, Henry AU - Volzke H AD - Institute for Community Medicine, SHIP/Clinical-Epidemiological Research, Greifswald, Germany. FAU - Nijpels, Giel AU - Nijpels G AD - Department of General Practice, VU University Medical Centre, Amsterdam, The Netherlands EMGO Institute for Health and Care Research, VU University Medical Centre, Amsterdam, The Netherlands. FAU - Willeit, Johann AU - Willeit J AD - Department of Neurology, Medical University Innsbruck, Austria. FAU - Franco, Oscar H AU - Franco OH AD - Department of Epidemiology, Erasmus University Medical Centre, Rotterdam, The Netherlands. FAU - Suarez, Carmen AU - Suarez C AD - Internal Medicine Department, Hospital Universitario de la Princesa, Universidad Autonoma de Madrid, Spain. FAU - Zhao, Dong AU - Zhao D AD - Department of Epidemiology, Beijing Institute of Heart, Lung and Blood Vessel Diseases, Beijing Anzhen Hospital, Capital Medical University, China. FAU - Ducimetiere, Pierre AU - Ducimetiere P AD - University Paris Sud Xi, Kremlin-Bicetre, Le Kremlin-Bicetre, France. FAU - Chien, Kuo-Liong AU - Chien KL AD - Institute of Epidemiology and Preventive Medicine, College of Public Health, National Taiwan University, Taipei, Taiwan. FAU - Robertson, Christine AU - Robertson C AD - Centre for Population Health Sciences, University of Edinburgh, UK. FAU - Bergstrom, Goran AU - Bergstrom G AD - Wallenberg Laboratory for Cardiovascular Research, Institution for Medicin, Department for Molecular and Clinical Medicine, Sahlgrenska Academy, Gothenburg University, Sweden. FAU - Kauhanen, Jussi AU - Kauhanen J AD - Institute of Public Health and Clinical Nutrition, University of Eastern Finland, Kuopio, Finland. FAU - Dorr, Marcus AU - Dorr M AD - Department B for Internal Medicine, University Medicine Greifswald, Germany German Centrefor Cardiovascular Research (DZHK), partner site Greifswald, Germany. FAU - Dekker, Jaqueline M AU - Dekker JM AD - Department of Epidemiology and Biostatistics, University Medical Centre, Amsterdam, The Netherlands. FAU - Kiechl, Stefan AU - Kiechl S AD - Department of Neurology, Medical University Innsbruck, Austria. FAU - Sitzer, Matthias AU - Sitzer M AD - Department of Neurology, Goethe University, Frankfurt am Main, Germany Department of Neurology, Klinikum Herford, Germany. FAU - Bickel, Horst AU - Bickel H AD - Department of Psychiatry and Psychotherapy, Technische Universitat Munchen, Germany. FAU - Sacco, Ralph L AU - Sacco RL AD - Department of Neurology, Miller School of Medicine, University of Miami, USA. FAU - Hofman, Albert AU - Hofman A AD - Department of Epidemiology, Erasmus University Medical Centre, Rotterdam, The Netherlands. FAU - Mathiesen, Ellisiv B AU - Mathiesen EB AD - Department of Clinical Medicine, University of Tromso, Norway Department of Neurology, University Hospital of Northern Norway, Tromso, Norway. FAU - Gabriel, Rafael AU - Gabriel R AD - Instituto de Investigacion IdiPAZ, Hospital Universitario La Paz, Madrid, Spain. FAU - Liu, Jing AU - Liu J AD - Department of Epidemiology, Beijing Institute of Heart, Lung and Blood Vessel Diseases, Beijing Anzhen Hospital, Capital Medical University, China. FAU - Berenson, Gerald AU - Berenson G AD - Department of Medicine, Pediatrics, Biochemistry, Epidemiology, Tulane University School of Medicine and School of Public Health and Tropical Medicine, New Orleans, USA. FAU - Kavousi, Maryam AU - Kavousi M AD - Department of Epidemiology and Biostatistics, Erasmus Medical Centre, Rotterdam, The Netherlands. FAU - Price, Jackie F AU - Price JF AD - Centre for Population Health Sciences, University of Edinburgh, UK. LA - eng GR - MR/L003120/1/Medical Research Council/United Kingdom GR - RG/08/014/24067/British Heart Foundation/United Kingdom PT - Journal Article PT - Meta-Analysis PT - Review PT - Research Support, Non-U.S. Gov't DEP - 20160108 PL - England TA - Eur J Prev Cardiol JT - European journal of preventive cardiology JID - 101564430 SB - IM MH - Atherosclerosis/diagnosis/*epidemiology MH - *Carotid Intima-Media Thickness MH - Disease Progression MH - Global Health MH - Humans MH - Incidence MH - Reference Values MH - Risk Factors OTO - NOTNLM OT - *Intima media thickness OT - *cardiovascular risk OT - *ethnicity OT - *geographic OT - *hazard ratio OT - *normal value EDAT- 2016/01/10 06:00 MHDA- 2017/12/27 06:00 CRDT- 2016/01/10 06:00 PHST- 2015/08/12 00:00 [received] PHST- 2015/12/15 00:00 [accepted] PHST- 2016/01/10 06:00 [entrez] PHST- 2016/01/10 06:00 [pubmed] PHST- 2017/12/27 06:00 [medline] AID - 2047487315625543 [pii] AID - 10.1177/2047487315625543 [doi] PST - ppublish SO - Eur J Prev Cardiol. 2016 Jul;23(11):1165-73. doi: 10.1177/2047487315625543. Epub 2016 Jan 8. PMID- 27312138 OWN - NLM STAT- MEDLINE DCOM- 20180910 LR - 20181202 IS - 1827-6806 (Print) IS - 1827-6806 (Linking) VI - 17 IP - 6 Suppl 1 DP - 2016 Jun TI - [ANMCO/ISS/AMD/ANCE/ARCA/FADOI/GICR-IACPR/SICI-GISE/SIBioC/SIC/SICOA/SID/SIF/SIME U/SIMG/SIMI/SISA Consensus document. Hypercholesterolemia and cardiovascular risk: diagnostic and therapeutic pathways in Italy]. PG - 3S-57 LID - 10.1714/2264.24358 [doi] AB - Atherosclerotic cardiovascular disease still represents the leading cause of death in western countries. A wealth of scientific evidence demonstrates that increased blood cholesterol levels have a major impact on the outbreak and progression of atherosclerotic plaques. Moreover, several cholesterol-lowering pharmacological agents, including statins and ezetimibe, have proven effective in improving clinical outcomes. This document is focused on the clinical management of hypercholesterolemia and has been conceived by 16 Italian medical associations with the support of the Italian National Institute of Health. The authors have considered with particular attention the role of hypercholesterolemia in the genesis of atherosclerotic cardiovascular disease. Besides, the implications of high cholesterol levels in the definition of the individual cardiovascular risk profile have been carefully analyzed, while all available therapeutic options for blood cholesterol reduction and cardiovascular risk mitigation have been considered. Finally, this document outlines the diagnostic and therapeutic pathways for the clinical management of patients with hypercholesterolemia. FAU - Gulizia, Michele Massimo AU - Gulizia MM AD - Associazione Nazionale Medici Cardiologi Ospedalieri (ANMCO). FAU - Colivicchi, Furio AU - Colivicchi F AD - Associazione Nazionale Medici Cardiologi Ospedalieri (ANMCO). FAU - Ricciardi, Gualtiero AU - Ricciardi G AD - Istituto Superiore di Sanita (ISS). FAU - Giampaoli, Simona AU - Giampaoli S AD - Istituto Superiore di Sanita (ISS). FAU - Maggioni, Aldo Pietro AU - Maggioni AP AD - Centro Studi ANMCO. FAU - Averna, Maurizio AU - Averna M AD - Societa Italiana per lo Studio della Arteriosclerosi (SISA). FAU - Graziani, Maria Stella AU - Graziani MS AD - Societa Italiana di Biochimica Clinica e Biologia Molecolare Clinica (SIBioC). FAU - Ceriotti, Ferruccio AU - Ceriotti F AD - Societa Italiana di Biochimica Clinica e Biologia Molecolare Clinica (SIBioC). FAU - Mugelli, Alessandro AU - Mugelli A AD - Societa Italiana di Farmacologia (SIF). FAU - Rossi, Francesco AU - Rossi F AD - Societa Italiana di Farmacologia (SIF). FAU - Medea, Gerardo AU - Medea G AD - Societa Italiana di Medicina Generale (SIMG). FAU - Parretti, Damiano AU - Parretti D AD - Societa Italiana di Medicina Generale (SIMG). FAU - Abrignani, Maurizio Giuseppe AU - Abrignani MG AD - Associazione Nazionale Medici Cardiologi Ospedalieri (ANMCO). FAU - Arca, Marcello AU - Arca M AD - Societa Italiana per lo Studio della Arteriosclerosi (SISA). FAU - Filardi, Pasquale Perrone AU - Filardi PP AD - Societa Italiana di Cardiologia (SIC). FAU - Perticone, Francesco AU - Perticone F AD - Societa Italiana di Medicina Interna (SIMI). FAU - Catapano, Alberico AU - Catapano A AD - Societa Italiana per lo Studio della Arteriosclerosi (SISA). FAU - Griffo, Raffaele AU - Griffo R AD - Gruppo Italiano di Cardiologia Riabilitativa e Preventiva (GICR-IACPR). FAU - Nardi, Federico AU - Nardi F AD - Associazione Nazionale Medici Cardiologi Ospedalieri (ANMCO). FAU - Riccio, Carmine AU - Riccio C AD - Associazione Nazionale Medici Cardiologi Ospedalieri (ANMCO). FAU - Di Lenarda, Andrea AU - Di Lenarda A AD - Associazione Nazionale Medici Cardiologi Ospedalieri (ANMCO). FAU - Scherillo, Marino AU - Scherillo M AD - Associazione Nazionale Medici Cardiologi Ospedalieri (ANMCO). FAU - Musacchio, Nicoletta AU - Musacchio N AD - Associazione Medici Diabetologi (AMD). FAU - Panno, Antonio Vittorio AU - Panno AV AD - Cardiologia Italiana del Territorio (ANCE). FAU - Zito, Giovanni Battista AU - Zito GB AD - Associazioni Regionali Cardiologi Ambulatoriali (ARCA). FAU - Campanini, Mauro AU - Campanini M AD - Federazione delle Associazioni dei Dirigenti Ospedalieri Internisti (FADOI). FAU - Bolognese, Leonardo AU - Bolognese L AD - Federazione Italiana di Cardiologia (FIC). FAU - Faggiano, Pompilio Massimo AU - Faggiano PM AD - Gruppo Italiano di Cardiologia Riabilitativa e Preventiva (GICR-IACPR). FAU - Musumeci, Giuseppe AU - Musumeci G AD - Societa Italiana di Cardiologia Interventistica (SICI-GISE). FAU - Pusineri, Enrico AU - Pusineri E AD - Societa Italiana Cardiologia Ospedalita Accreditata (SICOA). FAU - Ciaccio, Marcello AU - Ciaccio M AD - Societa Italiana di Biochimica Clinica e Biologia Molecolare Clinica (SIBioC). FAU - Bonora, Enzo AU - Bonora E AD - Societa Italiana di Diabetologia (SID). FAU - Cantelli Forti, Giorgio AU - Cantelli Forti G AD - Societa Italiana di Farmacologia (SIF). FAU - Ruggieri, Maria Pia AU - Ruggieri MP AD - Societa Italiana di Medicina di Emergenza-Urgenza (SIMEU). FAU - Cricelli, Claudio AU - Cricelli C AD - Societa Italiana di Medicina Generale (SIMG). FAU - Romeo, Francesco AU - Romeo F AD - Societa Italiana di Cardiologia (SIC). FAU - Ferrari, Roberto AU - Ferrari R AD - Societa Italiana di Cardiologia (SIC). FAU - Maseri, Attilio AU - Maseri A AD - Fondazione "per il Tuo cuore" HCF Onlus. LA - ita PT - Journal Article PT - Practice Guideline TT - Documento di consenso intersocietario ANMCO/ISS/AMD/ANCE/ARCA/FADOI/ GICR-IACPR/SICI-GISE/SIBioC/SIC/SICOA/ SID/SIF/SIMEU/SIMG/SIMI/SISA Colesterolo e rischio cardiovascolare: percorso diagnostico-terapeutico in Italia. PL - Italy TA - G Ital Cardiol (Rome) JT - Giornale italiano di cardiologia (2006) JID - 101263411 RN - 0 (Anticholesteremic Agents) SB - IM MH - Anticholesteremic Agents/therapeutic use MH - Cardiovascular Diseases/*epidemiology MH - Consensus MH - Humans MH - Hypercholesterolemia/complications/*diagnosis/drug therapy MH - Italy MH - Risk Factors EDAT- 2016/06/18 06:00 MHDA- 2018/09/11 06:00 CRDT- 2016/06/18 06:00 PHST- 2016/06/18 06:00 [entrez] PHST- 2016/06/18 06:00 [pubmed] PHST- 2018/09/11 06:00 [medline] AID - 10.1714/2264.24358 [doi] PST - ppublish SO - G Ital Cardiol (Rome). 2016 Jun;17(6 Suppl 1):3S-57. doi: 10.1714/2264.24358. PMID- 26803429 OWN - NLM STAT- MEDLINE DCOM- 20161213 LR - 20161230 IS - 1879-1484 (Electronic) IS - 0021-9150 (Linking) VI - 246 DP - 2016 Mar TI - Progression of carotid vascular damage and cardiovascular events in non-alcoholic fatty liver disease patients compared to the general population during 10 years of follow-up. PG - 208-13 LID - 10.1016/j.atherosclerosis.2016.01.016 [doi] LID - S0021-9150(16)30016-8 [pii] AB - BACKGROUND AND AIM: Non-alcoholic fatty liver disease (NAFLD) is associated not only with liver related morbidity and mortality but also with an increased risk of cardiovascular disease. AIM: to evaluate in patients with NAFLD and in matched Controls after 10 years of follow-up 1 the incidence of major cardiovascular and cerebral events 2 the progression of vascular damage. METHODS: Clinical and cardio-metabolic data were collected in 125 NAFLD patients and 250 age and gender matched Controls at baseline and 10 years later. Incidence of cardiovascular and cerebral events was recorded. By ultrasonography, carotid intima-media thickness (cIMT), presence of plaques and presence of fatty liver were evaluated. RESULTS: 25% of the overall series was lost to follow-up. Sixty-eight (37%) Controls developed steatosis. Major cardiovascular events were observed in thirty-five subjects (17/91 (19%) NAFLD and 18/182 (10%) Controls), with an estimated cumulative risk significantly higher in NAFLD than in Controls, log-rank test for equality of failure functions p = 0.007. At multivariate analysis, presence of plaques (hazard ratio 5.08 (95% C.I. 2.56-10.96) and of steatosis (hazard ratio 1.99 (1.01-3.94)) were the strongest predictors for cardiovascular events. Grade of steatosis, ALT and GGT levels were higher in NAFLD patients who developed cardiovascular events. cIMT value after 10 years was significantly higher in NAFLD than in Controls, but the mean progression rate was higher in Controls (0.015 and 0.006 mm/year, p = 0.001). In conclusion our results suggest that NAFLD has to be included among risk factors for cardiovascular damage and underline the utility to evaluate, once NAFLD is diagnosed, the presence of atherosclerotic lesions. CI - Copyright (c) 2016 Elsevier Ireland Ltd. All rights reserved. FAU - Fracanzani, Anna Ludovica AU - Fracanzani AL AD - Department of Pathophysiology and Transplantation, Ca' Granda Foundation IRCCS Maggiore Policlinico Hospital, University of Milan, Milan, Italy. Electronic address: anna.fracanzani@unimi.it. FAU - Tiraboschi, Silvia AU - Tiraboschi S AD - Department of Pathophysiology and Transplantation, Ca' Granda Foundation IRCCS Maggiore Policlinico Hospital, University of Milan, Milan, Italy. Electronic address: silvia.tiraboschi@studenti.unimi.it. FAU - Pisano, Giuseppina AU - Pisano G AD - Department of Pathophysiology and Transplantation, Ca' Granda Foundation IRCCS Maggiore Policlinico Hospital, University of Milan, Milan, Italy. Electronic address: pinaz81@hotmail.com. FAU - Consonni, Dario AU - Consonni D AD - Epidemiology Unit, Ca' Granda Foundation IRCCS Maggiore Policlinico Hospital, University of Milan, Milan, Italy. Electronic address: dario.consonni@unimi.it. FAU - Baragetti, Andrea AU - Baragetti A AD - Department of Pharmacological and Biomolecular Sciences, University of Milan and Centro Studi Aterosclerosi, Milan Italy. Electronic address: andrea.baragetti@guest.unimi.it. FAU - Bertelli, Cristina AU - Bertelli C AD - Department of Pathophysiology and Transplantation, Ca' Granda Foundation IRCCS Maggiore Policlinico Hospital, University of Milan, Milan, Italy. Electronic address: cristinagiuliabertelli@yahoo.it. FAU - Norata, Danilo AU - Norata D AD - Department of Pharmacological and Biomolecular Sciences, University of Milan and Centro Studi Aterosclerosi, Milan Italy. Electronic address: danilo.norata@unimi.it. FAU - Valenti, Luca AU - Valenti L AD - Department of Pathophysiology and Transplantation, Ca' Granda Foundation IRCCS Maggiore Policlinico Hospital, University of Milan, Milan, Italy. Electronic address: luca.valenti@unimi.it. FAU - Grigore, Liliana AU - Grigore L AD - Centro Studi Aterosclerosi, Bassini Hospital Milan, Italy. Electronic address: centroaterocat@gmail.com. FAU - Porzio, Marianna AU - Porzio M AD - Department of Pathophysiology and Transplantation, Ca' Granda Foundation IRCCS Maggiore Policlinico Hospital, University of Milan, Milan, Italy. Electronic address: marianna.porzio@unimi.it. FAU - Catapano, Alberico AU - Catapano A AD - Department of Pharmacological and Biomolecular Sciences, University of Milano, and Multimedica IRCCS Milan, Italy. Electronic address: alberico.catapano@unimi.it. FAU - Fargion, Silvia AU - Fargion S AD - Department of Pathophysiology and Transplantation, Ca' Granda Foundation IRCCS Maggiore Policlinico Hospital, University of Milan, Milan, Italy. Electronic address: silvia.fargion@unimi.it. LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20160112 PL - Ireland TA - Atherosclerosis JT - Atherosclerosis JID - 0242543 SB - IM CIN - Atherosclerosis. 2016 Jun;249:228-9. PMID: 27012655 MH - Adult MH - Aged MH - Cardiovascular Diseases/diagnosis/*epidemiology MH - Carotid Arteries/diagnostic imaging MH - Carotid Artery Diseases/diagnostic imaging/*epidemiology MH - Carotid Intima-Media Thickness MH - Case-Control Studies MH - Chi-Square Distribution MH - Disease Progression MH - Female MH - Follow-Up Studies MH - Humans MH - Incidence MH - Italy/epidemiology MH - Kaplan-Meier Estimate MH - Linear Models MH - Logistic Models MH - Longitudinal Studies MH - Male MH - Middle Aged MH - Multivariate Analysis MH - Non-alcoholic Fatty Liver Disease/diagnosis/*epidemiology MH - Odds Ratio MH - Plaque, Atherosclerotic MH - Proportional Hazards Models MH - Prospective Studies MH - Risk Assessment MH - Risk Factors MH - Time Factors OTO - NOTNLM OT - Cardiovascular events OT - Carotid plaques OT - Intima-media thickness OT - NAFLD OT - NASH EDAT- 2016/01/25 06:00 MHDA- 2016/12/15 06:00 CRDT- 2016/01/25 06:00 PHST- 2015/09/04 00:00 [received] PHST- 2015/12/27 00:00 [revised] PHST- 2016/01/09 00:00 [accepted] PHST- 2016/01/25 06:00 [entrez] PHST- 2016/01/25 06:00 [pubmed] PHST- 2016/12/15 06:00 [medline] AID - S0021-9150(16)30016-8 [pii] AID - 10.1016/j.atherosclerosis.2016.01.016 [doi] PST - ppublish SO - Atherosclerosis. 2016 Mar;246:208-13. doi: 10.1016/j.atherosclerosis.2016.01.016. Epub 2016 Jan 12. PMID- 26946077 OWN - NLM STAT- MEDLINE DCOM- 20161219 LR - 20171116 IS - 1932-8737 (Electronic) IS - 0160-9289 (Linking) VI - 39 IP - 3 DP - 2016 Mar TI - Comparison of PCSK9 Inhibitor Evolocumab vs Ezetimibe in Statin-Intolerant Patients: Design of the Goal Achievement After Utilizing an Anti-PCSK9 Antibody in Statin-Intolerant Subjects 3 (GAUSS-3) Trial. PG - 137-44 LID - 10.1002/clc.22518 [doi] AB - Statins are the accepted standard for lowering low-density lipoprotein cholesterol (LDL-C). However, 5% to 10% of statin-treated patients report intolerance, mostly due to muscle-related adverse effects. Challenges exist to objective identification of statin-intolerant patients. Evolocumab is a monoclonal antibody that binds proprotein convertase subtilisin/kexin type 9 (PCSK9), resulting in marked LDL-C reduction. We report the design of Goal Achievement After Utilizing an Anti-PCSK9 Antibody in Statin-Intolerant Subjects 3 (GAUSS-3), a phase 3, multicenter, randomized, double-blind, ezetimibe-controlled study to compare effectiveness of 24 weeks of evolocumab 420 mg monthly vs ezetimibe 10 mg daily in hypercholesterolemic patients unable to tolerate an effective statin dose. The study incorporates a novel atorvastatin-controlled, double-blind, crossover phase to objectively identify statin intolerance. Eligible patients had LDL-C above the National Cholesterol Education Project Adult Treatment Panel III target level for the appropriate coronary heart disease risk category and were unable to tolerate >/=3 statins or 2 statins (one of which was atorvastatin /=3% 10-year risk of fatal CVD according to European guidelines, and/or >/=10% 10-year risk of fatal + non-fatal CHD according to US guidelines. As a secondary priority after LDL-cholesterol reduction, we recommend a desirable level for Lp(a) <80th percentile (less than approximately 50 mg/dL). Treatment should primarily be niacin 1-3 g/day, as a meta-analysis of randomized, controlled intervention trials demonstrates reduced CVD by niacin treatment. In extreme cases, LDL-apheresis is efficacious in removing Lp(a). CONCLUSION: We recommend screening for elevated Lp(a) in those at intermediate or high CVD/CHD risk, a desirable level <50 mg/dL as a function of global cardiovascular risk, and use of niacin for Lp(a) and CVD/CHD risk reduction. FAU - Nordestgaard, Borge G AU - Nordestgaard BG AD - Department of Clinical Biochemistry, Herlev Hospital, Copenhagen University Hospital, University of Copenhagen, DK-2730 Herlev, Denmark. brno@heh.regionh.dk FAU - Chapman, M John AU - Chapman MJ FAU - Ray, Kausik AU - Ray K FAU - Boren, Jan AU - Boren J FAU - Andreotti, Felicita AU - Andreotti F FAU - Watts, Gerald F AU - Watts GF FAU - Ginsberg, Henry AU - Ginsberg H FAU - Amarenco, Pierre AU - Amarenco P FAU - Catapano, Alberico AU - Catapano A FAU - Descamps, Olivier S AU - Descamps OS FAU - Fisher, Edward AU - Fisher E FAU - Kovanen, Petri T AU - Kovanen PT FAU - Kuivenhoven, Jan Albert AU - Kuivenhoven JA FAU - Lesnik, Philippe AU - Lesnik P FAU - Masana, Luis AU - Masana L FAU - Reiner, Zeljko AU - Reiner Z FAU - Taskinen, Marja-Riitta AU - Taskinen MR FAU - Tokgozoglu, Lale AU - Tokgozoglu L FAU - Tybjaerg-Hansen, Anne AU - Tybjaerg-Hansen A CN - European Atherosclerosis Society Consensus Panel LA - eng GR - R01 HL073030/HL/NHLBI NIH HHS/United States PT - Consensus Development Conference PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20101021 PL - England TA - Eur Heart J JT - European heart journal JID - 8006263 RN - 0 (Lipoprotein(a)) SB - IM MH - Age Factors MH - Animals MH - Cardiovascular Diseases/*blood/genetics/prevention & control MH - Coronary Disease/blood/genetics/prevention & control MH - Early Diagnosis MH - Female MH - Humans MH - Hyperlipoproteinemias/*diagnosis/genetics/therapy MH - Immunoassay/methods MH - Lipoprotein(a)/*blood/genetics MH - Male MH - Mice MH - Mice, Transgenic MH - Patient Selection MH - Risk Factors MH - Sex Factors PMC - PMC3295201 EDAT- 2010/10/23 06:00 MHDA- 2011/07/16 06:00 CRDT- 2010/10/23 06:00 PHST- 2010/10/23 06:00 [entrez] PHST- 2010/10/23 06:00 [pubmed] PHST- 2011/07/16 06:00 [medline] AID - ehq386 [pii] AID - 10.1093/eurheartj/ehq386 [doi] PST - ppublish SO - Eur Heart J. 2010 Dec;31(23):2844-53. doi: 10.1093/eurheartj/ehq386. Epub 2010 Oct 21. PMID- 20678595 OWN - NLM STAT- MEDLINE DCOM- 20110510 LR - 20100924 IS - 1873-0183 (Electronic) IS - 1568-9972 (Linking) VI - 9 IP - 12 DP - 2010 Oct TI - From endothelial dysfunction to atherosclerosis. PG - 830-4 LID - 10.1016/j.autrev.2010.07.016 [doi] AB - It has recently emerged that endothelial dysfunction is an early step in the development of atherosclerosis and is mainly characterised by a reduction in the bioavailability of nitric oxide. All of the traditional cardiovascular (CV) risk factors (dyslipidemia, arterial hypertension, hyperglycemia and diabetes) are associated with endothelial dysfunction, and oxidised low-density lipoproteins, the renin-angiotensin axis and insulin resistance play important roles in the pathogenesis of impaired endothelial function. The increased expression of adhesion molecules and pro-inflammatory cytokines leads to abnormal endothelium-dependent vasodilation which could be investigated using vasoreactivity tests such as flow-mediated dilation in the brachial artery. Recently, new evidences showed that the immune system plays an important role in the pathogenesis of endothelial dysfunction and atherosclerosis with a particular regard towards autoimmunity. The high prevalence of the atherosclerotic process in systemic autoimmune diseases supports the hypothesis of the immune pathogenesis. Evaluating coronary microvascular dysfunction by means of transthoracic echocardiography with non-invasive coronary flow reserve assessment is particularly interesting as it could detect preclinical impairment of coronary microvascular function. The discovery that the mechanisms responsible for endothelial damage have a genetic basis could improve the approach to CV diseases. This review summarises the most important aspects of the pathogenesis and development of endothelial dysfunction, with particular attention to the role of traditional CV risk factors, the usefulness of vasoreactivity tests, and the future perspectives opened by genetic studies. CI - Copyright (c) 2010 Elsevier B.V. All rights reserved. FAU - Sitia, S AU - Sitia S AD - IRCCS Galeazzi Orthopedic Institute, Department of Health Technologies, Universita di Milano, Milan, Italy. FAU - Tomasoni, L AU - Tomasoni L FAU - Atzeni, F AU - Atzeni F FAU - Ambrosio, G AU - Ambrosio G FAU - Cordiano, C AU - Cordiano C FAU - Catapano, A AU - Catapano A FAU - Tramontana, S AU - Tramontana S FAU - Perticone, F AU - Perticone F FAU - Naccarato, P AU - Naccarato P FAU - Camici, P AU - Camici P FAU - Picano, E AU - Picano E FAU - Cortigiani, L AU - Cortigiani L FAU - Bevilacqua, M AU - Bevilacqua M FAU - Milazzo, L AU - Milazzo L FAU - Cusi, D AU - Cusi D FAU - Barlassina, C AU - Barlassina C FAU - Sarzi-Puttini, P AU - Sarzi-Puttini P FAU - Turiel, M AU - Turiel M LA - eng PT - Journal Article PT - Review DEP - 20100730 PL - Netherlands TA - Autoimmun Rev JT - Autoimmunity reviews JID - 101128967 RN - 0 (Calmodulin-Binding Proteins) RN - 0 (adducin) SB - IM MH - Animals MH - Atherosclerosis/diagnosis/*immunology/pathology/physiopathology MH - *Autoimmunity MH - Calmodulin-Binding Proteins/genetics/metabolism MH - Coronary Vessels/*metabolism/pathology/surgery MH - Echocardiography MH - Endothelium, Vascular/*immunology/pathology MH - Genetic Predisposition to Disease MH - Humans MH - Hypertension/genetics MH - Laser-Doppler Flowmetry MH - Polymorphism, Genetic MH - Renin-Angiotensin System/*immunology MH - Risk EDAT- 2010/08/04 06:00 MHDA- 2011/05/11 06:00 CRDT- 2010/08/04 06:00 PHST- 2010/07/24 00:00 [accepted] PHST- 2010/08/04 06:00 [entrez] PHST- 2010/08/04 06:00 [pubmed] PHST- 2011/05/11 06:00 [medline] AID - S1568-9972(10)00154-0 [pii] AID - 10.1016/j.autrev.2010.07.016 [doi] PST - ppublish SO - Autoimmun Rev. 2010 Oct;9(12):830-4. doi: 10.1016/j.autrev.2010.07.016. Epub 2010 Jul 30. PMID- 18004690 OWN - NLM STAT- MEDLINE DCOM- 20081216 LR - 20080722 IS - 0172-4622 (Print) IS - 0172-4622 (Linking) VI - 29 IP - 8 DP - 2008 Aug TI - Side effects of anabolic androgenic steroids abuse. PG - 679-87 AB - Long-term side effects of high doses of anabolic androgenic steroids self-administration were evaluated in this study. Twenty male bodybuilders, voluntarily starting steroid self-administration, were followed every 6 months over 2 years. Physical examination, haematological, metabolic and endocrine variables, semen analysis, hepatic and prostate ultrasound and echocardiographic evaluations were performed. LH values (baseline 3.43 +/- 1.75) were suppressed at 18 (1.98 +/- 1.99) (p = 0.026) and 24 (2.43 +/- 2.17) (p = 0.026), and FSH (3.95 +/- 2.01) at 6 (3.01 +/- 2.16) (p = 0.031), 12 (2.45 +/- 2.54) (p = 0.029), 18 (2.02 +/- 2.29) (p = 0.032) and 24 (3.42 +/- 2.64) (p = 0.032) months and SHBG (34.11 +/- 10.88) values significantly lowered at 12 (24.81 +/- 12.49) (p < 0.05), 18 (21.28 +/- 11.15) (p < 0.01), 24 months (25.42 +/- 11.16) (p < 0.01). A significant decrease in spermatozoa count (p < 0.01), and fertility index (p = 0.01) occurred. HDL-cholesterol (baseline 56.94 +/- 13.54) was reduced at 18 (41.86 +/- 14.17) (p < 0.01) and 24 (43.82 +/- 18.67) (p < 0.05) months and Apo A-1 at 12 (p < 0.001), 18 (p = 0.05) and 24 (p = 0.05) months. The most important long-term adverse effects were lower fertility and the impairment of lipid profile associated with an increased cardiovascular risk. FAU - Bonetti, A AU - Bonetti A AD - Department of Clinical Science, Curriculum of Sports Science and Physical Exercise, University of Parma, Parma, Italy. antonio.bonetti@unipr.it FAU - Tirelli, F AU - Tirelli F FAU - Catapano, A AU - Catapano A FAU - Dazzi, D AU - Dazzi D FAU - Dei Cas, A AU - Dei Cas A FAU - Solito, F AU - Solito F FAU - Ceda, G AU - Ceda G FAU - Reverberi, C AU - Reverberi C FAU - Monica, C AU - Monica C FAU - Pipitone, S AU - Pipitone S FAU - Elia, G AU - Elia G FAU - Spattini, M AU - Spattini M FAU - Magnati, G AU - Magnati G LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20071114 PL - Germany TA - Int J Sports Med JT - International journal of sports medicine JID - 8008349 RN - 0 (Anabolic Agents) RN - 0 (Androgens) SB - IM MH - Adult MH - Anabolic Agents/administration & dosage/*adverse effects MH - Analysis of Variance MH - Androgens/administration & dosage/*adverse effects MH - Chi-Square Distribution MH - Humans MH - Male MH - Risk Factors MH - Self Administration MH - Statistics, Nonparametric MH - *Weight Lifting EDAT- 2007/11/16 09:00 MHDA- 2008/12/17 09:00 CRDT- 2007/11/16 09:00 PHST- 2007/11/16 09:00 [pubmed] PHST- 2008/12/17 09:00 [medline] PHST- 2007/11/16 09:00 [entrez] AID - 10.1055/s-2007-965808 [doi] PST - ppublish SO - Int J Sports Med. 2008 Aug;29(8):679-87. doi: 10.1055/s-2007-965808. Epub 2007 Nov 14. PMID- 18258418 OWN - NLM STAT- MEDLINE DCOM- 20080320 LR - 20171116 IS - 1590-3729 (Electronic) IS - 0939-4753 (Linking) VI - 18 IP - 2 DP - 2008 Feb TI - Non-pharmacological control of plasma cholesterol levels. PG - S1-16 LID - 10.1016/j.numecd.2007.10.004 [doi] AB - The importance of non-pharmacological control of plasma cholesterol levels in the population is increasing, along with the number of subjects whose plasma lipid levels are non-optimal, or frankly elevated, according to international guidelines. In this context, a panel of experts, organized and coordinated by the Nutrition Foundation of Italy, has evaluated the nutritional and lifestyle interventions to be adopted in the control of plasma cholesterol levels (and specifically of LDL cholesterol levels). This Consensus document summarizes the view of the panel on this topic, with the aim to provide an updated support to clinicians and other health professionals involved in cardiovascular prevention. FAU - Poli, Andrea AU - Poli A AD - Nutrition Foundation of Italy, Italy. FAU - Marangoni, Franca AU - Marangoni F FAU - Paoletti, Rodolfo AU - Paoletti R FAU - Mannarino, Elmo AU - Mannarino E FAU - Lupattelli, Graziana AU - Lupattelli G FAU - Notarbartolo, Alberto AU - Notarbartolo A FAU - Aureli, Paolo AU - Aureli P FAU - Bernini, Franco AU - Bernini F FAU - Cicero, Arrigo AU - Cicero A FAU - Gaddi, Antonio AU - Gaddi A FAU - Catapano, Alberico AU - Catapano A FAU - Cricelli, Claudio AU - Cricelli C FAU - Gattone, Marinella AU - Gattone M FAU - Marrocco, Walter AU - Marrocco W FAU - Porrini, Marisa AU - Porrini M FAU - Stella, Roberto AU - Stella R FAU - Vanotti, Alfredo AU - Vanotti A FAU - Volpe, Massimo AU - Volpe M FAU - Volpe, Roberto AU - Volpe R FAU - Cannella, Carlo AU - Cannella C FAU - Pinto, Alessandro AU - Pinto A FAU - Del Toma, Eugenio AU - Del Toma E FAU - La Vecchia, Carlo AU - La Vecchia C FAU - Tavani, Alessandra AU - Tavani A FAU - Manzato, Enzo AU - Manzato E FAU - Riccardi, Gabriele AU - Riccardi G FAU - Sirtori, Cesare AU - Sirtori C FAU - Zambon, Alberto AU - Zambon A CN - Nutrition Foundation of Italy LA - eng PT - Journal Article PT - Practice Guideline DEP - 20080207 PL - Netherlands TA - Nutr Metab Cardiovasc Dis JT - Nutrition, metabolism, and cardiovascular diseases : NMCD JID - 9111474 RN - 0 (Cholesterol, Dietary) RN - 0 (Cholesterol, LDL) RN - 0 (Dietary Carbohydrates) RN - 0 (Dietary Fats) RN - 0 (Dietary Fiber) RN - 0 (Fatty Acids) RN - 0 (Fatty Acids, Monounsaturated) RN - 0 (Fatty Acids, Omega-3) RN - 0 (Fatty Acids, Omega-6) RN - 0 (Micronutrients) RN - 0 (Phytosterols) RN - 0 (Soybean Proteins) RN - 0 (Trans Fatty Acids) RN - 97C5T2UQ7J (Cholesterol) SB - IM MH - Cardiovascular Diseases/blood/etiology/physiopathology/*prevention & control MH - Cholesterol/*blood MH - Cholesterol, Dietary/administration & dosage MH - Cholesterol, LDL/blood MH - Diet, Mediterranean MH - Dietary Carbohydrates/administration & dosage MH - Dietary Fats/*administration & dosage MH - Dietary Fiber/administration & dosage MH - Evidence-Based Medicine MH - *Exercise MH - Fatty Acids/administration & dosage MH - Fatty Acids, Monounsaturated/administration & dosage MH - Fatty Acids, Omega-3/administration & dosage MH - Fatty Acids, Omega-6/administration & dosage MH - Female MH - Humans MH - Hypercholesterolemia/blood/complications/*diet therapy/physiopathology MH - *Life Style MH - Male MH - Micronutrients/administration & dosage MH - *Nutritional Physiological Phenomena MH - Osteoporosis, Postmenopausal/prevention & control MH - Phytosterols/administration & dosage MH - Soybean Proteins/administration & dosage MH - Trans Fatty Acids/administration & dosage MH - *Weight Loss EDAT- 2008/02/09 09:00 MHDA- 2008/03/21 09:00 CRDT- 2008/02/09 09:00 PHST- 2007/06/27 00:00 [received] PHST- 2007/10/24 00:00 [revised] PHST- 2007/10/25 00:00 [accepted] PHST- 2008/02/09 09:00 [pubmed] PHST- 2008/03/21 09:00 [medline] PHST- 2008/02/09 09:00 [entrez] AID - S0939-4753(07)00187-1 [pii] AID - 10.1016/j.numecd.2007.10.004 [doi] PST - ppublish SO - Nutr Metab Cardiovasc Dis. 2008 Feb;18(2):S1-16. doi: 10.1016/j.numecd.2007.10.004. Epub 2008 Feb 7. PMID- 18187076 OWN - NLM STAT- MEDLINE DCOM- 20080124 LR - 20161124 IS - 1555-7162 (Electronic) IS - 0002-9343 (Linking) VI - 121 IP - 1 DP - 2008 Jan TI - Carotid artery intima-media thickness in nonalcoholic fatty liver disease. PG - 72-8 LID - 10.1016/j.amjmed.2007.08.041 [doi] AB - PURPOSE: To evaluate, in patients with nonalcoholic fatty liver disease with no or mild alterations of liver function tests, carotid artery intima-media thickness and the presence of plaques and to define determinants of vascular damage. METHODS: A paired-sample case-control study: 125 patients with nonalcoholic fatty liver disease and 250 controls, without a prior diagnosis of diabetes, hypertension, and cardiovascular disease, matched for sex, age, and body mass index. B-mode ultrasound was used for evaluation of carotid intima-media thickness and presence of small plaques. RESULTS: A significant difference in mean values of intima-media thickness (0.89+/-0.26 and 0.64+/-0.14 mm, P = .0001) and prevalence of plaques (26 [21%] and 15 [6%], P < .001) was observed in nonalcoholic fatty liver disease patients and controls. Variables significantly associated with intima-media thickness higher than 0.64 mm (median value in controls), in both patients and controls were: age (P = .0001), systolic blood pressure (P = .004), total and low-density lipoprotein cholesterol (P < or = .02 and P = .01, respectively), fasting glucose (P = .0001), and cardiovascular risk (P = .0001) and, only in controls, metabolic syndrome (P = .0001), HOMA-insulin resistance (P = .01), and body mass index (P = .0003). At multivariate logistic regression performed in the overall series of subjects, independent risk predictors of intima-media thickness higher than 0.64 mm were presence of steatosis (odds ratio [OR] = 6.9), age (OR 6.0), and systolic blood pressure (OR 2.3). CONCLUSION: Patients with nonalcoholic fatty liver disease, even with no or mild alterations of liver tests, should be considered at high risk for cardiovascular complications. FAU - Fracanzani, Anna Ludovica AU - Fracanzani AL AD - Centro Malattie Metaboliche del Fegato, Dipartimento Medicina Interna, Universita di Milano, Milano, Italy. FAU - Burdick, Larry AU - Burdick L FAU - Raselli, Sara AU - Raselli S FAU - Pedotti, Paola AU - Pedotti P FAU - Grigore, Liliana AU - Grigore L FAU - Santorelli, Gennaro AU - Santorelli G FAU - Valenti, Luca AU - Valenti L FAU - Maraschi, Alessandra AU - Maraschi A FAU - Catapano, Alberico AU - Catapano A FAU - Fargion, Silvia AU - Fargion S LA - eng PT - Comparative Study PT - Journal Article PT - Research Support, Non-U.S. Gov't PL - United States TA - Am J Med JT - The American journal of medicine JID - 0267200 SB - AIM SB - IM MH - Biopsy MH - Carotid Artery, Common/*diagnostic imaging MH - Fatty Liver/blood/*diagnosis MH - Female MH - Follow-Up Studies MH - Humans MH - Male MH - Middle Aged MH - Prognosis MH - Retrospective Studies MH - Risk Factors MH - Severity of Illness Index MH - Tunica Intima/*diagnostic imaging MH - Ultrasonography EDAT- 2008/01/12 09:00 MHDA- 2008/01/25 09:00 CRDT- 2008/01/12 09:00 PHST- 2007/03/16 00:00 [received] PHST- 2007/08/18 00:00 [revised] PHST- 2007/08/20 00:00 [accepted] PHST- 2008/01/12 09:00 [pubmed] PHST- 2008/01/25 09:00 [medline] PHST- 2008/01/12 09:00 [entrez] AID - S0002-9343(07)00976-X [pii] AID - 10.1016/j.amjmed.2007.08.041 [doi] PST - ppublish SO - Am J Med. 2008 Jan;121(1):72-8. doi: 10.1016/j.amjmed.2007.08.041. PMID- 16004682 OWN - NLM STAT- MEDLINE DCOM- 20050926 LR - 20151119 IS - 0300-7995 (Print) IS - 0300-7995 (Linking) VI - 21 IP - 7 DP - 2005 Jul TI - Lipid altering-efficacy of ezetimibe co-administered with simvastatin compared with rosuvastatin: a meta-analysis of pooled data from 14 clinical trials. PG - 1123-30 AB - OBJECTIVE: Results of direct comparative studies between ezetimibe/simvastatin and rosuvastatin therapies have not been reported. Both of these treatment options offer significant reductions in LDL-C. To evaluate the lipid efficacy of each of these therapies relative to each other, a meta-analysis of data from 14 randomized, double-blind clinical trials that compared the effectiveness of two new options for cholesterol lowering was performed. DATA SOURCES: PubMed, EMBASE and BIOSIS databases were searched up to March 14, 2004. METHODS OF STUDY SELECTION: Efficacy results from clinical trials with the co-administration of ezetimibe 10 mg with simvastatin or with the ezetimibe/simvastatin combination product (ezetimibe/simvastatin 10/10 mg, 10/20 mg, 10/40 mg, and 10/80 mg) were compared with efficacy results from clinical trials of rosuvastatin 5 mg, 10 mg, 20 mg, and 40 mg in patients with primary hypercholesterolemia. Trials in healthy patients, heterozygous familial hypercholesterolemia or combined hyperlipidemia, and pharmacokinetic trials were excluded. DATA EXTRACTION AND SYNTHESIS: This analysis used pooled data for LDL-C, HDL-C, non-HDL-C, triglycerides, total cholesterol, apolipoprotein (apo) A-I, and apo B for the two therapies at their lowest doses (ezetimibe/simvastatin 10/10 mg and rosuvastatin 5 mg) through their highest doses (ezetimibe/simvastatin 10/80 mg and rosuvastatin 40 mg), and estimated within-treatment percentage changes in these parameters. Percentage reductions from baseline in LDL-C for the pooled data were 46.2% and 41.8% for ezetimibe/simvastatin 10/10 mg and rosuvastatin 5 mg, respectively; 50.6% and 47.4% for ezetimibe/simvastatin 10/20 mg and rosuvastatin 10 mg, respectively; 55.9% and 52.1% for ezetimibe/simvastatin 10/40 mg and rosuvastatin 20 mg, respectively; and 59.7% and 58.5% for ezetimibe/simvastatin 10/80 mg and rosuvastatin 40 mg, respectively. CONCLUSIONS: The results of this meta-analysis suggest greater LDL-C lowering with ezetimibe/simvastatin compared with rosuvastatin. These results need to be confirmed in a head-to-head comparison of both therapies. FAU - Catapano, Alberico AU - Catapano A AD - Marie Curie Training Centre for Cardiovascular Diseases, Milan, Italy. Alberico.Carapano@unimi.it FAU - Brady, William E AU - Brady WE FAU - King, Thomas R AU - King TR FAU - Palmisano, Joanne AU - Palmisano J LA - eng PT - Comparative Study PT - Journal Article PT - Meta-Analysis PT - Research Support, Non-U.S. Gov't PL - England TA - Curr Med Res Opin JT - Current medical research and opinion JID - 0351014 RN - 0 (Anticholesteremic Agents) RN - 0 (Azetidines) RN - 0 (Cholesterol, LDL) RN - 0 (Fluorobenzenes) RN - 0 (Pyrimidines) RN - 0 (Sulfonamides) RN - 83MVU38M7Q (Rosuvastatin Calcium) RN - AGG2FN16EV (Simvastatin) RN - EOR26LQQ24 (Ezetimibe) SB - IM MH - Anticholesteremic Agents/administration & dosage/pharmacokinetics/*therapeutic use MH - Azetidines/administration & dosage/pharmacokinetics/*therapeutic use MH - Cholesterol, LDL/blood MH - Clinical Trials as Topic MH - Drug Therapy, Combination MH - Ezetimibe MH - Fluorobenzenes/administration & dosage/pharmacokinetics/*therapeutic use MH - Humans MH - Hypercholesterolemia/*drug therapy MH - Pyrimidines/administration & dosage/pharmacokinetics/*therapeutic use MH - Rosuvastatin Calcium MH - Simvastatin/administration & dosage/pharmacokinetics/*therapeutic use MH - Sulfonamides/administration & dosage/pharmacokinetics/*therapeutic use MH - Treatment Outcome EDAT- 2005/07/12 09:00 MHDA- 2005/09/27 09:00 CRDT- 2005/07/12 09:00 PHST- 2005/07/12 09:00 [pubmed] PHST- 2005/09/27 09:00 [medline] PHST- 2005/07/12 09:00 [entrez] AID - 10.1185/030079905X50642 [doi] PST - ppublish SO - Curr Med Res Opin. 2005 Jul;21(7):1123-30. doi: 10.1185/030079905X50642. PMID- 15591215 OWN - NLM STAT- MEDLINE DCOM- 20050802 LR - 20161124 IS - 1524-4636 (Electronic) IS - 1079-5642 (Linking) VI - 25 IP - 2 DP - 2005 Feb TI - Inherited apolipoprotein A-V deficiency in severe hypertriglyceridemia. PG - 411-7 AB - OBJECTIVE: Mutations in LPL or APOC2 genes are recognized causes of inherited forms of severe hypertriglyceridemia. However, some hypertrigliceridemic patients do not have mutations in either of these genes. Because inactivation or hyperexpression of APOA5 gene, encoding apolipoprotein A-V (apoA-V), causes a marked increase or decrease of plasma triglycerides in mice, and because some common polymorphisms of this gene affect plasma triglycerides in humans, we have hypothesized that loss of function mutations in APOA5 gene might cause hypertriglyceridemia. METHODS AND RESULTS: We sequenced APOA5 gene in 10 hypertriglyceridemic patients in whom mutations in LPL and APOC2 genes had been excluded. One of them was found to be homozygous for a mutation in APOA5 gene (c.433 C>T, Q145X), predicted to generate a truncated apoA-V devoid of key functional domains. The plasma of this patient was found to activate LPL in vitro less efficiently than control plasma, thus suggesting that apoA-V might be an activator of LPL. Ten carriers of Q145X mutation were found in the patient's family; 5 of them had mild hypertriglyceridemia. CONCLUSIONS: As predicted from animal studies, apoA-V deficiency is associated with severe hypertriglyceridemia in humans. This observation suggests that apoA-V regulates the secretion and/or catabolism of triglyceride-rich lipoproteins. Mutations in APOA5 gene might be the cause of severe hypertriglyceridemia in subjects in whom mutations in LPL or APOC2 genes have been excluded. We detected a nonsense mutation in APOA5 gene (Q145X) in a boy with hyperchylomicronemia syndrome. This is the first observation of a complete apoA-V deficiency in humans. FAU - Priore Oliva, Claudio AU - Priore Oliva C AD - Department of Biomedical Sciences, University of Modena and Reggio Emilia, Italy. FAU - Pisciotta, Livia AU - Pisciotta L FAU - Li Volti, Giovanni AU - Li Volti G FAU - Sambataro, Maria Paola AU - Sambataro MP FAU - Cantafora, Alfredo AU - Cantafora A FAU - Bellocchio, Antonella AU - Bellocchio A FAU - Catapano, Alberico AU - Catapano A FAU - Tarugi, Patrizia AU - Tarugi P FAU - Bertolini, Stefano AU - Bertolini S FAU - Calandra, Sebastiano AU - Calandra S LA - eng PT - Case Reports PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20041209 PL - United States TA - Arterioscler Thromb Vasc Biol JT - Arteriosclerosis, thrombosis, and vascular biology JID - 9505803 RN - 0 (APOA5 protein, human) RN - 0 (Apolipoprotein A-V) RN - 0 (Apolipoproteins) RN - 0 (Apolipoproteins A) RN - 0 (Fatty Acids, Omega-3) RN - 0 (Lipids) RN - 0 (Lipoproteins) RN - 0 (RNA, Messenger) RN - EC 3.1.1.34 (Lipoprotein Lipase) SB - IM MH - Amino Acid Substitution MH - Apolipoprotein A-V MH - Apolipoproteins/blood/*deficiency/genetics MH - Apolipoproteins A MH - Child MH - Consanguinity MH - DNA Mutational Analysis MH - Enzyme Activation MH - Exons/genetics MH - Fatty Acids, Omega-3/therapeutic use MH - Genotype MH - Humans MH - Hyperlipoproteinemia Type IV/blood/drug therapy/*genetics MH - Italy MH - Lipids/blood MH - Lipoprotein Lipase/blood MH - Lipoproteins/blood MH - Male MH - *Mutation, Missense MH - Pedigree MH - *Point Mutation MH - RNA, Messenger/biosynthesis/genetics MH - Tunisia/ethnology EDAT- 2004/12/14 09:00 MHDA- 2005/08/03 09:00 CRDT- 2004/12/14 09:00 PHST- 2004/12/14 09:00 [pubmed] PHST- 2005/08/03 09:00 [medline] PHST- 2004/12/14 09:00 [entrez] AID - 01.ATV.0000153087.36428.dd [pii] AID - 10.1161/01.ATV.0000153087.36428.dd [doi] PST - ppublish SO - Arterioscler Thromb Vasc Biol. 2005 Feb;25(2):411-7. doi: 10.1161/01.ATV.0000153087.36428.dd. Epub 2004 Dec 9. PMID- 15576637 OWN - NLM STAT- MEDLINE DCOM- 20050802 LR - 20161124 IS - 1524-4636 (Electronic) IS - 1079-5642 (Linking) VI - 25 IP - 2 DP - 2005 Feb TI - Acute effect of high-fat meal on endothelial function in moderately dyslipidemic subjects. PG - 406-10 AB - OBJECTIVE: Hypercholesterolemia markedly impairs endothelial function. Whether this is the case for hypertriglyceridemia is less clear, however, and limited evidence exists on the effect of an acute increase in triglyceridemia caused by a high-fat meal. METHODS AND RESULTS: In 16 normotensive subjects with an untreated mild hypertriglyceridemia and dyslipidemia and in 7 normal controls, we measured radial artery diameter and blood flow by an echo-tracking device (NIUS02). Data were obtained at baseline, at the release of a 4-minute ischemia of the hand, which causes an increase in arterial diameter dependent on nitric oxide (NO) secretion, and at the release of a 12-minute exclusion of the arm by an arm cuff to obtain a larger increase in arterial diameter mainly of nonendothelial nature. Measurements were performed before and 6 hours after a high-fat meal (680 kcal/m(2) body surface; 82% lipids). In mild dyslipidemic hypertriglyceridemic subjects, the high-fat meal did not alter baseline blood pressure (beat-to-beat finger measurement), heart rate, radial artery diameter, and blood flow. It also did not alter the increase in blood flow induced by the 4-minute ischemia (+42.7+/-10.4 and +43.7+/-10.4 mL/min), whereas it markedly attenuated the concomitant increase in arterial diameter (+0.31+/-0.06 versus 0.13+/-0.06 mm; P<0.05). The alteration of the diameter response did not correlate with changes in total cholesterol, but it showed a significant correlation with the increase in serum triglycerides induced by high-fat meal (r=0.49, P<0.05). This attenuation was not seen in control subjects and in subjects in whom measurements were repeated after a 6-hour observation period. It was also not paralleled by an alteration of the endothelially independent response to a 12-minute ischemia whose larger effects on arterial diameter and blood flow were similar before and after the high-fat meal. CONCLUSIONS: Endothelial function is markedly impaired by a high-fat meal that causes an acute hypertriglyceridemia. This impairment is evident in dyslipidemic patients with baseline hypertriglyceridemia but not in normotriglyceridemic controls. An oral fat load was administered to 55 HIV-positive and 10 HIV-negative individuals. Postprandial clearance of triglyceride-rich lipoproteins was delayed in HIV-positive individuals. Compared with HIV-positive subjects not on PIs, those taking PIs do not have increased postprandial triglyceride-rich lipoproteins but do have increased postprandial intermediate-density and low-density lipoproteins. Hypercholesterolemia impairs endothelial function, whereas the effect of hypertriglyceridemia is less clear. In normotensive subjects with an untreated hypertriglyceridemia and hypercholesterolemia, we measured endothelial function before and 6 hours after a high-fat meal. The results demonstrate that in moderately dyslipidemic patients, endothelial function is impaired by acute hypertriglyceridemia. FAU - Giannattasio, C AU - Giannattasio C AD - Clinica Medica, University of Milano-Bicocca and San Gerardo Hospital, Monza, Italy. FAU - Zoppo, A AU - Zoppo A FAU - Gentile, G AU - Gentile G FAU - Failla, M AU - Failla M FAU - Capra, A AU - Capra A FAU - Maggi, F M AU - Maggi FM FAU - Catapano, A AU - Catapano A FAU - Mancia, G AU - Mancia G LA - eng PT - Journal Article DEP - 20041202 PL - United States TA - Arterioscler Thromb Vasc Biol JT - Arteriosclerosis, thrombosis, and vascular biology JID - 9505803 RN - 0 (Dietary Fats) RN - 31C4KY9ESH (Nitric Oxide) SB - IM MH - Adult MH - Arm/blood supply MH - Blood Flow Velocity/drug effects MH - Blood Pressure/drug effects MH - Dietary Fats/administration & dosage/*adverse effects MH - Endothelium, Vascular/*drug effects/physiopathology MH - Female MH - Hand/blood supply MH - Heart Rate/drug effects MH - Humans MH - Hypercholesterolemia/physiopathology MH - Hypertriglyceridemia/*physiopathology MH - Ischemia/physiopathology MH - Male MH - Middle Aged MH - Nitric Oxide/physiology MH - Radial Artery/diagnostic imaging MH - Ultrasonography MH - Vasodilation/*drug effects EDAT- 2004/12/04 09:00 MHDA- 2005/08/03 09:00 CRDT- 2004/12/04 09:00 PHST- 2004/12/04 09:00 [pubmed] PHST- 2005/08/03 09:00 [medline] PHST- 2004/12/04 09:00 [entrez] AID - 01.ATV.0000152231.93590.17 [pii] AID - 10.1161/01.ATV.0000152231.93590.17 [doi] PST - ppublish SO - Arterioscler Thromb Vasc Biol. 2005 Feb;25(2):406-10. doi: 10.1161/01.ATV.0000152231.93590.17. Epub 2004 Dec 2. PMID- 14564675 OWN - NLM STAT- MEDLINE DCOM- 20031106 LR - 20181130 IS - 0026-0495 (Print) IS - 0026-0495 (Linking) VI - 52 IP - 10 DP - 2003 Oct TI - Effect of a standardized grape seed extract on low-density lipoprotein susceptibility to oxidation in heavy smokers. PG - 1250-7 AB - The aim of our study was to evaluate the effect of a standardized formulation of a polyphenolic extract of grapes (Leucoselect-Phytosome [LP]) on low-density lipoprotein (LDL) susceptibility to oxidation in a group of heavy smokers. A randomized, double-blind, crossover study was undertaken in 24 healthy male heavy smokers, aged > or = 50 years. Enrolled subjects were given 2 capsules twice daily for 4 weeks (phase 1). Each capsule contained 75 mg of a grape procyanidin extracts and soy-phosphatidlcholine or placebo consisiting of 75 mg lactose and soy-phosphatidlcholine. A wash out period of 3 weeks was then followed by 4 weeks of the opposite treatment (phase 2). Blood samples were taken at baseline and at the end of each phase and assayed for plasma lipids and LDL susceptibility to oxidation. Compliance was good, and no adverse effects were recorded. Subjects did not show significant modification of total cholesterol (TC), triglycerides (TG), high-density lipoprotein-cholesterol (HDL-C) and LDL-C during LP treatment. Among oxidative indices, thiobarbituric acid reactive substances (TBARS) concentration was significantly reduced in subjects taking LP (-14.7% +/- 21.1% v +5.0% +/- 18.1%, P <.01), and the lag phase prolonged (+15.4% +/- 24.4% v -0.1% +/- 16.0%, P <.05) compared with placebo and basal values. The antioxidant potential of grape seed extract polyphenols may prove effective in a model of oxidative stress (smoking); however more investigational data are needed before use in wider clinical settings. FAU - Vigna, Giovanni B AU - Vigna GB AD - Department of Clinical and Experimental Medicine, Section of Internal Medicine II, University of Ferrara, Ferrara, Italy. FAU - Costantini, Fabrizio AU - Costantini F FAU - Aldini, Giancarlo AU - Aldini G FAU - Carini, Marina AU - Carini M FAU - Catapano, Alberico AU - Catapano A FAU - Schena, Fabio AU - Schena F FAU - Tangerini, Arianna AU - Tangerini A FAU - Zanca, Rosanna AU - Zanca R FAU - Bombardelli, Egidio AU - Bombardelli E FAU - Morazzoni, Paolo AU - Morazzoni P FAU - Mezzetti, Andrea AU - Mezzetti A FAU - Fellin, Renato AU - Fellin R FAU - Maffei Facino, Roberto AU - Maffei Facino R LA - eng PT - Clinical Trial PT - Journal Article PT - Randomized Controlled Trial PL - United States TA - Metabolism JT - Metabolism: clinical and experimental JID - 0375267 RN - 0 (Antioxidants) RN - 0 (Biflavonoids) RN - 0 (Cholesterol, HDL) RN - 0 (Cholesterol, LDL) RN - 0 (Plant Extracts) RN - 0 (Proanthocyanidins) RN - 0 (Triglycerides) RN - 01YAE03M7J (beta Carotene) RN - 11103-57-4 (Vitamin A) RN - 36-88-4 (Carotenoids) RN - 4852-22-6 (procyanidin) RN - 8R1V1STN48 (Catechin) RN - R0ZB2556P8 (Tocopherols) RN - SB0N2N0WV6 (Lycopene) SB - IM MH - Antioxidants/administration & dosage/chemistry/*pharmacology MH - *Biflavonoids MH - Carotenoids/blood MH - Catechin/administration & dosage/chemistry/*pharmacology MH - Cholesterol, HDL/blood MH - Cholesterol, LDL/*blood MH - Cross-Over Studies MH - Double-Blind Method MH - Humans MH - Lycopene MH - Male MH - Middle Aged MH - Oxidation-Reduction MH - *Oxidative Stress MH - Plant Extracts/pharmacology MH - *Proanthocyanidins MH - Smoking/*blood MH - Time Factors MH - Tocopherols/blood MH - Treatment Outcome MH - Triglycerides/blood MH - Vitamin A/blood MH - *Vitis MH - beta Carotene/blood EDAT- 2003/10/18 05:00 MHDA- 2003/11/07 05:00 CRDT- 2003/10/18 05:00 PHST- 2003/10/18 05:00 [pubmed] PHST- 2003/11/07 05:00 [medline] PHST- 2003/10/18 05:00 [entrez] AID - S0026049503001926 [pii] PST - ppublish SO - Metabolism. 2003 Oct;52(10):1250-7. PMID- 12716811 OWN - NLM STAT- MEDLINE DCOM- 20031218 LR - 20081121 IS - 0149-5992 (Print) IS - 0149-5992 (Linking) VI - 26 IP - 5 DP - 2003 May TI - Effects of an automated electronic reminder in changing the antiplatelet drug-prescribing behavior among Italian general practitioners in diabetic patients: an intervention trial. PG - 1497-500 AB - OBJECTIVE: To evaluate whether an electronic reminder integrated into a routine computer system increases the use of antiplatelet drugs for diabetic patients among Italian general practitioners (GPs). RESEARCH DESIGN AND METHODS: A randomized controlled trial was carried out among 300 GPs and their patients selected from the Health Search Database. Among these, 150 GPs (intervention group) received instructions to activate an electronic reminder plus a letter summarizing the beneficial effects of antiplatelet drugs in diabetic patients with at least one additional cardiovascular risk factor ("high risk"), whereas the other 150 GPs (control group) received only the letter. The electronic reminder, integrated into a standard software system for the management of the daily clinical practice, was displayed when every participating GP opened the medical record of diabetic patients aged > or =30 years. Only high-risk diabetic patients were included in the analysis. Patients were considered under antiplatelet treatment if they received two or more prescriptions at baseline and during the follow-up. RESULTS: We selected 15,343 high-risk diabetic patients, 7,313 belonging to GPs of the control group and 8,030 belonging to GPs of the intervention group. Overall, 1,672 patients (22.9%) of the control group and 1,886 (23.5%) patients of the intervention group received antiplatelet drugs at baseline (P = N.S.). At the end of the follow-up, the number of treated patients was significantly increased in the intervention group (odds ratio 1.99, 95% CI 1.79-2.22) versus the control group. The effect of the electronic reminder was more relevant among those patients with one or more cardiovascular risk factors but without previous cardiovascular diseases (CVDs), compared with those with CVDs. CONCLUSIONS: These findings provide evidence for the effect of an electronic reminder in affecting the prescriptive behavior of GPs. FAU - Filippi, Alessandro AU - Filippi A AD - Italian College of General Practitioners, Florence, Italy. FAU - Sabatini, Andrea AU - Sabatini A FAU - Badioli, Letizia AU - Badioli L FAU - Samani, Fabio AU - Samani F FAU - Mazzaglia, Giampiero AU - Mazzaglia G FAU - Catapano, Alberico AU - Catapano A FAU - Cricelli, Claudio AU - Cricelli C LA - eng PT - Clinical Trial PT - Journal Article PT - Multicenter Study PT - Randomized Controlled Trial PL - United States TA - Diabetes Care JT - Diabetes care JID - 7805975 RN - 0 (Platelet Aggregation Inhibitors) SB - IM MH - Adult MH - Aged MH - Automation/methods MH - Cardiovascular Diseases/drug therapy/epidemiology MH - Databases, Factual MH - Diabetic Angiopathies/*drug therapy MH - *Drug Prescriptions MH - Electronics MH - Family Practice MH - Female MH - Follow-Up Studies MH - Humans MH - Hypertension/drug therapy/epidemiology MH - Italy MH - Male MH - Middle Aged MH - *Patient Compliance MH - Platelet Aggregation Inhibitors/*administration & dosage/*therapeutic use MH - Risk Factors MH - Time Factors EDAT- 2003/04/30 05:00 MHDA- 2003/12/19 05:00 CRDT- 2003/04/30 05:00 PHST- 2003/04/30 05:00 [pubmed] PHST- 2003/12/19 05:00 [medline] PHST- 2003/04/30 05:00 [entrez] PST - ppublish SO - Diabetes Care. 2003 May;26(5):1497-500. PMID- 12583967 OWN - NLM STAT- MEDLINE DCOM- 20030321 LR - 20150616 IS - 0140-6736 (Print) IS - 0140-6736 (Linking) VI - 361 IP - 9356 DP - 2003 Feb 8 TI - Heart Protection Study. PG - 528; author reply 529-30 FAU - Poli, Andrea AU - Poli A FAU - Catapano, Alberico AU - Catapano A LA - eng PT - Comment PT - Letter PL - England TA - Lancet JT - Lancet (London, England) JID - 2985213R RN - 0 (Cholesterol, LDL) RN - AGG2FN16EV (Simvastatin) SB - AIM SB - IM CON - Lancet. 2002 Jul 6;360(9326):7-22. PMID: 12114036 MH - Cholesterol, LDL/blood MH - Coronary Disease/blood/*drug therapy MH - Data Interpretation, Statistical MH - Humans MH - Hypercholesterolemia/blood/*drug therapy MH - Randomized Controlled Trials as Topic/statistics & numerical data MH - Risk MH - Simvastatin/*therapeutic use EDAT- 2003/02/14 04:00 MHDA- 2003/03/22 04:00 CRDT- 2003/02/14 04:00 PHST- 2003/02/14 04:00 [pubmed] PHST- 2003/03/22 04:00 [medline] PHST- 2003/02/14 04:00 [entrez] AID - S0140-6736(03)12473-7 [pii] AID - 10.1016/S0140-6736(03)12473-7 [doi] PST - ppublish SO - Lancet. 2003 Feb 8;361(9356):528; author reply 529-30. doi: 10.1016/S0140-6736(03)12473-7. PMID- 10436249 OWN - NLM STAT- MEDLINE DCOM- 20000405 LR - 20131121 IS - 0940-5429 (Print) IS - 0940-5429 (Linking) VI - 36 IP - 1-2 DP - 1999 Jun TI - The effect of gemfibrozil on lipid profile and glucose metabolism in hypertriglyceridaemic well-controlled non-insulin-dependent diabetic patients. For the Gemfibrozil Study Group. PG - 27-33 AB - We assessed the efficacy of gemfibrozil therapy on lipid profile and glucose metabolism in a large cohort of (type 2) non-insulin-dependent diabetic patients. We enrolled 217 type 2 diabetic patients with plasma triglyceride concentrations equal to or above 2 mmol/l: 110 were randomized to gemfibrozil (600 mg twice daily) and 107 to placebo treatment in a double blind fashion. Each treatment was followed for 20 weeks. To assess postprandial glucose metabolism and insulin secretion, at time 0 and 20 weeks, a standard meal containing 12.5 g of proteins, 40.1 g of carbohydrate, 10 g of lipids was given. No differences in demographic characteristics were observed between patients randomized either to gemfibrozil or to placebo therapy. No differences were observed in total cholesterol and LDL-cholesterol concentration changes between the baseline observations and week 20 of both treatments. At variance, both treatments significantly increased HDL cholesterol. Gemfibrozil treatment significantly decreased plasma triglyceride concentration from 316+/-84 to 214+/-82 mg/dl (P < 0.001), whereas with placebo triglyceride levels increased from 318 + 93 to 380 + 217 mg/dl. No changes were observed in non-esterified fatty acid concentrations or in fasting plasma glucose concentrations, in HbA(1C) values, insulin and C-peptide concentrations. Gemfibrozil treatment: 1) significantly reduces circulating triglyceride concentration; 2) does not significantly affect cholesterol concentration; 3) does not worsen glucose metabolism. FAU - Avogaro, A AU - Avogaro A AD - Division of Metabolic Diseases, Via Giustiniani 2, I-35100 Padova, Italy. FAU - Piliego, T AU - Piliego T FAU - Catapano, A AU - Catapano A FAU - Miola, M AU - Miola M FAU - Tiengo, A AU - Tiengo A LA - eng PT - Clinical Trial PT - Journal Article PT - Multicenter Study PT - Randomized Controlled Trial PL - Germany TA - Acta Diabetol JT - Acta diabetologica JID - 9200299 RN - 0 (Blood Glucose) RN - 0 (Cholesterol, HDL) RN - 0 (Cholesterol, LDL) RN - 0 (Fatty Acids, Nonesterified) RN - 0 (Hypoglycemic Agents) RN - 0 (Hypolipidemic Agents) RN - 0 (Lipids) RN - 0 (Placebos) RN - 0 (Triglycerides) RN - 97C5T2UQ7J (Cholesterol) RN - Q8X02027X3 (Gemfibrozil) SB - IM MH - Blood Glucose/drug effects/*metabolism MH - Cholesterol/blood MH - Cholesterol, HDL/blood MH - Cholesterol, LDL/blood MH - Diabetes Mellitus, Type 2/blood/complications/*drug therapy MH - Double-Blind Method MH - Fatty Acids, Nonesterified/blood MH - Female MH - Gemfibrozil/*therapeutic use MH - Humans MH - Hypertriglyceridemia/blood/complications/*drug therapy MH - Hypoglycemic Agents/*therapeutic use MH - Hypolipidemic Agents/*therapeutic use MH - Italy MH - Lipids/*blood MH - Male MH - Middle Aged MH - Placebos MH - Triglycerides/blood EDAT- 1999/08/07 00:00 MHDA- 1999/08/07 00:01 CRDT- 1999/08/07 00:00 PHST- 1999/08/07 00:00 [pubmed] PHST- 1999/08/07 00:01 [medline] PHST- 1999/08/07 00:00 [entrez] AID - 90360027.592 [pii] PST - ppublish SO - Acta Diabetol. 1999 Jun;36(1-2):27-33. PMID- 9604920 OWN - NLM STAT- MEDLINE DCOM- 19980618 LR - 20170908 IS - 0002-9149 (Print) IS - 0002-9149 (Linking) VI - 81 IP - 8A DP - 1998 Apr 23 TI - What kinds of data should be available to probe the effects of nutrients, food supplements or vitamins on serum lipoprotein levels and/or atherosclerosis? PG - 80F-83F FAU - Davidson, M AU - Davidson M AD - Chicago Center for Clinical Research, Illinois, USA. FAU - Kanter, M AU - Kanter M FAU - Catapano, A AU - Catapano A FAU - Saidman, C AU - Saidman C LA - eng PT - Journal Article PT - Review PL - United States TA - Am J Cardiol JT - The American journal of cardiology JID - 0207277 RN - 0 (Lipoproteins) RN - 0 (Vitamins) SB - AIM SB - IM MH - Arteriosclerosis/blood/*diet therapy MH - Dietary Supplements/*standards MH - Food Labeling/*standards MH - Guideline Adherence MH - Humans MH - Lipoproteins/*blood MH - *Nutritional Requirements MH - Practice Guidelines as Topic MH - United States MH - United States Food and Drug Administration MH - Vitamins/*therapeutic use RF - 0 EDAT- 1998/05/30 00:00 MHDA- 1998/05/30 00:01 CRDT- 1998/05/30 00:00 PHST- 1998/05/30 00:00 [pubmed] PHST- 1998/05/30 00:01 [medline] PHST- 1998/05/30 00:00 [entrez] AID - S0002-9149(98)00274-4 [pii] PST - ppublish SO - Am J Cardiol. 1998 Apr 23;81(8A):80F-83F. PMID- 1599980 OWN - NLM STAT- MEDLINE DCOM- 19920713 LR - 20131121 IS - 0939-4974 (Print) IS - 0939-4974 (Linking) VI - 30 IP - 3 DP - 1992 Mar TI - A collaborative trial for the evaluation of blood cholesterol measurement in clinical laboratories in Italy. PG - 157-61 AB - A collaborative trial for the evaluation of blood cholesterol measurement in Italy was carried out, with the use of two lyophilized controls, whose target values, respectively 4.42 and 6.21 mmol/l, were established by means of "definitive" methodology (isotope dilution/mass spectrometry). Results from 480 participants showed a somewhat broad dispersion (CV 6.1% and 6.3% respectively), and a definite bias (-0.25 mmol/l and -0.61 mmol/l respectively) with respect to the target values. The different analytical systems were characterized by different combinations of inaccuracy and imprecision; however, the bias observed for the higher concentration sample was a constant finding. The behaviour of the control materials, in comparison with that exhibited by patients' sera, was assessed in a manual enzymatic procedure and in the Kodak Ektachem 700 and Technicon Chem 1 systems. The peculiar property of one control material to behave differently from patients' sera in some analytical systems, i.e. the lack of commutability, was found to be partially responsible for the observed bias in the three methods studied. The importance of testing for commutability of the control materials to be used for the control of accuracy is stressed. FAU - Malavasi, B AU - Malavasi B AD - Institute of Pharmacological Sciences, University of Milan, Italy. FAU - Catapano, A AU - Catapano A FAU - Galli, G AU - Galli G FAU - Franzini, C AU - Franzini C LA - eng PT - Comparative Study PT - Journal Article PL - Germany TA - Eur J Clin Chem Clin Biochem JT - European journal of clinical chemistry and clinical biochemistry : journal of the Forum of European Clinical Chemistry Societies JID - 9105775 RN - 97C5T2UQ7J (Cholesterol) SB - IM MH - Blood Chemical Analysis/*methods/statistics & numerical data MH - Cholesterol/*blood MH - Evaluation Studies as Topic MH - Humans MH - Italy MH - Laboratories EDAT- 1992/03/01 00:00 MHDA- 1992/03/01 00:01 CRDT- 1992/03/01 00:00 PHST- 1992/03/01 00:00 [pubmed] PHST- 1992/03/01 00:01 [medline] PHST- 1992/03/01 00:00 [entrez] PST - ppublish SO - Eur J Clin Chem Clin Biochem. 1992 Mar;30(3):157-61. PMID- 2370048 OWN - NLM STAT- MEDLINE DCOM- 19900817 LR - 20181113 IS - 0340-6717 (Print) IS - 0340-6717 (Linking) VI - 85 IP - 2 DP - 1990 Jul TI - Lecithin cholesterol acyl transferase deficiency: molecular analysis of a mutated allele. PG - 195-9 AB - The enzyme, lecithin cholesterol acyltransferase (LCAT), is responsible for the esterification of plasma cholesterol mediating the transfer of an acyl group from lecithin to the 3-hydroxy group of cholesterol. Deficiency of the enzyme is a well-known syndrome with a widespread geographic occurrence. We have cloned an allele from a patient homozygous for the LCAT deficiency. The only change that we could detect is a C to T transition in the fourth exon of the gene; this causes a substitution of Arg for Trp at position 147 of the mature protein. The functional significance of such a substitution with respect to the enzyme defect was demonstrated by transfecting the mutated LCAT gene in the cell line COS-1. FAU - Taramelli, R AU - Taramelli R AD - Dipartimento di Genetica e di Biologia dei Microrganismi, Milan, Italy. FAU - Pontoglio, M AU - Pontoglio M FAU - Candiani, G AU - Candiani G FAU - Ottolenghi, S AU - Ottolenghi S FAU - Dieplinger, H AU - Dieplinger H FAU - Catapano, A AU - Catapano A FAU - Albers, J AU - Albers J FAU - Vergani, C AU - Vergani C FAU - McLean, J AU - McLean J LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't PL - Germany TA - Hum Genet JT - Human genetics JID - 7613873 RN - 0 (DNA Probes) SB - IM MH - *Alleles MH - Amino Acid Sequence MH - DNA Probes MH - *Exons MH - Gene Amplification MH - *Homozygote MH - Humans MH - Hypolipoproteinemias/*genetics MH - *Introns MH - Lecithin Cholesterol Acyltransferase Deficiency/*genetics MH - Male MH - Molecular Sequence Data MH - *Mutation MH - Transfection EDAT- 1990/07/01 00:00 MHDA- 1990/07/01 00:01 CRDT- 1990/07/01 00:00 PHST- 1990/07/01 00:00 [pubmed] PHST- 1990/07/01 00:01 [medline] PHST- 1990/07/01 00:00 [entrez] PST - ppublish SO - Hum Genet. 1990 Jul;85(2):195-9. PMID- 2495256 OWN - NLM STAT- MEDLINE DCOM- 19890512 LR - 20131121 IS - 0172-4622 (Print) IS - 0172-4622 (Linking) VI - 10 IP - 1 DP - 1989 Feb TI - Effects of anabolic steroids, testosterone, and HGH on blood lipids and echocardiographic parameters in body builders. PG - 62-6 AB - To evaluate the metabolic or cardiovascular effects induced by self-administration of human growth hormone (HGH) alone or combined with testosterone and anabolic steroids, we conducted a study with 15 male body builders. Of these, 8 (control group) did not take any hormonal substances; 6 (experimental group) self-administered testosterone, anabolic steroids, and HGH for 6 weeks in various dosages; 1 subject self-administered only HGH for an equal period of time. At the end of the period of treatment with the hormonal combination, the experimental group continued for 2 additional weeks with anabolic steroids and testosterone only. All maintained the same, unaltered type and intensity of training, and constant diet. Before the beginning of treatment with hormonal substances, after 6 weeks, and at the end of treatment (for a total of 8 weeks), they were tested for total and HDL-cholesterol (t-chol and HDL-chol), apolipoproteins A-1 and B (apo A-1 and B), and triglycerides (tg). Before the start and after 6 weeks, an echocardiographic examination was performed to assess left ventricular dimensions and function in all 15 body builders. The most interesting result is a significant decrease of HDL-chol and apo A-1 derived from self-administration of anabolic steroids and HGH together. FAU - Zuliani, U AU - Zuliani U AD - Cattedra di Medicina dello Sport, University of Parma, Italy. FAU - Bernardini, B AU - Bernardini B FAU - Catapano, A AU - Catapano A FAU - Campana, M AU - Campana M FAU - Cerioli, G AU - Cerioli G FAU - Spattini, M AU - Spattini M LA - eng PT - Journal Article PL - Germany TA - Int J Sports Med JT - International journal of sports medicine JID - 8008349 RN - 0 (Anabolic Agents) RN - 0 (Apolipoprotein A-I) RN - 0 (Apolipoproteins A) RN - 0 (Apolipoproteins B) RN - 0 (Cholesterol, HDL) RN - 0 (Lipids) RN - 0 (Triglycerides) RN - 3XMK78S47O (Testosterone) RN - 9002-72-6 (Growth Hormone) SB - IM MH - Adult MH - Anabolic Agents/*pharmacology MH - Apolipoprotein A-I MH - Apolipoproteins A/blood MH - Apolipoproteins B/blood MH - Cholesterol, HDL/blood MH - *Echocardiography MH - Growth Hormone/*pharmacology MH - Heart Ventricles/drug effects MH - Humans MH - Lipids/*blood MH - Male MH - *Sports MH - Testosterone/*pharmacology MH - Triglycerides/blood MH - *Weight Lifting EDAT- 1989/02/01 00:00 MHDA- 1989/02/01 00:01 CRDT- 1989/02/01 00:00 PHST- 1989/02/01 00:00 [pubmed] PHST- 1989/02/01 00:01 [medline] PHST- 1989/02/01 00:00 [entrez] AID - 10.1055/s-2007-1024877 [doi] PST - ppublish SO - Int J Sports Med. 1989 Feb;10(1):62-6. doi: 10.1055/s-2007-1024877. PMID- 3338256 OWN - NLM STAT- MEDLINE DCOM- 19880304 LR - 20161123 IS - 0143-5221 (Print) IS - 0143-5221 (Linking) VI - 74 IP - 1 DP - 1988 Jan TI - A study of the structure of the gene for lecithin: cholesterol acyltransferase in four unrelated individuals with familial lecithin: cholesterol acyltransferase deficiency. PG - 91-6 AB - 1. We have used polyclonal antibodies and a complementary DNA clone for human lecithin:cholesterol acyltransferase (LCAT) to study LCAT protein and the structure of the LCAT gene, respectively, in patients with familial LCAT deficiency from Norway, Ireland, Germany and Italy. 2. The patients had low levels of non-functional LCAT protein in their serum as measured by rocket immunoelectrophoresis; its mol. wt. of approximately 68,000 was identical with that of LCAT in normal plasma, as judged by immunoblotting. 3. Enzymatic digestion of DNA samples from the patients produced LCAT gene fragments which were indistinguishable from those found in normal individuals. 4. We conclude that LCAT deficiency in these patients is not caused by a large deletion or rearrangement of the LCAT gene sequences. FAU - Humphries, S E AU - Humphries SE AD - Department of Biochemistry, St Mary's Hospital Medical School, London. FAU - Chaves, M E AU - Chaves ME FAU - Tata, F AU - Tata F FAU - Lima, V L AU - Lima VL FAU - Owen, J S AU - Owen JS FAU - Borysiewicz, L K AU - Borysiewicz LK FAU - Catapano, A AU - Catapano A FAU - Vergani, C AU - Vergani C FAU - Gjone, E AU - Gjone E FAU - Clemens, M R AU - Clemens MR AU - et al. LA - eng GR - Wellcome Trust/United Kingdom PT - Journal Article PT - Research Support, Non-U.S. Gov't PL - England TA - Clin Sci (Lond) JT - Clinical science (London, England : 1979) JID - 7905731 RN - EC 2.3.1.43 (Phosphatidylcholine-Sterol O-Acyltransferase) SB - IM MH - Genes MH - Germany MH - Humans MH - Hypolipoproteinemias/*genetics MH - Ireland MH - Italy MH - Lecithin Cholesterol Acyltransferase Deficiency/*genetics MH - Norway MH - Phosphatidylcholine-Sterol O-Acyltransferase/*genetics EDAT- 1988/01/01 00:00 MHDA- 1988/01/01 00:01 CRDT- 1988/01/01 00:00 PHST- 1988/01/01 00:00 [pubmed] PHST- 1988/01/01 00:01 [medline] PHST- 1988/01/01 00:00 [entrez] PST - ppublish SO - Clin Sci (Lond). 1988 Jan;74(1):91-6. PMID- 3796552 OWN - NLM STAT- MEDLINE DCOM- 19870204 LR - 20061115 IS - 0026-4946 (Print) IS - 0026-4946 (Linking) VI - 38 IP - 20 DP - 1986 Oct 31 TI - [Familial hypercholesterolemia. Study of low-density lipoprotein receptors. Treatment with plasmapheresis]. PG - 893-902 FAU - Bellini, C AU - Bellini C FAU - Bonioli, E AU - Bonioli E FAU - Ruffa, G AU - Ruffa G FAU - Franchini, E AU - Franchini E FAU - Rivabella, L AU - Rivabella L FAU - Cinollo, G AU - Cinollo G FAU - Catapano, A AU - Catapano A FAU - Fumagalli, R AU - Fumagalli R FAU - Corsini, A AU - Corsini A FAU - Gemme, G AU - Gemme G LA - ita PT - Case Reports PT - English Abstract PT - Journal Article TT - Ipercolesterolemia familiare. Studio del recettore per le LDL. Trattamento con plasmaferesi. PL - Italy TA - Minerva Pediatr JT - Minerva pediatrica JID - 0400740 RN - 0 (Receptors, LDL) SB - IM MH - Child MH - Child, Preschool MH - Humans MH - Hyperlipoproteinemia Type II/metabolism/*therapy MH - Male MH - Pedigree MH - *Plasmapheresis MH - Receptors, LDL/*analysis EDAT- 1986/10/31 00:00 MHDA- 1986/10/31 00:01 CRDT- 1986/10/31 00:00 PHST- 1986/10/31 00:00 [pubmed] PHST- 1986/10/31 00:01 [medline] PHST- 1986/10/31 00:00 [entrez] PST - ppublish SO - Minerva Pediatr. 1986 Oct 31;38(20):893-902. PMID- 6321869 OWN - NLM STAT- MEDLINE DCOM- 19840426 LR - 20180703 IS - 0024-3205 (Print) IS - 0024-3205 (Linking) VI - 34 IP - 11 DP - 1984 Mar 12 TI - beta-Adrenergic receptors in brain microvessels of diabetic rats. PG - 1095-100 AB - A significant decrease in the number of beta-adrenergic receptors was observed in cerebral microvessels of fatty (fa/fa) and streptozotocin-induced diabetic rats, without receptor affinity changes. These results suggest that alterations of central adrenergic regulation of small vessels may be involved in brain microvasculature disturbances that occur with diabetes. FAU - Magnoni, M S AU - Magnoni MS FAU - Kobayashi, H AU - Kobayashi H FAU - Trezzi, E AU - Trezzi E FAU - Catapano, A AU - Catapano A FAU - Spano, P F AU - Spano PF FAU - Trabucchi, M AU - Trabucchi M LA - eng PT - Journal Article PL - Netherlands TA - Life Sci JT - Life sciences JID - 0375521 RN - 0 (Blood Glucose) RN - 0 (Receptors, Adrenergic, beta) SB - IM MH - Animals MH - Blood Glucose/analysis MH - Brain/*blood supply MH - Capillaries/analysis MH - Cerebrovascular Circulation MH - Cricetinae MH - Diabetes Mellitus, Experimental/*physiopathology MH - Male MH - Mice MH - Rats MH - Rats, Inbred Strains MH - Rats, Zucker MH - Receptors, Adrenergic, beta/*analysis EDAT- 1984/03/12 00:00 MHDA- 1984/03/12 00:01 CRDT- 1984/03/12 00:00 PHST- 1984/03/12 00:00 [pubmed] PHST- 1984/03/12 00:01 [medline] PHST- 1984/03/12 00:00 [entrez] AID - 0024-3205(84)90023-7 [pii] PST - ppublish SO - Life Sci. 1984 Mar 12;34(11):1095-100. PMID- 6101731 OWN - NLM STAT- MEDLINE DCOM- 19800417 LR - 20170920 IS - 0140-6736 (Print) IS - 0140-6736 (Linking) VI - 1 IP - 8162 DP - 1980 Feb 2 TI - New case of apoprotein C-II deficiency. PG - 268 FAU - Capurso, A AU - Capurso A FAU - Pace, L AU - Pace L FAU - Bonomo, L AU - Bonomo L FAU - Catapano, A AU - Catapano A FAU - Schiliro, G AU - Schiliro G FAU - La Rosa, M AU - La Rosa M FAU - Assmann, G AU - Assmann G LA - eng PT - Case Reports PT - Letter PL - England TA - Lancet JT - Lancet (London, England) JID - 2985213R RN - 0 (Apoproteins) RN - 0 (Triglycerides) SB - AIM SB - IM MH - Apoproteins/*deficiency MH - Child, Preschool MH - Female MH - Humans MH - Hyperlipoproteinemia Type V/blood MH - Triglycerides/*blood EDAT- 1980/02/02 00:00 MHDA- 1980/02/02 00:01 CRDT- 1980/02/02 00:00 PHST- 1980/02/02 00:00 [pubmed] PHST- 1980/02/02 00:01 [medline] PHST- 1980/02/02 00:00 [entrez] AID - S0140-6736(80)90768-0 [pii] PST - ppublish SO - Lancet. 1980 Feb 2;1(8162):268. PMID- 189780 OWN - NLM STAT- MEDLINE DCOM- 19770315 LR - 20131121 IS - 0021-9150 (Print) IS - 0021-9150 (Linking) VI - 26 IP - 1 DP - 1977 Jan TI - Metaformin: an antiatherosclerotic agent modifying very low density lipoproteins in rabbits. PG - 79-89 AB - The composition of very low density lipoproteins (VLDL: d less than 1.019) of New Zealand male rabbits reciving cholesterol (2 g/day) and metformin (135 mg/kg/day) is investigated. These rabbits, while showing only a slight reduction of plasma cholesterol levels, as compared to cholesterol-fed (h.c.) animals, show a marked decrease of the aortic cholesterol esters and atheromatous process. VLDL from the cholesterol + metformin group (h.c. + met), as compared to the h.c. animals, are homogenous in size and not separable into VLDL-1 and VLDL-2 subfractions by Sepharose 4B chromatography. These findings are confirmed by electron microscopy, which shows homogeneity of particle size, as well a decreased tendency of h.c. + met VLDL to aggregate. Chemical composition of h.c. + met VLDL is characterized by increased triglycerides and phospholipids, while the percentage of cholesterol esters is not significantly decreased. Phospholipid distribution of h.c. + met VLDL shows a significant decrease of sphingomyelin and increased phosphatidylinositol, the latter both as compared to h.c. and control VLDL. Apoprotein pattern of h.c. + met VLDL in polyacrylamide gels shows a relative increase of peptides with C mobility and a decrease of proteins corresponding to the arg-rich peptides. These findings exemplify a case of altered lipoprotein composition and decreased atheromatosis, in the presence of marked hypercholesteremia. FAU - Sirtori, C R AU - Sirtori CR FAU - Catapano, A AU - Catapano A FAU - Ghiselli, G C AU - Ghiselli GC FAU - Innocenti, A L AU - Innocenti AL FAU - Rodriguez, J AU - Rodriguez J LA - eng PT - Journal Article PL - Ireland TA - Atherosclerosis JT - Atherosclerosis JID - 0242543 RN - 0 (Apolipoproteins) RN - 0 (Blood Glucose) RN - 0 (Fatty Acids) RN - 0 (Lipoproteins, VLDL) RN - 0 (Phospholipids) RN - 9100L32L2N (Metformin) RN - 97C5T2UQ7J (Cholesterol) SB - IM MH - Animals MH - Aorta/metabolism MH - Apolipoproteins/blood MH - Blood Glucose/analysis MH - Cholesterol/metabolism MH - Fatty Acids/metabolism MH - Hypercholesterolemia/*blood MH - Lipoproteins, VLDL/analysis/*blood MH - Liver/metabolism MH - Male MH - Metformin/*pharmacology MH - Microscopy, Electron MH - Particle Size MH - Phospholipids/metabolism MH - Rabbits EDAT- 1977/01/01 00:00 MHDA- 1977/01/01 00:01 CRDT- 1977/01/01 00:00 PHST- 1977/01/01 00:00 [pubmed] PHST- 1977/01/01 00:01 [medline] PHST- 1977/01/01 00:00 [entrez] AID - 0021-9150(77)90142-3 [pii] PST - ppublish SO - Atherosclerosis. 1977 Jan;26(1):79-89. PMID- 179294 OWN - NLM STAT- MEDLINE DCOM- 19760802 LR - 20161109 IS - 0065-2598 (Print) IS - 0065-2598 (Linking) VI - 67 IP - 00 DP - 1976 TI - Turnover and aortic uptake of very low density lipoproteins (VLDL) from hypercholesteremic rabbits as a model for testing antiatherosclerotic compounds. PG - 169-89 AB - VLDL from hypercholesteremic (HC) rabbits display features which are suggestive of inherent atherogenicity. The lipid composition, compared to that of control VLDL, shows an enrichment of cholesterol esters, which have a very high 18:1/18:2 ratio in their fatty acids, and an increased sphingomyelin content, with decreased PC/Sph ratio. This lipid composition is very similar to that of the atherosclerotic plaqua. Apoprotein peptides of HC VLDL show a predominance of arg-rich proteins, similar to human conditions (Type III hyperlipoproteinemia and hypothyroidism) characterized by early and severe atherosclerosis. Turnover of 125I-labelled HC VLDL is significantly slower than that of control VLDL, both when the lipoprotein is injected into the donor animals and into controls. Conversion of HC VLDL into lipoproteins of higher density is also very small, as compared to control VLDL. Uptake of radioactivity into the aortic wall after injection is about doubled, as compared to control VLDL, when HC rabbits receive HC VLDL. This experimental model suggests that structural modifications of the HC VLDL make them poorly metabolizable, and possible more akin to the recently described arterial lipoprotein complexing factor (ALCF). Metformin was selected as the test compound, because it has been shown to decrease aortic and liver lipid accumulation in cholesterol fed rabbits, while only slightly affecting plasma cholesterol levels. VLDL from rabbits fed cholesterol and metformin (HC+Met), while still enriched in cholesterol esters, have a higher protein content, less sphingomyelin and more phosphatidylethanolamine and phosphatidylinositol than HC VLDL, while fatty acid composition of cholesterol esters does not differ. Turnover of HC+Met VLDL is extremely rapid, with a t1/2 even shorter than that of control VLDL. FAU - Rodriguez, J AU - Rodriguez J FAU - Catapano, A AU - Catapano A FAU - Ghiselli, G C AU - Ghiselli GC FAU - Sirtori, C R AU - Sirtori CR LA - eng PT - Journal Article PL - United States TA - Adv Exp Med Biol JT - Advances in experimental medicine and biology JID - 0121103 RN - 0 (Apoproteins) RN - 0 (Lipoproteins, VLDL) RN - 0 (Phospholipids) RN - 0 (Sphingomyelins) RN - 0 (Triglycerides) RN - 9100L32L2N (Metformin) RN - 97C5T2UQ7J (Cholesterol) SB - IM MH - Animals MH - Aorta/*metabolism MH - Apoproteins/analysis MH - Arteriosclerosis/metabolism MH - Cholesterol/blood MH - *Disease Models, Animal MH - Hypercholesterolemia/*metabolism MH - Lipoproteins, VLDL/analysis/blood/*metabolism MH - Male MH - Metformin/*pharmacology MH - Phospholipids/blood MH - Rabbits/*metabolism MH - Sphingomyelins/analysis MH - Triglycerides/blood EDAT- 1976/01/01 00:00 MHDA- 1976/01/01 00:01 CRDT- 1976/01/01 00:00 PHST- 1976/01/01 00:00 [pubmed] PHST- 1976/01/01 00:01 [medline] PHST- 1976/01/01 00:00 [entrez] PST - ppublish SO - Adv Exp Med Biol. 1976;67(00):169-89. PMID- 233766 OWN - NLM STAT- MEDLINE DCOM- 19880701 LR - 20031114 IS - 0021-9150 (Print) IS - 0021-9150 (Linking) VI - 23 IP - 1 DP - 1976 Jan-Feb TI - Very low density lipoproteins in normal and cholesterol-fed rabbits: lipid and protein composition and metabolism. Part 2. Metabolism of very low density lipoproteins in rabbits. PG - 85-96 AB - The metabolic fate of very low density lipoproteins (VLDL) in normal and hypercholesteremic (h.c.) rabbits has been investigated. VLDL were labelled with 125I in the protein moieties and injected into normal and h.c. animals. The turnover of h.c. VLDL is markedly delayed as compared to that of normal VLDL, and conversion into lipoprotein classes of higher density is considerably decreased. This is observed when h.c. VLDL are injected either into h.c., or into normal rabbits. Arterial uptake of radioactivity is much higher with h.c. VLDL than with the normal lipoproteins, and it is highest when h.c. VLDL are injected into normal recipients. These data, together with those reported in the previous study, support the hypothesis that h.c. VLDL have an inherent atherogenicity. Injection of h.c. VLDL into normal animals also offers an experimental model for testing drugs or diets against atherosclerosis, using untreated animals. FAU - Rodriguez, J L AU - Rodriguez JL AD - Center E. Grossi Paoletti for the Study of Metabolic Diseases and Hyperlipidemias, University of Milan, Italy. FAU - Catapano, A AU - Catapano A FAU - Ghiselli, G C AU - Ghiselli GC FAU - Sirtori, C R AU - Sirtori CR LA - eng PT - Journal Article PL - Ireland TA - Atherosclerosis JT - Atherosclerosis JID - 0242543 RN - 0 (Lipoproteins, VLDL) SB - IM MH - Animals MH - Hypercholesterolemia/*metabolism MH - Lipoproteins, VLDL/blood/*metabolism MH - Male MH - Rabbits EDAT- 1976/01/01 00:00 MHDA- 1976/01/01 00:01 CRDT- 1976/01/01 00:00 PHST- 1976/01/01 00:00 [pubmed] PHST- 1976/01/01 00:01 [medline] PHST- 1976/01/01 00:00 [entrez] AID - 0021-9150(76)90120-9 [pii] PST - ppublish SO - Atherosclerosis. 1976 Jan-Feb;23(1):85-96.