Hyperlipidemias: USA

Navaneethan SD, Pansini F, Perkovic V, Manno C, Pellegrini F, Johnson DW, Craig JC, Strippoli GF. · Department of Nephrology and Hypertension, Glickman Urological and Kidney institute, Cleveland Clinic, Cleveland, OH 44195, USA. · Cochrane Database Syst Rev. · Pubmed #19370693 No free full text.

Abstract: BACKGROUND: Dyslipidaemia occurs frequently in chronic kidney disease (CKD) patients and contributes both to cardiovascular disease and worsening renal function. Statins are widely used in non-dialysis dependent CKD patients (pre-dialysis) even though evidence favouring their use is lacking. OBJECTIVES: To evaluate the benefits and harms of statins in CKD patients who were not receiving renal replacement therapy. SEARCH STRATEGY: We searched MEDLINE, EMBASE, CENTRAL (in The Cochrane Library), and hand-searched reference lists of textbooks, articles and scientific proceedings. SELECTION CRITERIA: Randomised controlled trials (RCTs) and quasi-RCTs comparing statins with placebo, no treatment or other statins in adult pre-dialysis CKD patients. DATA COLLECTION AND ANALYSIS: Two authors independently assessed study quality and extracted data. Results were expressed as mean difference (MD) for continuous outcomes (lipids, creatinine clearance and proteinuria) and risk ratio (RR) for dichotomous outcomes (all-cause mortality, cardiovascular mortality, fatal and non-fatal cardiovascular events, elevated liver enzymes, rhabdomyolysis and withdrawal rates) with 95% confidence intervals (CI). MAIN RESULTS: Twenty six studies (25,017 participants) comparing statins with placebo were identified. Total cholesterol decreased significantly with statins (18 studies, 1677 patients: MD -41.48 mg/dL, 95% CI -49.97 to -33.99). Similarly, LDL cholesterol decreased significantly with statins (16 studies, 1605 patients: MD -42.38 mg/dL, 95% CI -50.71 to -34.05). Statins decreased both the risk of all-cause (21 RCTs, 18,781 patients, RR 0.81, 95% CI 0.74, 0.89) and cardiovascular deaths (20 studies, 18,746 patients: RR 0.80, 95% CI 0.70 to 0.90). Statins decreased 24-hour urinary protein excretion (6 studies, 311 patients: MD -0.73 g/24 h, 95% CI -0.95 to -0.52), but there was no significant improvement in creatinine clearance - a surrogate marker of renal function (11 studies, 548 patients: MD 1.48 mL/min, 95% CI -2.32 to 5.28).The incidence of rhabdomyolysis, elevated liver enzymes and withdrawal rates due to adverse events (well known complications of statins use), were not significantly different between patients receiving statins and placebo. AUTHORS' CONCLUSIONS: Statins significantly reduced the risk of all-cause and cardiovascular mortality in CKD patients who are not receiving renal replacement therapy. They do not impact on the decline in renal function as measured by creatinine clearance, but may reduce protein excretion in urine. Statins appear to be safe in this population. Guidelines recommendations on hyperlipidaemia management in CKD patients could therefore be followed targeting higher proportions of patients receiving a statin, with appropriate monitoring of adverse events.

Penumathsa SV, Maulik N. · Molecular Cardiology and Angiogenesis Laboratory, Department of Surgery, University of Connecticut Health Center, 263 Farmington Avenue, Farmington, CT 06030-1110, USA. · Can J Physiol Pharmacol. · Pubmed #19370081 No free full text.

Abstract: The inverse association between alcohol intake and coronary heart disease has been consistently reported in cross-culture, case-control, and cohort studies. Over the past couple of decades, however, many studies have explained promising health benefits associated with wine consumption. Some studies suggest that red wine is more cardioprotective than white wine, possibly due to the increased content of flavanoid antioxidants found in red wine. Several experimental studies, including ours, support the evidence that these beneficial effects are due to resveratrol, the polyphenolic compound present in red wine. Many studies have provided evidence that resveratrol possesses antioxidant and antiapoptotic effects apart from activation of longevity proteins (such as SIRT-1). We have recently reported the angiogenic, antihypercholesterolemic, and antidiabetic effects of resveratrol and the mechanisms involved in reduced ventricular remodeling and increased cardiac functions. We have also shown different strategic target molecules involved in resveratrol-mediated cardioprotection. Therefore, this review discusses the potential effect of resveratrol and the mechanisms involved in resveratrol-mediated cardioprotection during myocardial infarction, hypercholesterolemia, and diabetes rendering its beneficial effects during health and disease.

Beigneux AP, Weinstein MM, Davies BS, Gin P, Bensadoun A, Fong LG, Young SG. · Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, California, USA. · Curr Opin Lipidol. · Pubmed #19369870 No free full text.

Abstract: PURPOSE OF REVIEW: This review will provide an update on the structure of GPIHBP1, a 28-kDa glycosylphosphatidylinositol-anchored glycoprotein, and its role in the lipolytic processing of triglyceride-rich lipoproteins. RECENT FINDINGS: Gpihbp1 knockout mice on a chow diet have milky plasma and plasma triglyceride levels of more than 3000 mg/dl. GPIHBP1 is located on the luminal surface of endothelial cells in tissues where lipolysis occurs: heart, skeletal muscle, and adipose tissue. The pattern of lipoprotein lipase (LPL) release into the plasma after an intravenous injection of heparin is abnormal in Gpihbp1-deficient mice, suggesting that GPIHBP1 plays a direct role in binding LPL within the tissues of mice. Transfection of CHO cells with a GPIHBP1 expression vector confers on cells the ability to bind both LPL and chylomicrons. Two regions of GPIHBP1 are required for the binding of LPL - an amino-terminal acidic domain and the cysteine-rich Ly6 domain. GPIHBP1 expression in mice changes with fasting and refeeding and is regulated in part by peroxisome proliferator-activated receptor-gamma. SUMMARY: GPIHBP1, an endothelial cell-surface glycoprotein, binds LPL and is required for the lipolytic processing of triglyceride-rich lipoproteins.

Lindberg DA. · Gastroenterology & Hepatology Clinic, Dartmouth-Hitchcock Medical Center, Lebanon, New Hampshire 03756, USA. · Gastroenterol Nurs. · Pubmed #19357469 No free full text.

Abstract: Pancreatitis is a condition characterized by painful inflammation of the pancreas and can be either chronic or acute. The most common causes of acute pancreatitis (AP) in the United States are gallstones and excessive alcohol consumption. In addition, significantly elevated serum triglyceride levels can precipitate episodes of AP. Genetic defects are associated with severe elevations in serum triglyceride levels, whereas poorly controlled diabetes, obesity, and high-fat diets can contribute to elevated triglyceride levels substantial enough to provoke pancreatitis (secondary hypertriglyceridemia). Treatment of hypertriglyceridemia-induced AP consists of immediate reduction in serum triglyceride levels and long-term medications and lifestyle modifications. Nurses are instrumental in patient education about lifelong treatment strategies.

Karalis DG. · Drexel University College of Medicine, Philadelphia, PA, USA. · Mayo Clin Proc. · Pubmed #19339653 No free full text.

Abstract: Coronary artery disease (CAD) is the leading cause of morbidity and mortality in the United States, and a high concentration of low-density lipoprotein cholesterol (LDL-C) is a major risk factor for CAD. Current guidelines recommend the use of statins to lower LDL-C levels for the primary prevention of CAD based on an individual's risk factor profile and baseline LDL-C level. For moderaterisk individuals, those with 2 or more major risk factors for CAD and a Framingham risk score of 10% to 20%, the recommendation is to use a statin to lower LDL-C levels to less than 130 mg/dL. However, up to 40% of individuals who develop CAD have LDL-C levels lower than this cutoff. In 2004, the National Cholesterol Education Program Adult Treatment Panel III guidelines were updated to include an LDL-C goal of less than 100 mg/dL for individuals at moderately high risk of developing CAD. The guidelines identified several risk factors that when present would favor the use of pharmacological therapy to achieve this more aggressive LDL-C goal. This review evaluates the evidence supporting an LDL-C target of less than 100 mg/dL for moderately high-risk individuals and reviews those risk factors that when present help identify patients who would benefit from achieving this lower LDL-C goal. English-language publications in MEDLINE and references from relevant articles published between January 1, 1980, and November 30, 2008, were reviewed. Main keywords searched were coronary artery disease, hyperlipidemia, statins, cardiac risk factors, inflammatory markers, metabolic syndrome, and coronary artery calcium.

Chan EJ, Cho L. · Women's Cardiovascular Center, Jb1, Cleveland Clinic, Cleveland, OH 44195, USA. · Cleve Clin J Med. · Pubmed #19339640 links to  free full text

Abstract: Omega-3 fatty acids are abundant in fish oil. A high dietary intake of omega-3 fatty acids has been strongly linked to lower rates of cardiovascular disease in epidemiologic studies. Fish oil supplements lower triglyceride levels and may have other benefits such as preventing arrhythmias, reducing inflammation (although they have minimal impact on C-reactive protein), inhibiting platelet aggregation, and lowering blood pressure, all of which should reduce cardiovascular risk.

Pfefferkorn JA. · Pfizer Global Research & Development, Cardiovascular and Metabolic Disease Chemistry, Eastern Point Road, Groton, CT 06340, USA. · Curr Opin Investig Drugs. · Pubmed #19333882 No free full text.

Abstract: Coronary heart disease (CHD) is a leading cause of death in the US, and hypercholesterolemia is a key risk factor for this disease. The current standard of care for treating hypercholesterolemia is the use of HMG-CoA reductase inhibitors, also known as statins, which block the rate-limiting step of cholesterol biosynthesis. In widespread clinical use, statins have proven safe and effective for both primary prevention of CHD and secondary prevention of coronary events. Results from several recent clinical trials have demonstrated that increasingly aggressive cholesterol-lowering therapy might offer additional protection against CHD compared with less aggressive treatment standards. While higher doses of current statin therapies are capable of achieving these more aggressive treatment goals, in certain cases statin-induced myalgia, the muscle pain or weakness that sometimes accompanies high-dose statin therapy, limits patient compliance with a treatment regimen. To address this limitation, efforts have been undertaken to develop highly hepatoselective statins that are capable of delivering best-in-class efficacy with minimized risk of dose-limiting myalgia. In this review, the preclinical and early clinical data for these next generation statins are discussed.

Huffmyer J, Raphael J. · Department of Anesthesiology, University of Virginia Health Sciences System, Charlottesville, Virginia 22908, USA. · Semin Cardiothorac Vasc Anesth. · Pubmed #19329471 No free full text.

Abstract: Perioperative myocardial ischemia and infarction are not only major sources of morbidity and mortality in patients undergoing surgery but also important causes of prolonged hospital stay and resource utilization. Ischemic and pharmacological preconditioning and postconditioning have been known for more than 2 decades to provide protection against myocardial ischemia and reperfusion and limit myocardial infarct size in many experimental animal models, as well as in clinical studies. This article reviews the physiology and pharmacology of ischemic and drug-induced preconditioning and postconditioning of the myocardium with special emphasis on the mechanisms by which volatile anesthetics provide myocardial protection. Insights gained from animal and clinical studies are reviewed and recommendations given for the use of perioperative anesthetics and medications.

Tsuang W, Navaneethan U, Ruiz L, Palascak JB, Gelrud A. · Department of Internal Medicine, University of Cincinnati Medical Center, Cincinnati, Ohio, USA. · Am J Gastroenterol. · Pubmed #19293788 No free full text.

Abstract: Hypertriglyceridemia (HTG) is reported to cause 1-4% of acute pancreatitis (AP) episodes. HTG is also implicated in more than half of gestational pancreatitis cases. Disorders of lipoprotein metabolism are conventionally divided into primary (genetic) and secondary causes, including diabetes, hypothyroidism, and obesity. Serum triglyceride (TG) levels above 1,000 mg/dl are usually considered necessary to ascribe causation for AP. The mechanism for hypertriglyceridemic pancreatitis (HTGP) is postulated to involve hydrolysis of TG by pancreatic lipase and release of free fatty acids that induce free radical damage. Multiple small studies on HTGP management have evaluated the use of insulin, heparin, or both. Many series have also reported use of apheresis to reduce TG levels. Subsequent control of HTG with dietary restrictions, antihyperlipidemic agents, and even regular apheresis has been shown anecdotally in case series to prevent future episodes of AP. However, large multicenter studies are needed to optimize future management guidelines for patients with HTGP.

Dall TL, Bays H. · Advanced Lipidology, Delafield, WI 53018, USA. · South Med J. · Pubmed #19279539 No free full text.

Abstract: Decreasing very high triglyceride (TG) levels (>or=500 mg/dL) is recommended to prevent pancreatitis. Decreasing low-density lipoprotein cholesterol (LDL-C) is the primary lipid treatment target to reduce the risk of atherosclerotic coronary heart disease. A secondary lipid treatment target for patients at LDL-C goal, but with persistent TG elevations, includes achievement of non-high density lipoprotein cholesterol goals (non-HDL-C). Statins are the mainstay of therapy to lower LDL-C, but statin monotherapy may not achieve all lipid treatment goals. Thus, in patients with multiple lipid abnormalities, combination lipid-altering therapy is often necessary. Drugs such as niacin and fibrates provide lipid benefits beyond LDL-C when used in combination with a statin. Prescription omega-3-fatty acids combined with statin therapy also provide improvements in lipid parameters beyond cholesterol alone.

Jacobs DR, Gross MD, Tapsell LC. · School of Public Health, University of Minnesota, Minneapolis, MN, USA. · Am J Clin Nutr. · Pubmed #19279083 No free full text.

Abstract: Research and practice in nutrition relate to food and its constituents, often as supplements. In food, however, the biological constituents are coordinated. We propose that "thinking food first"' results in more effective nutrition research and policy. The concept of food synergy provides the necessary theoretical underpinning. The evidence for health benefit appears stronger when put together in a synergistic dietary pattern than for individual foods or food constituents. A review of dietary supplementation suggests that although supplements may be beneficial in states of insufficiency, the safe middle ground for consumption likely is food. Also, food provides a buffer during absorption. Constituents delivered by foods taken directly from their biological environment may have different effects from those formulated through technologic processing, but either way health benefits are likely to be determined by the total diet. The concept of food synergy is based on the proposition that the interrelations between constituents in foods are significant. This significance is dependent on the balance between constituents within the food, how well the constituents survive digestion, and the extent to which they appear biologically active at the cellular level. Many examples are provided of superior effects of whole foods over their isolated constituents. The food synergy concept supports the idea of dietary variety and of selecting nutrient-rich foods. The more we understand about our own biology and that of plants and animals, the better we will be able to discern the combinations of foods, rather than supplements, which best promote health.

Raman VS, Heptulla RA. · Department of Pediatrics, Division of Endocrinology and Metabolism, Baylor College of Medicine and Texas Children's Hospital, Houston, TX, USA. · Tex Med. · Pubmed #19221942 No free full text.

Abstract: Vandana S. Raman, MD, and Rubina A. Heptulla, MD, explain the clinical assessment and management strategies for childhood hyperlipidemia.

Toth PP. · Sterling Rock Falls Clinic, Ltd., 101 East Miller Road, Sterling, IL 61081, USA. · Endocrinol Metab Clin North Am. · Pubmed #19217517 No free full text.

Abstract: The protectiveness of elevated HDL-C against CHD and its long-term sequelae is a subject of intense investigation throughout the world. HDL has the capacity to modulate a large number of atherogenic mechanisms, such as inflammation, oxidation, thrombosis, and cell proliferation. Among lipoproteins, HDL is also unique, in that it promotes the mobilization and clearance of excess lipid via the series of reactions collectively termed "reverse cholesterol transport." Numerous therapeutic agents are being developed in an attempt to modulate serum levels of HDL-C as well as its functionality. This article discusses the development of newer treatments targeted at raising HDL-C and HDL particle numbers to reduce residual risk in patients at risk for CHD.

Goldberg IJ. · Division of Preventive Medicine and Nutrition, Department of Medicine, Columbia University College of Physicians and Surgeons, 630 West 168th Street, New York, NY10032, USA. · Endocrinol Metab Clin North Am. · Pubmed #19217516 No free full text.

Abstract: The treatment of elevated levels of low-density lipoprotein cholesterol is standard medical practice supported by conclusive outcome data. Less definitive information exists for hypertriglyceridemia. Only in the setting of severe hyperchylomicronemia is the benefit of triglyceride lowering clear: it is a means to reduce the risk of pancreatitis. The relationship of triglycerides and cardiovascular disease is still unclear. Moreover, the cardiovascular benefits of reducing triglycerides and of using triglyceride-lowering medications remain unproved. Nonetheless it has become almost standard to reduce the levels of triglyceride-rich lipoproteins that are a major component of plasma non-high-density lipoprotein cholesterol.

Stein EA. · Metabolic and Atherosclerosis Research Center, 4685 Forest Avenue, Cincinnati, OH, USA. · Endocrinol Metab Clin North Am. · Pubmed #19217514 No free full text.

Abstract: Although the past 30 years have been fruitful and productive in lipid research, from basic science to drug development to demonstration of clinical benefit, cardiovascular disease remains the major cause of mortality and morbidity in industrialized societies. With the rapid industrialization of countries, such as India and China, cardiovascular disease rapidly is becoming the leading cause of global death and disability. Although most of the effective lipid-lowering drugs, the statins, have become generic and inexpensive, there remains a need for effective and safe agents. Hopefully, some of those discussed in this article will fill that need.

Hou R, Goldberg AC. · Endocrine Unit, University of Rochester, 601 Elmwood Avenue, Box 693, Rochester, NY 14642, USA. · Endocrinol Metab Clin North Am. · Pubmed #19217513 No free full text.

Abstract: Statins, ezetimibe, and bile acid-binding resins can be used individually or in combination for lowering low-density lipoprotein cholesterol (LDL-C) levels. Statins are the most potent drugs for lowering LDL-C and are well tolerated in most patients. The addition of a bile acid sequestrant or ezetimibe to a statin produces additional LDL-C reduction allowing many patients to reach LDL-C targets. This article discusses the efficacy and safety of available statins, bile acid sequestrants, and ezetimibe in the treatment of hyperlipidemia.

Katcher HI, Hill AM, Lanford JL, Yoo JS, Kris-Etherton PM. · Department of Nutritional Sciences, Pennsylvania State University, 119 Chandlee Lab, University Park, PA 16802, USA. · Endocrinol Metab Clin North Am. · Pubmed #19217512 No free full text.

Abstract: This article discusses specific dietary factors as well as dietary patterns that affect the major coronary heart disease (CHD) lipid risk factors (ie, LDL-C, HDL-C, and TG). Based on a very large evidence base, it is clear that diet and lifestyle practices can markedly affect these major CHD lipid risk factors, and consequently decrease CHD risk substantively.

Garbarino J, Sturley SL. · Institute of Human Nutrition, Columbia University Medical Center, New York, New York 10032, USA. · Curr Opin Clin Nutr Metab Care. · Pubmed #19202381 No free full text.

Abstract: PURPOSE OF REVIEW: To present current perspectives on the mediators and mechanisms of cyto-lipotoxic events and their relevance to human health. RECENT FINDINGS: The relatively recent isolation of lipid acyltransferase genes from yeast to mice and humans has resulted in a paradigm shift that now establishes all fatty acids as toxic, albeit in tissue specific patterns and by different mechanisms. Furthermore, the dysregulation of glucose homeostasis in combination with excess fatty acids provides a synergistic effect leading to glucolipotoxicity and cell death. These findings are relevant to the development of disease states associated with the pathogenesis of the metabolic syndrome. SUMMARY: In an era when an astounding number of people are diagnosed with metabolic disorders, it is imperative that we understand the consequences of a chronic metabolic surplus. Excessive fat, saturated or otherwise, has to be accommodated. Multiple aspects of this homeostasis are emerging, some of which are described here.

Zhou Q, Liao JK. · Vascular Medicine Research Unit, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts 02139, USA. · Curr Pharm Des. · Pubmed #19199975 No free full text.

Abstract: Statins are 3-hydroxy-3-methyglutaryl coenzyme A (HMG-CoA) reductase inhibitors, which are prescribed extensively for cholesterol lowering in the primary and secondary prevention of cardiovascular disease. Recent compelling evidence suggests that the beneficial effects of statins may not only be due to their cholesterol lowering effects, but also, to their cholesterol-independent or pleiotropic effects. Through these so-called pleiotropic effects, statins are directly involved in restoring or improving endothelial function, attenuating vascular remodeling, inhibiting vascular inflammatory response, and perhaps, stabilizing atherosclerotic plaques. These cholesterol-independent effects of statins are predominantly due to their ability to inhibit isoprenoid synthesis, the products of which are important lipid attachments for intracellular signaling molecules, such as Rho, Rac and Cdc42. In particular, inhibition of Rho and its downstream target, Rho-associated coiled-coil containing protein kinase (ROCK), has emerged as the principle mechanisms underlying the pleiotropic effects of statins. This review provides an update of statin-mediated vascular effects beyond cholesterol lowering and highlights recent findings from bench to bedside to support the concept of statin pleiotropy.

Neeli H, Gadi R, Rader DJ. · Institute for Translational Medicine and Therapeutics, University of Pennsylvania School of Medicine, 654 BRB II/III, 421 Curie Boulevard, Philadelphia, PA 19104, USA. · Curr Diab Rep. · Pubmed #19192419 No free full text.

Abstract: Cardiovascular disease is a significant cause of morbidity and mortality in patients with diabetes mellitus. The lipid profile of type 2 diabetes mellitus is characterized by increased triglycerides (TGs), decreased high-density lipoprotein cholesterol (HDL-C), increased very low density lipoproteins (VLDLs), and small, dense low-density lipoprotein particles, the combination of which is highly atherogenic. In diabetic patients, current treatment guidelines target low-density lipoprotein cholesterol (LDL-C) <or= 100 mg/dL with statins. In patients with elevated TGs, non-HDL-C is considered a secondary target of therapy. Despite the use of statin therapy in diabetes, a significant number of fatal and nonfatal coronary heart disease (CHD) events still occur, indicating the need to target other modifiable risk factors for CHD, including high TGs and low HDL-C.

Brooks JO, Chang HS, Krasnykh O. · UCLA Semel Institute, MC 175919, 760 Westwood Plaza, B8-233B NPI, Los Angeles, CA 90024, USA. · Curr Psychiatry Rep. · Pubmed #19187706 No free full text.

Abstract: Metabolic syndrome is prevalent in older adults and increases the risk of cardiovascular disease. Second-generation antipsychotics (aripiprazole, clozapine, olanzapine, quetiapine, risperidone, and ziprasidone) increase the risk of metabolic syndrome and present many challenges for psychiatrists. In this article, we review the relationships between second-generation antipsychotics and metabolic syndrome with a focus on older adults. Because few studies focus exclusively on older adults, we augment this review with relevant findings from younger adults. The differential risk factors of each medication are reviewed, as are recent findings in monitoring and treating metabolic syndrome. Olanzapine and clozapine are more strongly associated with metabolic risks, whereas aripiprazole and ziprasidone are less associated. Although lifestyle modifications can help to reduce some aspects of metabolic syndrome, lifestyle modifications in conjunction with metformin therapy appear to be most effective.

Stahl SM, Mignon L, Meyer JM. · Department of Psychiatry, University of California, San Diego School of Medicine, San Diego, CA 92008, USA. · Acta Psychiatr Scand. · Pubmed #19178394 No free full text.

Abstract: OBJECTIVE: To provide an overview for practicing clinicians on the pharmacological basis of cardiometabolic risk induced by antipsychotic drugs in patients with serious mental illness, to propose hypotheses to explain these risks and to give tips for managing cardiometabolic risk during antipsychotic treatment. METHOD: A MEDLINE search using terms for atypical antipsychotics (including individual drug names), metabolic, cardiovascular, weight gain and insulin resistance, cross-referenced with schizophrenia was performed on articles published between 1990 and May 2008. RESULTS: Strong evidence exists for significant cardiometabolic risk differences among several antipsychotic agents. Histamine H1 and serotonin 5HT2C antagonism are associated with risk of weight gain, but receptor targets for dyslipidemia and insulin resistance have not yet been identified. Convincing data indicate that hypertriglyceridemia and insulin resistance may occur in the absence of weight gain with certain antipsychotics. CONCLUSION: Although lifestyle and genetics may contribute independent risks of cardiometabolic dysfunction in schizophrenia and other serious mental illness, antipsychotic treatment also represents an important contributor to risk of cardiometabolic dysfunction, particularly for certain drugs and for vulnerable patients. Mental health professionals must learn to recognize the clinical signposts indicating antipsychotic-related cardiometabolic problems to forestall progression to type II diabetes, cardiovascular events and premature death.

Kaysen GA. · Division of Nephrology, Department of Medicine and of Biochemistry and Molecular Medicine, UC Davis, Davis, Calif. 95616, USA. · Blood Purif. · Pubmed #19169024 No free full text.

Abstract: The risk of cardiovascular disease increases with declining glomerular filtration rate. Hyperlipidemia and dyslipidemia, characterized by increased triglycerides and low levels of high-density lipoprotein, are both associated with cardiovascular outcome as well as the risk of progression of loss of renal function. Both hyperlipidemia and dyslipidemia respond to pharmacologic therapy, including hydroxymethylglutaryl-CoA reductase inhibitors and fibric acid derivatives, to alteration in diet as well as to extreme measures such as bariatric surgery. However, the effects of these modalities on cardiovascular or renal outcomes are dependent upon the level of renal function. There is strong evidence that patients with stages 1-3 chronic kidney disease attain benefit from lipid-lowering therapy both with reduction in cardiovascular risk and possibly reduction in the rate of decline in renal function. Among dialysis patients little risk reduction appears to be achieved by treatment of low-density lipoprotein cholesterol level. Bariatric surgery reduces hyperlipidemia in patients with chronic kidney disease, but has also been associated with subsequent rapid decline in renal function secondary to oxalate deposition.

Dembowski E, Davidson MH. · The University of Chicago, Pritzker School of Medicine, Chicago, Illinois 60637, USA. · J Cardiopulm Rehabil Prev. · Pubmed #19158581 No free full text.

Abstract: Lipid management in primary and secondary prevention reduces cardiovascular morbidity and mortality. Lowering of low-density lipoprotein cholesterol (LDL-C) levels with statins remains the primary goal of therapy. For secondary prevention patients, those with coronary heart disease (CHD) or CHD risk equivalents, intensive LDL-C lowering is recommended, although the precise target value is still debated. For primary prevention, reduction in LDL-C levels is based on patient risk for CHD. In clinical outcome trials to date, statins benefit those who are at moderate to high risk and appear to have less clinical benefit for those at low risk. Yet despite aggressive LDL-C management with statins, there remains a residual risk for CHD events in high-risk patients. Secondary targets have been proposed to decrease this risk, including non-high-density lipoprotein cholesterol, high-sensitivity C-reactive protein, and apolipoprotein B, as well as other emerging targets, including LDL particle number and lipoprotein(a). In many high-risk patients, statin monotherapy is unlikely to achieve goals, and combination therapy with other agents is a safe, effective, and optimal therapeutic approach.

Collins N, Tighe AP, Brunton SA, Kris-Etherton PM. · RD411.com, Inc, Weston, Florida,USA. · J Am Coll Nutr. · Pubmed #19155425 No free full text.

Abstract: The medical management of many diseases and conditions can include either restriction or provision of specific essential nutrients. When such nutrients are needed, there are often both prescription and nonprescription products available, as in the case of nicotinic acid or omega-3 fatty acids. Although they may seem to contain similar ingredients, there may be important differences between the prescription and dietary-supplement preparations. The manufacturing of prescription pharmaceutical products is regulated by the US Food and Drug Administration (FDA), which mandates standards for consistency and quality assurance. Dietary supplements are available to consumers under the provisions of the Dietary Supplement Health and Education Act of 1994, for which the FDA has the burden of proving a dietary supplement is harmful rather than requiring the manufacturer prove that the supplement is safe. Consumers and medical professionals should be aware of the important qualitative and quantitative differences between the FDA-approved prescription formulations and dietary supplements, particularly when an essential nutrient is part of the medical management of a disease or condition.