Hyperlipidemias: Europe

Wierzbicki AS, Humphries SE, Minhas R, Anonymous00232. · St Thomas' Hospital, London SE1 7EH. · BMJ. · Pubmed #18753174 No free full text.

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Clement D, Kolh P, Motte S, Sprynger M, Van Damme H, Verhamme P, Vermassen F, Wautrecht JC, Anonymous00147. · University of Ghent, Belgium. · Acta Chir Belg. · Pubmed #18277433 No free full text.

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Poli A, Marangoni F, Paoletti R, Mannarino E, Lupattelli G, Notarbartolo A, Aureli P, Bernini F, Cicero A, Gaddi A, Catapano A, Cricelli C, Gattone M, Marrocco W, Porrini M, Stella R, Vanotti A, Volpe M, Volpe R, Cannella C, Pinto A, Del Toma E, La Vecchia C, Tavani A, Manzato E, Riccardi G, Sirtori C, Zambon A, Anonymous00119. · Nutrition Foundation of Italy, Italy. · Nutr Metab Cardiovasc Dis. · Pubmed #18258418 No free full text.

Abstract: 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.

Rydén L, Standl E, Bartnik M, Van den Berghe G, Betteridge J, de Boer MJ, Cosentino F, Jönsson B, Laakso M, Malmberg K, Priori S, Ostergren J, Tuomilehto J, Thrainsdottir I, Vanhorebeek I, Stramba-Badiale M, Lindgren P, Qiao Q, Priori SG, Blanc JJ, Budaj A, Camm J, Dean V, Deckers J, Dickstein K, Lekakis J, McGregor K, Metra M, Morais J, Osterspey A, Tamargo J, Zamorano JL, Deckers JW, Bertrand M, Charbonnel B, Erdmann E, Ferrannini E, Flyvbjerg A, Gohlke H, Juanatey JR, Graham I, Monteiro PF, Parhofer K, Pyörälä K, Raz I, Schernthaner G, Volpe M, Wood D, Anonymous00256, Anonymous00257. · Department of Cardiology, Karolinska University Hospital, Sweden. · Eur Heart J. · Pubmed #17220161 links to  free full text

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Marín R, Goicoechea MA, Gorostidi M, Cases A, Díez J, Escolar G, Fernández-Vega F, Palomar R, Rodrigo E, Martínez I, Segura J, Anonymous00167. · Servicio de Nefrología, Hospital Universitario Central de Asturias, Celestino Villamil, s/n 33006 Oviedo, Asturias. · Nefrologia. · Pubmed #16649424 links to  free full text

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Civeira F, Anonymous00222. · Lipid Unit, Hospital Universitario Miguel Servet, Avda Isabel La Católica 1-3, 50009 Zaragoza, Spain. · Atherosclerosis. · Pubmed #15177124 No free full text.

Abstract: Familial hypercholesterolemia (FH) is a genetic disorder of lipoprotein metabolism characterized by very high plasma concentrations of low density lipoprotein cholesterol (LDLc), tendon xanthomas and increased risk of premature coronary heart disease (CHD). FH is a public health problem throughout the world. There are 10,000,000 people with FH worldwide, mainly heterozygotes, and approximately 85% of males and 50% of females with FH will suffer a coronary event before 65 years old if appropriate preventive efforts are not implemented. Early identification of persons with FH and their relatives, and the early start of treatment are essential issues in the prevention of premature cardiovascular disease (CVD) and death in this population. However, guidelines for the general population formally exclude FH from their diagnostic and treatment recommendations. These guidelines have been elaborated by a group of international experts with the intention to answer the main questions about heterozygous FH (heFH) subjects that physicians worldwide face in the diagnosis and management of these patients.

Dietz R, Rauch B, Anonymous00264, Anonymous00265, Anonymous00266. · Kardiologie Campus Berlin-Buch, Universitätsklinikum Charité, Medizinische Fakultät der Humboldt Universität zu Berlin, Germany. · Z Kardiol. · Pubmed #12905980 No free full text.

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Schuster H, Anonymous00170. · Humboldt University Berlin, Droysenstr. 1, 10629 Berlin, Germany. · Atheroscler Suppl. · Pubmed #12714033 No free full text.

Abstract: Populations of patients at high risk of coronary heart disease (CHD) include those with type 2 diabetes and those with heterozygous familial hypercholesterolemia (HeFH). Despite benefits of statin lipid-lowering therapy in reducing CHD risk in diabetic patients, screening for dyslipidemia in such patients is inadequate, and patients frequently fail to achieve recommended low-density lipoprotein goals. Diagnosis of HeFH is also suboptimal, despite the reliability of family lipid screening in confirming clinical diagnosis and utility of screening in identifying other family members who are at risk. Patients with HeFH frequently require large reductions in low-density lipoprotein (LDL) cholesterol to achieve target levels. In both of these populations, statins that produce large reductions in LDL cholesterol offer advantages in achieving lipid-lowering goals and in simplifying medical therapy to reduce CHD risk.

Gaddi A, Galetti C, Pauciullo P, Arca M. · Centro per lo Studio dell'Arteriosclerosi e delle Malattie Dismetaboliche Giancarlo Descovich, Servizio di Gerontologia, Policlinico S. Orsola-Malpighi, Bologna, Italy. · Nutr Metab Cardiovasc Dis. · Pubmed #10765523 No free full text.

Abstract: The Atherosclerosis and Dysmetabolic Disorders Study Group, headed by Prof. Rodolfo Paoletti, decided in 1994 to compose a committee of experts to formulate a clear description of familial combined hyperlipoproteinemia (FCH), a disorder illustrated in the literature, but still unknown to most physicians in spite of its severity and relative diffusion. The Committee consists of experts from the Lipid Clinics of the Universities of Ancona, Bari, Bologna, Ferrara, Genoa, Milan, Naples, Padua, Palermo, Perugia, Rome, Sassari, Turin, Verona and Venice. It has held several meetings coordinated by the national secretary at the "Giancarlo Descovich" Atherosclerosis Centre of the University of Bologna. This paper summarizes its conclusions.

Deans KA, Dominiczak MH. · Department of Biochemistry, Gartnavel General Hospital, Glasgow, UK. · Curr Opin Lipidol. · Pubmed #18957887 No free full text.

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Panza F, Solfrizzi V, D'Introno A, Colacicco AM, Santamato A, Seripa D, Pilotto A, Capurso A, Capurso C. · Department of Geriatrics, Center for Lipoprotein Metabolism, University of Bari, Policlinico, Piazza Giulio Cesare, 11, 70124 Bari, Italy. · Neurobiol Aging. · Pubmed #18179846 No free full text.

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DeSilvey DL. · Waldo Cardiovascular Medicine, Belfast, ME 04915, USA. · Am J Geriatr Cardiol. · Pubmed #17086036 links to  free full text

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Vartiainen E. · · Duodecim. · Pubmed #16457069 No free full text.

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Rabelink TJ. · University Medical Center Utrecht, Internal Medicine, Room G 02.228, PO Box 85500, 3508 GA Utrecht, The Netherlands. · Nephrol Dial Transplant. · Pubmed #14671033 links to  free full text

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Vogt L, Laverman GD, Dullaart RP, Navis G. · Department of internal Medicine, Division of Nephrology, University Medical Center Groningen, Hanzeplein 1, 9713 GX Groningen, The Netherlands. · Nephrol Dial Transplant. · Pubmed #14671028 links to  free full text

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Ackermann M, Fraefel C. · Institute of Virology, Veterinary Medical Faculty, University of Zurich, Switzerland. · Mol Ther. · Pubmed #12718898 No free full text.

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Langford NJ, Kendall MJ. · Clinical Pharmacology Section, Department of Medicine, University of Birmingham, Queen Elizabeth Hospital, Edgbaston, Birmingham B15 2TH, UK. · J Clin Pharm Ther. · Pubmed #11722675 No free full text.

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Grassi G, Taddei S. · Clinica Medica, University of Milano-Bicocca, Ospedale San Gerardo, Monza, Milano, Italy. · J Hypertens. · Pubmed #11330868 No free full text.

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Parazzini F, Ricci E, Chiaffarino F, Trinchieri A. · Clinica Mangiagalli, Università degli Studi di Milano e Fondazione Policlinico-Mangiagalli-Regina Elena, Milano, Italy. · Arch Ital Urol Androl. · Pubmed #19499755 No free full text.

Abstract: In this narrative review we have briefly revised the main epidemiological evidences on the relation between erectile dysfunction (ED) and cardiovascular risk factors and diseases. There are consistent epidemiological evidences which link ED and cardiovascular diseases, diabetes or cholesterol levels. Most of studies which have taken into account in the analysis of the relation between ED and hypertension, cardiovascular diseases, smoking and weight (or body mass index) have shown that these factors have an independent role on the risk of ED. Otherwise, ED is a risk factor for subsequent development of cardiovascular diseases. In the routine clinical practice the presence of ED should be considered a "marker" for the development of cardiovascular diseases. The physician should consider to ask each patient regarding the presence of ED in order to focus preventive measures.

Staels B. · Universite Lille Nord de France, Inserm U545, UDSL, Lille, France. · Postgrad Med. · Pubmed #19494475 No free full text.

Abstract: Clinical evidence has demonstrated that bile acid sequestrants reduce glucose levels in patients with type 2 diabetes mellitus (T2DM). This effect has been confirmed in multiple double-blind, placebo-controlled clinical studies with the bile acid sequestrant colesevelam hydrochloride (HCl). Colesevelam HCl was approved by the US Food and Drug Administration in January 2008 as an adjunctive therapy for patients with T2DM to improve glycemic control. However, the mechanism of action for the glucose-lowering effect of bile acid sequestrants is unclear. Bile acid sequestrants are nonsystemic pharmacological agents that bind bile acids in the gastrointestinal tract, thereby diverting bile acids from the enterohepatic circulation. This, in turn, upregulates bile acid synthesis (via cholesterol 7-alpha-hydroxylase), which utilizes cholesterol, resulting in reduced low-density lipoprotein cholesterol levels. Recent research has revealed that bile acids are tightly controlled signaling molecules that have metabolic effects beyond their primary role in bile to aid in the digestion of lipids and fat. Bile acids signal via various membrane and nuclear receptors. Therefore, bile acid sequestrants may exert glycemic effects by altering the interaction of these bile acid pathways. This article reviews the role for bile acids in glucose regulation and discusses the potential mechanism(s) of action for the glycemic effects of bile acid sequestrants.

Olsson AG, Nilsson PM. · Institutionen för medicin och hälsa, Hälsouniversitetet, Linköping. · Lakartidningen. · Pubmed #19452786 No free full text.

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Bláha V, Mistrík E. · Klinika gerontologická a metabolická Lékarské fakulty UK a FN Hradec Králové. · Vnitr Lek. · Pubmed #19449750 No free full text.

Abstract: Diabetes mellitus associates with high cardiovascular risk. The absolute values of cardiovascular risk tend to be even higher than as calculated from the SCORE tables. Recent randomized clinical trials have shown evidence of benefit and safety of more intensive LDL-cholesterol lowering in patients with diabetes and established cardiovascular disease supporting guidelines for a more intensive LDL goal of therapy. A recent meta-analysis has confirmed benefit on major coronary events and ischaemic stroke in many diabetic patient subgroups, including those with type 1 disease. The pathological combination of several lipoprotein metabolism abnormalities and the need to reach lipoprotein goals need combination therapy of hypolipidemic drugs with different mechanisms of action. Despite statin treatment, cardiovascular disease residual risk remains high. After LDL the next lipoprotein goal is to increase HDL. Although there has been disappointment with the first cholesteryl-ester-transfer-protein-inhibitor, there is encouraging evidence that increasing HDL with the peroxisome-proliferator-activator-receptor (PPAR) gamma agonist, pioglitazone and nicotinic acid derivatives may contribute beyond statin therapy.

Giorgi PL. · Università, Ancona. · Recenti Prog Med. · Pubmed #19445282 No free full text.

Abstract: Probiotics are defined viable microorganisms which in sufficient amount reach the intestine in an active state, to be able to exert positive health benefit on the host. Thus far, they have shown particular promise on prevention or treatment of various pathologic conditions. Our aim has been to report the most recent articles (until October 2008), resulting from randomized, double controlled trials, according to the conventional and molecular methods. In this review we have taken into consideration almost all the fields in which the probiotics have been given, either with a prophylactic or therapeutic intent. So far we have summarized the actual results concerning lactose intolerance, acute rotavirus diarrhea, traveller's diarrhea, antibiotic associated diarrhea, Clostridium difficile infection, and the role as adjuvant in Helicobacter pylori eradication. Furthermore, we have synthesised articles concerning the probiotic connection in irritable bowel syndrome, and in inflammatory bowel diseases. Last but not least, the prevention by probiotics of allergic diseases, of bacterial vaginosis, of respiratory infections, and the possible advantage in hypercholesteremic subjects.

Fudickar A, Bein B. · Department of Anesthesiology and Intensive Care Medicine, University Hospital Schleswig-Holstein, Kiel, Germany. · Minerva Anestesiol. · Pubmed #19412155 links to  free full text

Abstract: Propofol infusion syndrome (PRIS) is defined as acute bradycardia progressing to asystole combined with lipemic plasma, fatty liver enlargement, metabolic acidosis with negative base excess >10 mmol l(-1), rhabdomyolysis or myoglobinuria associated with propofol infusion. The purpose of this review was to provide a new update of reported case reports and to describe recent retrospective studies and animal research relevant for the pathophysiology and clinical presentation of PRIS. New case reports of PRIS have confirmed previously identified risk factors, and have also further revealed the incidence of PRIS in patients previously not estimated to be at risk for this syndrome. Retrospective studies contributed new evidence to the incidence of PRIS and development of PRIS even at propofol doses commonly used for surgical anesthesia. An animal study confirmed potential pathophysiological pathways and showed new organ manifestations possibly associated with propofol infusion. Further clinical and experimental evidence has confirmed the existence of PRIS as a rare but highly lethal complication of propofol use not limited to prolonged use of propofol. PRIS has to be kept in mind if propofol is used for anesthesia or sedation. Recommendations for the limitation of propofol use have to be adhered to. Early warning signs must prompt immediate cessation of propofol infusion and adequate treatment.

Giannattasio C, Failla M, Corsi D, Capra A, Meles E, Gentile G, Fantini E, Boffi L, Maestroni S, Scotti V, Mancia G. · Clinica Medica, Università degli Studi di Milano-Bicocca, Ospedale San Gerardo, Monza, MI. · Ital Heart J Suppl. · Pubmed #19400052 No free full text.

Abstract: The reduction of large arterial distensibility has several adverse consequences for the cardiovascular system. This paper reviews the evidence we have obtained by measuring distensibility through quantification of changes in arterial diameter vs blood pressure changes at large elastic and middle size muscle artery sites. Evidence shows that arterial distensibility is reduced in conditions such as hypercholesterolemia, hypertension, diabetes, and congestive heart failure. In some conditions (e.g. hypertension) the alterations are not uniformly distributed in the arteries of different structure and size whereas in others (e.g. diabetes and heart failure) they are widespread. In diabetes evidence is available that distensibility changes occur early in the course of the disease. Evidence is also available that in all above conditions treatment can improve arterial distensibility thereby reversing the initial abnormality. This is due to a variable combination of structural and functional factors. However, technical ability to determine their precise role in distensibility changes in humans is limited.