Hyperlipidemias: Finland

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

This publication has no abstract.

Kauppila LI. · Terveystalo Healthcare, Helsinki, Finland. · Eur J Vasc Endovasc Surg. · Pubmed #19328027 No free full text.

Abstract: OBJECTIVES: Atherosclerosis can obstruct branching arteries of the abdominal aorta, including four paired lumbar arteries and the middle sacral artery that feed the lumbar spine. The diminished blood flow could result in various back problems. The aim of this systematic literature review was to assess associations between atherosclerosis and disc degeneration (DD) or low-back pain (LBP). DATA SOURCES: A systematic search of the Medline/PubMed database for all original articles on atherosclerosis and DD/LBP published until October 2008. The search was performed with the medical subject headings atherosclerosis, cardiovascular risk factor, or vascular disease and keywords "disc degeneration", "disc herniation", and "back pain" on the basis of MeSH tree and as a text search. In addition reference lists were studied and searched manually. Observational studies investigating the association of atherosclerosis or its risk factors and lumbar DD/LBP were selected. REVIEW METHODS: The following data were extracted: study characteristics, duration of follow-up, year of publication, findings of atherosclerosis/cardiovascular risk factors and DD/LBP. Disc herniation was regarded as a form of disc degeneration and cardiovascular risk factors were regarded as surrogate for atherosclerosis in epidemiological studies. RESULTS: One hundred and seventy-nine papers were identified. After exclusion of case reports, letters, editorials, papers not related to the lumbar spine, and animal studies, 25 papers were included. Post-mortem studies showed an association between atheromatous lesions in the aorta and DD, as well as between occluded lumbar arteries and life-time LBP. In clinical studies, aortic calcification was associated with LBP, and stenosis of lumbar arteries was associated with both DD and LBP. In epidemiological studies, smoking and high serum cholesterol levels were found to have the most consistent associations with DD and LBP. CONCLUSION: Aortic atherosclerosis and stenosis of the feeding arteries of the lumbar spine were associated with DD and LBP. Cardiovascular risk factors had weaker associations, being clearly apparent only in cohorts on elderly people or in large study samples. More prospective clinical studies are needed to further clarify the association of atherosclerosis and low-back disorders.

Murtola TJ, Visakorpi T, Lahtela J, Syvälä H, Tammela TLj. · Department of Epidemiology, School of Public Health, University of Tampere, Tampere, Finland. · Nat Clin Pract Urol. · Pubmed #18542103 No free full text.

Abstract: Statins are cholesterol-lowering drugs that are widely used to prevent and treat atherosclerotic cardiovascular disease. Recent research from both in vitro and in vivo studies suggests that there is an association between the use of statins and a reduction in the incidence of and mortality from prostate cancer. Several mechanisms of action that might bring about these beneficial effects of statins have been proposed, most of which include direct effects of statins on intracellular signaling. In this Review we discuss the current knowledge on the use of statins to prevent prostate cancer. We will also look at future directions for clinical research on this topic.

Kesäniemi A. · Department of Internal Medicine, Oulu University Hospital, Oulu, Finland. · Fundam Clin Pharmacol. · Pubmed #18001318 No free full text.

Abstract: There is a large ongoing endpoint trial program using ezetimibe 10 mg combined with simvastatin 20, 40 or 80 mg in a number of patients with a high risk of major cardiovascular events. These studies include the measurement of carotid intima-media thickness in patients with familial hypercholesterolemia, aggressive lowering of LDL in patients with degenerative aortic stenosis, LDL lowering effects on cardiovascular risk and loss of renal function in patients with chronic kidney disease, and treatment of patients with acute coronary syndrome to very low LDL levels.

Rissanen TT, Ylä-Herttuala S. · 1Department of Biotechnology and Molecular Medicine, A. I. Virtanen Institute, Kuopio University, Kuopio, Finland. · Mol Ther. · Pubmed #17505481 No free full text.

Abstract: Gene transfer for the therapeutic modulation of cardiovascular diseases is an expanding area of gene therapy. During the last decade several approaches have been designed for the treatment of hyperlipidemias, post-angioplasty restenosis, hypertension, and heart failure, and for protection of vascular by-pass grafts and promotion of therapeutic angiogenesis. Adenoviruses (Ads) and adeno-associated viruses (AAVs) are currently the most efficient vectors for delivering therapeutic genes into the cardiovascular system. Gene transfer using local gene delivery techniques have been shown to be superior to less-targeted intra-arterial or intra-venous applications. To date, no gene therapy drugs have been approved for clinical use in cardiovascular applications. In preclinical studies of therapeutic angiogenesis, various growth factors such as vascular endothelial growth factors (VEGFs) and fibroblast growth factors (FGFs), have shown positive results. Gene therapy also appears to have potential clinical applications in improving the patency of vascular grafts and in treating heart failure. Post-angioplasty restenosis, hypertension, and hyperlipidemias (excluding homozygotic familial hypercholesterolemia) can usually be managed satisfactorily by conventional approaches, and are therefore less favored areas for gene therapy. The development of technologies that can ensure long-term, targeted, and regulated gene transfer, and a careful selection of target patient populations, will be very important for the progress of cardiovascular gene therapy in clinical applications.

Järvisalo MJ, Raitakari OT. · Department of Internal Medicine, Satakunta Central Hospital, Pori, Finland. · Vasc Health Risk Manag. · Pubmed #17319108 links to  free full text

Abstract: Although the clinical complications of atherosclerosis arise from developed lesions in old age, the atherosclerotic disease is a lifelong process with roots in childhood. Endothelial dysfunction is currently considered an early stage in the pathogenesis of atherosclerosis, which precedes the formation of structural atherosclerotic changes. Improvements in noninvasive imaging modalities, mainly in ultrasound imaging, have made it possible to assess the endothelial health of asymptomatic children with or without cardiovascular risk factors. By using noninvasive ultrasound for endothelial function, important insights have been gained into the early stages of atherosclerosis and the effects of cardiovascular risk factors on vasculature in childhood. The ultrasound test of endothelial function is affordable, available, and safe and may be considered a potent aid in clinical risk stratification of children at high risk for subsequent clinical atherosclerosis in adulthood. At present, this methodology serves only research purposes, as many issues including reproducibility and normal values for healthy children need to be solved before clinical use can be considered. In adults, however, recent studies have shown that attenuated endothelial function predicts the occurrence of future cardiovascular events.

Ikonen E. · Institute of Biomedicine/Anatomy, University of Helsinki, Helsinki, Finland. · Physiol Rev. · Pubmed #17015489 links to  free full text

Abstract: This review summarizes the mechanisms of cellular cholesterol transport and monogenic human diseases caused by defects in intracellular cholesterol processing. In addition, selected mouse models of disturbed cholesterol trafficking are discussed. Current pharmacological strategies to prevent atherosclerosis are largely based on altering cellular cholesterol balance and are introduced in this context. Finally, because of the organizing potential of cholesterol in membranes, disturbances in cellular cholesterol transport have implications for a wide variety of human diseases, of which selected examples are given.

Naukkarinen J, Ehnholm C, Peltonen L. · Department of Molecular Medicine, National Public Health Institute, Helsinki, Finland. · Curr Opin Lipidol. · Pubmed #16680034 No free full text.

Abstract: PURPOSE OF REVIEW: To provide an overview of recent advances that have defined the first putative genes behind familial combined hyperlipidemia, the most common genetic dyslipidemia and a major risk factor for early coronary heart disease. RECENT FINDINGS: The first locus for familial combined hyperlipidemia on 1q21-23 revealed a gene encoding a transcription factor critical in lipid and glucose metabolism, USF1. All the associated variants represent noncoding single nucleotide polymorphisms, one of which affects the binding site of nuclear proteins with a putative effect on transcript levels of USF1. Transcript analyses of fat biopsies have exposed risk-allele related changes in the downstream genes. Another recent clue to the molecular pathogenesis of familial combined hyperlipidemia is the association of the high triglyceride trait with the APOA5 gene, located on 11q. More familial combined hyperlipidemia genes are expected to be found, since linkage evidence exists for additional loci on 16q24 and 20q12-q13.1. SUMMARY: Genetic research of familial combined hyperlipidemia families has revealed several linked loci guiding to susceptibility genes. The USF1 transcription factor is the major gene underlying the 1q21-23 linkage. Modifying genes, especially influencing the high triglyceride trait, include APOC3 and APOA5, the latter representing a downstream target of USF1 and implying a USF1-dependent pathway in the molecular pathogenesis of dyslipidemias.

Laakso M. · Department of Medicine, University of Kuopio, Kuopio, Finland. · Semin Vasc Med. · Pubmed #16222596 No free full text.

Abstract: Type 2 diabetes increases the risk of cardiovascular disease two- to fourfold compared to the risk in nondiabetic subjects. Although type 2 diabetes is associated with a clustering of risk factors, the cause for an excess risk of cardiovascular disease remains unknown. Lipid and lipoprotein abnormalities in type 2 diabetes include particularly elevated levels of total and very low-density lipoprotein triglycerides and reduced levels of high-density lipoprotein (HDL) cholesterol. Total and low-density lipoprotein (LDL) cholesterol levels are usually normal if glycemic control is adequate but LDL particles are small and dense. According to prospective population-based studies, total cholesterol is a similar risk factor for coronary heart disease (CHD) in patients with type 2 diabetes as it is in nondiabetic subjects. High total triglycerides and low HDL cholesterol may be even stronger risk factors for CHD in patients with type 2 diabetes than in nondiabetic subjects. Recent drug treatment trials have indicated that the lowering of total and LDL cholesterol by statins, and the lowering of total triglycerides and the raising of HDL cholesterol by fibrates, are at least as beneficial in diabetic patients as in nondiabetic subjects in the prevention of cardiovascular disease.

Tuomilehto J, Leiter LA, Kallend D. · National Public Health Institute, Helsinki, Finland. · Int J Clin Pract Suppl. · Pubmed #16035394 No free full text.

Abstract: It has been estimated that 92% of individuals with type 2 diabetes, without cardiovascular disease (CVD), have a dyslipidaemic profile. Several guidelines on cardiovascular risk now recommend that patients with diabetes should be considered at high risk of CVD and should thus receive lipid-lowering therapy to reduce low-density lipoprotein cholesterol (LDL-C) to below 2.5 mmol/L. Since their introduction in 1987, statins have revolutionized the management of CVD. The most recent statin to be introduced, rosuvastatin, has been shown to be the most effective at lowering LDL-C, as well as consistently raising HDL-C across the 10-40 mg dose range. This has been confirmed by many studies, including the Measuring Effective Reductions in Cholesterol Using Rosuvastatin Therapy (MERCURY I) study in which rosuvastatin 10 mg was shown to be more effective than commonly used doses of other statins, both for LDL-C reduction and achieving treatment target goals. The effectiveness of rosuvastatin has also been studied in type 2 diabetes patients in three studies: the URANUS (Use of Rosuvastatin vs. Atorvastatin iN type 2 diabetes mellitUS), ANDROMEDA (A raNdomized, Double-blind study to compare Rosuvastatin [10 & 20 mg] and atOrvastatin [10 & 20 Mg] in patiEnts with type II DiAbetes) and CORALL (COmpare Rosuvastatin [10-40 mg] with Atorvastatin [20-80 mg] on apo B/apo A-1 ratio in patients with type 2 diabetes meLLitus and dyslipidaemia) studies. URANUS and ANDROMEDA showed rosuvastatin to be more effective than atorvastatin at reducing LDL-C and achieving treatment target goals. CORALL demonstrated rosuvastatin 10, 20 and 40 mg to be more effective at lowering LDL-C than 20, 40 and 80 mg of atorvastatin, respectively. Ongoing studies will evaluate whether these properties of rosuvastatin translate into beneficial effects on atherosclerosis and significant reductions in cardiovascular events.

Helske S, Lindstedt K, Kovanen P. · Wihurin tutkimuslaitos, Helsinki. · Duodecim. · Pubmed #15999977 No free full text.

This publication has no abstract.

Miettinen TA, Gylling H. · Department of Medicine, Biomedicum Helsinki, University of Helsinki, Helsinki, Finland. · Am J Cardiol. · Pubmed #15992515 No free full text.

Abstract: Normal serum contains small amounts of noncholesterol sterols, including those reflecting cholesterol absorption and those that are markers of cholesterol synthesis. Absorption marker sterols include serum plant sterols, whereas cholesterol precursor sterols correlate with whole-body synthesis of cholesterol. Thus, serum noncholesterol sterols, and especially their ratios to cholesterol, can be used to evaluate the major features of cholesterol metabolism (ie, synthesis and absorption). Statin treatment reduces serum cholesterol precursors but increases serum plant sterols severalfold, especially in subjects with high-absorption marker sterol levels indicative of efficient cholesterol and sterol absorption in general. Statin therapy is most effective in subjects with high serum cholesterol precursor levels. In subjects with high-absorption sterol markers, dietary cholesterol absorption inhibition (eg, with plant stanol and sterol ester margarine) needs to be combined with a statin to achieve effective serum cholesterol reduction. However, whereas dietary plant stanol esters reduce statin-induced elevations of serum plant sterol levels, serum plant sterol levels remain elevated during dietary plant sterol ester consumption. The clinical implication of high serum plant sterol levels is under active investigation.

Tolonen H, Ferrario M, Kuulasmaa K, Anonymous00353. · Department of Epidemiology and Health Promotion, National Public Health Institute (KTL), Helsinki, Finland. · Eur J Cardiovasc Prev Rehabil. · Pubmed #15942425 No free full text.

Abstract: BACKGROUND: The estimation of population distribution of total cholesterol, as well as other blood lipids requires population surveys. Comparability of the estimates over time or between populations requires a predefined, standardized measurement protocol. This paper will assess the effect of variation in the pre-analytic procedures, on the estimation of population distribution of total cholesterol and the prevalence of hypercholesterolaemia. Implications of variation to real survey results are demonstrated on data collected during the WHO MONICA Project. DESIGN AND METHODS: The extent (%) of pre-analytic variations were determined by literature review. Simulations were then used to estimate the effect of these variations on the distribution of total cholesterol values. Three populations were selected as examples for different population distributions of total cholesterol levels and variations resulting from seasonal and postural changes, use of tourniquet, and serum versus plasma collection were simulated both individually and in combinations. RESULTS: Depending on the population distribution of total cholesterol, differences in pre-analytic procedures can explain a difference of up to 1.12 mmol/l in the mean total cholesterol between populations, and a difference up to 41% in the prevalence of hypercholesterolaemia (> or =6.5 mmol/l). CONCLUSIONS: Variation in results on measured total cholesterol levels due to differences in procedures during the pre-analytic stage can diminish substantially the reliability and comparability of measurements among surveys over time and between populations. The effect of pre-analytic variation in the population estimates of total cholesterol can be extensively reduced by standardization and training.

Taskinen MR. · Department of Medicine, University of Helsinki, Finland. · Curr Mol Med. · Pubmed #15892649 No free full text.

Abstract: Diabetic dyslipidemia is a cluster of plasma lipid and lipoprotein abnormalities that are metabolically interrelated. The recognition that the elevation of large VLDL 1 particles initiates a sequence of events that leads to the formation of small dense LDL and HDL species has focused the assembly of VLDL particles on the spotlight as a potential culprit of dyslipidemia. Notably dyslipidemia is associated with insulin resistance, visceral obesity and liver fat content. Insulin resistance is associated with excessive flux of substrates for VLDL assembly to the liver as well as the upregulation of the machinery generating large VLDL particles in excess. The regulation of different molecular steps in this cascade of events are complex and so far poorly understood. The disordered crosstalk between adipose tissue and the liver results in an imbalance of the machinery that orchestrates the regulation of VLDL production. A number of studies indicates that adipocytokines in particular adiponectin may be a seminal player in the regulation of fat metabolism in the liver. Future discoveries hopefully will delineate the regulatory steps to allow more targeted treatment of diabetic dyslipidemia.

Gylling H. · Department of Clinical Nutrition, University of Kuopio, and Kuopio University Hospital, Kuopio, Finland. · Int J Clin Pract. · Pubmed #15529520 No free full text.

Abstract: Cardiovascular diseases are the principal causes of mortality in middle-aged people and in older people. Coronary heart disease (CHD) is the most common of the cardiovascular diseases; high serum levels of cholesterol are associated with atherosclerosis and an increased risk of CHD. Cholesterol homeostasis is achieved by means of a fine balance between cholesterol intake, absorption/excretion and synthesis. All of these processes are tightly linked and a change in one of them can significantly influence the others. Results from both experimental studies and clinical trials have shown that inhibition of cholesterol synthesis with a statin increases absorption and that conversely, inhibition of cholesterol absorption increases synthesis. The tight linkage of cholesterol absorption and synthesis in maintaining cholesterol homeostasis suggests that treatment with an agent that influences only one of these two processes is likely to have distinct limits with respect to its effects on cholesterol levels. Better understanding of cholesterol homeostasis, particularly the close interrelationship between cholesterol synthesis and absorption, may result in the design of rational integrated treatment regimens that employ multiple agents with complementary actions that attack multiple mechanisms to lower cholesterol.

Vanhanen H. · Suomen Sydänliitto ry PL 50, 00621 Helsinki. · Duodecim. · Pubmed #15232853 No free full text.

This publication has no abstract.

Lindstedt KA, Leskinen MJ, Kovanen PT. · Wihuri Research Institute, Helsinki, Finland. · Arterioscler Thromb Vasc Biol. · Pubmed #15191939 links to  free full text

Abstract: The 2 major general concepts about the cell biology of atherogenesis, growth of smooth muscle cells, and lipid accumulation in macrophages, ie, foam cell formation, have not been able to satisfactorily explain the genesis of acute coronary syndromes. Rather, the basic pathology behind the acute atherothrombotic events relates to erosion and rupture of unstable coronary plaques. At the cellular level, we now understand that a switch from cellular growth to cellular death, notably apoptosis, could be involved in turning at least some types of atherosclerotic plaques unstable. Because intimal cells require a proper matrix environment for normal function and survival, the vulnerability of an atherosclerotic plaque may critically depend on the integrity of the pericellular matrix of the plaque cells. In vitro studies have revealed that plaque-infiltrating inflammatory cells, such as macrophages, T-lymphocytes, and mast cells, by secreting a variety of proteases capable of degrading pericellular matrix components, induce death of endothelial cells and smooth muscle cells, and so provide a mechanistic explanation for inflammation-dependent plaque erosion and rupture. Thus, a novel link between inflammation and acute coronary syndromes is emerging. For a more explicit understanding of the role of proteases released by inflammatory cells in the conversion of a clinically silent plaque into a dangerous and potentially killing plaque, animal models of plaque erosion and rupture need to be established.

Vuorio AF, Kovanen PT, Gylling H. · Department of Medicine, University of Helsinki and Helsinki University Central Hospital, PoBox 105, FIN-00029 HUS, Finland. · Expert Rev Cardiovasc Ther. · Pubmed #15151486 No free full text.

Abstract: In familial hypercholesterolemia, a defect in low-density lipoprotein receptors causes lifelong two- to threefold elevations in serum low-density lipoprotein-cholesterol levels. This leads to early atherosclerotic changes in infancy. Lifelong hypolipidemic treatment that can be started at a young age is thus greatly needed. Early diagnosis of familial hypercholesterolemia is important, and improved DNA tests for low-density lipoprotein receptor mutations have made it possible to carry out diagnosis at birth. A low saturated-fat, low cholesterol diet can be safely started at 7 months of age. This can be accompanied by dietary stanol esters from 2 years of age. At the age of 10, statin treatment can be safely started. In adults, more aggressive hypolipidemic treatment is required in order to reach the treatment goal for serum low-density lipoprotein-cholesterol levels less than 2.5 mmol/l. This can be achieved by using high doses of statin, or preferably by combining a statin with resin or ezetimibe (Zeita), Merck and Shering-Plough Pharmaceuticals). Once started, treatment of familial hypercholesterolemia is lifelong.

Tuomilehto J. · National Public Health Institute, University of Helsinki, Mannerheiminite 166, 00300 Helsinki, Finland. · Atheroscler Suppl. · Pubmed #15121030 No free full text.

Abstract: Cardiovascular disease (CVD) represents a major global healthcare problem. The prevalence of this condition increases with age. As many countries around the world are experiencing an increase in the proportion of elderly people in the population, this raises serious issues for cardiac and cerebrovascular disease prevention and management. A wealth of data has established smoking, dyslipidemia, hypertension and type 2 diabetes as major risk factors for cardiac and cerebrovascular events. This article reviews the evidence that links these metabolic risk factors with an increased risk of complications, and assesses the data concerning how risk changes with age. This review also focuses on how these conditions can be optimally managed and whether treatment outcomes are affected by age. The current status of research is assessed and issues which remain to be resolved are highlighted.

Miettinen TA, Gylling H. · Department of Medicine, Division of Internal Medicine, Universiry of Helsinki, Helsinki, Finland. · Ann Med. · Pubmed #15119832 No free full text.

Abstract: Statin trials have indicated that effective reduction of serum cholesterol should last up to one year before reduced risk of cardiovascular diseases can be detected. This observation can be applied most probably also to the use of plant stanol/sterol ester spreads for the treatment of hypercholesterolemia. However, despite the fact that the two spreads lower serum cholesterol similarly in short term studies, a comparison of one year results reveals an inconsistent effect of plant sterol spread as compared with that of plant stanol spread on cholesterol concentration in both men and women. This favors the use of plant stanol ester spread for long-term lowering of serum cholesterol. Doses of about 2 g/day of plant stanols as fatty acid ester spread enhances fecal elimination of cholesterol, but not of bile acids, through inhibition of cholesterol absorption by about 40%. This lowers serum total and low density lipoprotein (LDL) cholesterol despite enhanced compensatory increase in cholesterol synthesis by about 10% and 15% as compared with control spread, respectively, and by up to 20% as compared with the baseline diet. About one-third of mildly hypercholesterolemic subjects reach an accepted cholesterol level. A small dose of statin should be added to treatment in individuals resistant to monotherapy with plant stanol ester spread. A life-long consumption of plant stanol ester spread has been predicted to lower coronary events by about 20%.

Palomäki A. · Kanta-Hämeen keskussairaala 13530 Hämeenlinna. · Duodecim. · Pubmed #15065459 No free full text.

This publication has no abstract.

Laakso M. · Department of Medicine, University of Kuopio, Kuopio, Finland. · Curr Opin Lipidol. · Pubmed #15017354 No free full text.

Abstract: PURPOSE OF REVIEW: Both insulin resistance and dyslipidaemia are determined by genetic and environmental factors. Depending on their expression and their function, gene variants (mutations, polymorphisms) can primarily regulate either insulin action or dyslipidaemia. The purpose of this review is to give some examples from recent studies on gene variants regulating primarily insulin signalling or lipoprotein metabolism. RECENT FINDINGS: Common polymorphisms in the PC-1, insulin receptor substrate 1 and 2, and PPAR-gamma 2 genes have been linked to insulin resistance and dyslipidaemia, although the results have not been consistent. However, the Pro12Pro genotype of the PPAR-gamma 2 gene has been consistently associated with insulin resistance and the risk of type 2 diabetes. Promoter polymorphisms in the hepatic lipase gene, the 54Thr allele of the fatty acid binding protein 2 gene, and genes regulating LDL particle size have been associated with lipid metabolism, but on the other hand their association with insulin resistance is not consistent. SUMMARY: Although results have not always been consistent, gene variants affecting primary insulin action or dyslipidaemia, and particularly their interaction with the environment, are important modulators of glucose and lipoprotein metabolism.

Kaaja R. · HYKS:n naistenklinikka PL 140, 00029 HUS. · Duodecim. · Pubmed #14870505 No free full text.

This publication has no abstract.

Fuentes R, Uusitalo T, Puska P, Tuomilehto J, Nissinen A. · Department of Public Health and General Practice, Faculty of Medicine, University of Kuopio, Kuopio, Finland. · Eur J Cardiovasc Prev Rehabil. · Pubmed #14671463 No free full text.

Abstract: BACKGROUND: While the age-specific rates of cardiovascular diseases (CVD) are declining in many developed countries, the epidemic is accelerating in most developing countries. Elevated serum total cholesterol (TC) is one of the major risk factors for atherosclerotic CVD. This review was carried out to describe the current situation in mean TC and in the prevalence of hypercholesterolaemia in developing countries. DESIGN AND METHODS: A search for papers published in medical journals from 1990 to 2002 was performed using the MEDLINE database. A total of 37 articles were selected according to previously defined criteria containing information on mean blood total cholesterol and/or hypercholesterolaemia from 38 developing countries. RESULTS: Hypercholesterolaemia is a public health problem in most of the developing countries reviewed. A positive association between the population mean TC and the GNP per capita was evidenced. CONCLUSIONS: Differences in methodology between national surveys make international comparisons difficult. Nevertheless, low-cost dietary interventions and the development of primary prevention strategies are needed to reduce the already existing public health problem of elevated TC in developing countries.

Tuomilehto J. · Diabetes and Genetic Epidemiology Unit, National Public Health Institute, Mannerheimintie 166, 00300 Helsinki, Finland. · Diabetes Res Clin Pract. · Pubmed #12880692 No free full text.

Abstract: Efforts to reduce the burden of coronary heart disease (CHD) associated with type 2 diabetes should include increased emphasis on preventing progression to diabetes in individuals with impaired glucose tolerance. Recent large-scale studies have shown that lifestyle intervention can reduce progression to diabetes by nearly 60%. Dyslipidaemia is a risk factor for CHD in diabetic patients. Accumulation of evidence indicating significant reductions in CHD risk with statin treatment to lower low-density lipoprotein (LDL)-cholesterol has led to the recommendation that reduction of LDL-cholesterol be considered the highest priority in treating diabetic dyslipidaemia; additional aims of treatment include raising high-density lipoprotein (HDL)-cholesterol and reducing triglyceride levels. In a recent trial of rosuvastatin alone or combined with fenofibrate in diabetic patients with combined hyperlipidaemia, rosuvastatin 40 mg monotherapy produced marked beneficial changes in LDL-cholesterol (-47%), HDL-cholesterol (+6%) and triglycerides (-30%), with the combination of lower-dose rosuvastatin (10 mg) and fenofibrate producing a significantly greater triglyceride reduction (-47%) and comparable changes in other lipid measures. Combination therapies for dyslipidaemia may be the key to optimizing CHD risk reduction in type 2 diabetes.