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Articles by Peter P. Toth
Total Records ( 20 ) for Peter P. Toth
  Peter P. Toth and Kevin C. Maki
  not available
  Peter P. Toth , Victoria Zarotsky , Jane M. Sullivan and Dave Laitinen
 

Background

National clinical treatment guidelines recommend pharmacologic treatment in addition to therapeutic lifestyle modifications in patients with mixed dyslipidemia and multiple risk factors for coronary heart disease (CHD).

Objectives

To evaluate real-world pharmacologic treatment of mixed dyslipidemia patients with cardiovascular disease (CVD) risk factors.

Methods

Commercial health plan members in a large, United States managed-care database with complete lipid panel results (ie, high-density lipoprotein cholesterol [HDL-C], low-density lipoprotein cholesterol [LDL-C], total cholesterol [TC], triglycerides [TG]) between January 1, 2006 and December 31, 2006 were included. Mixed dyslipidemia was defined as any two nonoptimal lipid parameters (LDL-C, HDL-C, TG) according to National Cholesterol Education Program/Adult Treatment Panel III guidelines. Subjects were observed for 182 days pre-index to determine CVD risk factors (ie, male aged 45+ years, female 55+ years, CHD history, hypertension, diabetes mellitus). Lipid treatment status 6 months pre- and post-index dates was determined using pharmacy claims for any lipid monotherapy (statin, fibrate, niacin, “other”), or combination therapy (statin + fenofibrate; statin + niacin; statin + other).

Results

Lipid treatment increased post-index for all mixed dyslipidemia groups and by total number of risk factors. The increased LDL-C and low HDL-C group had the lowest treatment rates; the group with low HDL-C and elevated TG had the highest. In the latter group, when treated, primarily statin monotherapy (51%) was used post-index; only 26% received niacin or fibrate therapy targeting HDL-C or TG abnormalities. Across all mixed dyslipidemia patients, >30% with three to four CVD risk factors were not treated ≥6 months post-index.

Conclusions

In real-world clinical practice, pharmacologic treatment rates increased upon assessment of multiple lipid abnormalities and by total risk factors for CHD. However, mixed dyslipidemia remained undertreated with low rates of niacin and fibrate usage.

  Peter P. Toth and Michael H. Davidson
  The high-density lipoproteins (HDLs) are complex, polymolecular assemblies produced by the jejunum, liver, in serum, and on the surface of macrophages. HDL cholesterol (HDL-C) levels are an independent predictor of risk for cardiovascular events in both men and women. High serum levels of this lipoprotein are associated with reduced risk for atherosclerosis and its clinical sequelae, such as myocardial infarction, ischemic stroke, and death. The molecular basis for the apparent vasculoprotection afforded by elevated HDL-C is widely attributed to the ability of HDL particles to drive reverse cholesterol transport. The proteosome (protein cargo) of HDL also appears to endow this lipoprotein with a capacity to reduce oxidized lipids, promote endothelial cell nitric oxide production, reduce adhesion molecule expression, inhibit platelet activation, stimulate endothelial proliferation and inhibit apoptosis, and reduce inflammatory mediator expression, among other functions. Recent investigation suggests that among patients with coronary artery disease, HDL can also be dysfunctional, yielding a pro-inflammatory and pro-oxidative phenotype. Numerous drugs are currently in development in an effort to devise the means by which to optimally increase serum levels of functional, antiatherogenic HDL species. These drugs exploit a diverse range of mechanisms with potential for beneficially impacting the development and progression of atherosclerotic disease.
  Peter P. Toth
  The proteosome of high-density lipoprotein particles is quite complex and consists of up to 75 different proteins and enzymes. The specific protein cargo of HDL particles regulates their functionality. In addition to their documented capacity to engage in reverse cholesterol transport, reduce oxidized lipid, and function as apoprotein donors, HDL particles can activate a variety of signaling systems in endothelial cells, smooth muscle cells, and platelets. The HDLs can deliver sphingolipids to the surface of these cell types and activate sphingosine phosphate receptors. Sphingosine phosphate receptors are coupled to numerous different intracellular signaling cascades exerting roles in vasodilatation, inflammation, cell migration and apoptosis, inhibition of platelet activation, and endothelial adhesion molecule expression, among other functions. The ability of HDL to influence such a diverse array of cellular functions lends biological plausibility to the substantial epidemiological and clinical evidence suggesting that the HDLs are unique among lipoproteins in that they are vasculoprotective and antiatherogenic.
  Anne C. Goldberg , Paul N. Hopkins , Peter P. Toth , Christie M. Ballantyne , Daniel J. Rader , Jennifer G. Robinson , Stephen R. Daniels , Samuel S. Gidding , Sarah D. de Ferranti , Matthew K. Ito , Mary P. McGowan , Patrick M. Moriarty , William C. Cromwell , Joyce L. Ross and Paul E. Ziajka
  The familial hypercholesterolemias (FH) are a group of genetic defects resulting in severe elevations of blood cholesterol levels and increased risk of premature coronary heart disease. FH is among the most commonly occurring congenital metabolic disorders. FH is a treatable disease. Aggressive lipid lowering is necessary to achieve the target LDL cholesterol reduction of at least 50% or more. Even greater target LDL cholesterol reductions may be necessary for FH patients who have other CHD risk factors. Despite the prevalence of this disease and the availability of effective treatment options, FH is both underdiagnosed and undertreated, particularly among children. Deficiencies in the diagnosis and treatment of FH indicate the need for greatly increased awareness and understanding of this disease, both on the part of the public and of healthcare practitioners. This document provides recommendations for the screening, diagnosis and treatment of FH in pediatric and adult patients developed by the National Lipid Association Expert Panel on Familial Hypercholesterolemia. This report goes beyond previously published guidelines by providing specific clinical guidance for the primary care clinician and lipid specialist with the goal of improving care of patients with FH and reducing their elevated risk for CHD.
  Michael H. Davidson , Christie M. Ballantyne , Terry A. Jacobson , Vera A. Bittner , Lynne T. Braun , Alan S. Brown , W. Virgil Brown , William C. Cromwell , Ronald B. Goldberg , James M. McKenney , Alan T. Remaley , Allan D. Sniderman , Peter P. Toth , Sotirios Tsimikas , Paul E. Ziajka , Kevin C. Maki and Mary R. Dicklin
  The National Cholesterol Education Program Adult Treatment Panel guidelines have established low-density lipoprotein cholesterol (LDL-C) treatment goals, and secondary non-high-density lipoprotein (HDL)-C treatment goals for persons with hypertriglyceridemia. The use of lipid-lowering therapies, particularly statins, to achieve these goals has reduced cardiovascular disease (CVD) morbidity and mortality; however, significant residual risk for events remains. This, combined with the rising prevalence of obesity, which has shifted the risk profile of the population toward patients in whom LDL-C is less predictive of CVD events (metabolic syndrome, low HDL-C, elevated triglycerides), has increased interest in the clinical use of inflammatory and lipid biomarker assessments. Furthermore, the cost effectiveness of pharmacological intervention for both the initiation of therapy and the intensification of therapy has been enhanced by the availability of a variety of generic statins. This report describes the consensus view of an expert panel convened by the National Lipid Association to evaluate the use of selected biomarkers [C-reactive protein, lipoprotein-associated phospholipase A2, apolipoprotein B, LDL particle concentration, lipoprotein(a), and LDL and HDL subfractions] to improve risk assessment, or to adjust therapy. These panel recommendations are intended to provide practical advice to clinicians who wrestle with the challenges of identifying the patients who are most likely to benefit from therapy, or intensification of therapy, to provide the optimum protection from CV risk.
  Peter P. Toth
 

Background

Because a significant percentage of patients who require high-dose statin therapy for dyslipidemia experience treatment-related muscle symptoms and an inconsistent clinical response, alternative or adjunctive approaches to the management of dyslipidemia are needed. One alternative approach, antisense therapy, may offer an effective and well-tolerated option for patients not satisfactorily responsive to or intolerant to standard pharmacologic dyslipidemia therapies.

Objective

This review provides an overview of antisense technology and its potential role in the management of dyslipidemia.

Methods

Source material was obtained primarily from the published literature identified through a search of the PubMed database.

Results

Antisense technology is an evolving approach to therapy that has gone through a series of refinements to enhance molecular stability, potency, and tolerability. Mipomersen is an antisense molecule capable of producing clinically meaningful reductions in low-density lipoprotein cholesterol in patients with severe familial hypercholesterolemia. Further long-term clinical studies are required to more clearly quantify its impact on risk for cardiovascular events and establish whether it increases risk for hepatosteatosis.

Conclusion

Antisense therapy represents a potentially effective and well-tolerated emerging treatment modality for numerous diseases. In the treatment of hypercholesterolemia, the antisense therapy mipomersen may provide a possible treatment option for patients with treatment-resistant dyslipidemia.

  Matthew Konerman , Krishnaji Kulkarni , Peter P. Toth and Steven R. Jones
  Lipoprotein(a) [Lp(a)] is a complex lipoprotein consisting of a low-density lipoprotein (LDL)-like ApoB100-containing core particle covalently bound to apo(a), a large functionally complex glycoprotein. The mechanisms of Lp(a) metabolism and its interactions with cell-surface lipoprotein receptors are incompletely understood. In this study, we investigated the relationship of Lp(a) to other lipoproteins at high and normal levels of serum triglycerides (TGs). We measured serum lipid and Lp(a) particle concentrations in 148 unselected primary- and secondary-prevention patients. Subjects with TG > 200 mg/dL were classified as having high TG in accordance with National Cholesterol Education Program Adult Treatment Panel III guidelines. Our analysis revealed mean TG levels of 100 and 270 mg/dL in the normal and high TG groups, respectively. Lp(a)-C, Lp(a)-P, and Lp(a) cholesterol content per particle [Lp(a)-C/Lp(a)-P] did not differ between groups. At normal TG levels, stepwise multiple linear regression revealed that Lp(a)-P correlated with Lp(a)-C (P < 10−6), ApoAI (P = .0001), the high-density lipoprotein cholesterol subfraction ratio (HDL2-C/HDL3-C; P = .002), and dense very-low-density lipoprotein cholesterol (VLDL3-C; P = .04), overall model R = 0.74. At high TG levels, Lp(a)-P very strongly correlated primarily with HDL2-C/HDL3-C and TG-related variables with minimal dependence on Lp(a)-C (P = .09), overall model R = 0.96. These findings provide evidence of shared metabolic mechanisms for Lp(a), HDL, TG, and very low-density lipoprotein at high serum TG. Future studies are needed to elucidate common mechanisms, enzymes, and receptors involved in Lp(a) and HDL/TG metabolism with a focus on how these mechanisms are modified in the setting of hypertriglyceridemia.
  Peter P. Toth , Christie M. Ballantyne , Michael H. Davidson , Joanne E. Tomassini , Dena Rosen Ramey , David Neff , Andrew M. Tershakovec , X. Henry Hu and Kaan Tunceli
 

Background

Recent trends suggest a decreased use of ezetimibe/simvastatin combination and coadministered ezetimibe plus statin therapies.

Objective

This analysis evaluated changes in prescription patterns for ezetimibe/simvastatin, ezetimibe plus statins, and statin therapies and expected effects on low-density lipoprotein cholesterol (LDL-C) lowering during 2007 to 2008.

Methods

Prescription pattern changes were assessed by the use of patient-level data from the IMS Health Longitudinal Rx database during two time periods, July 14, 2007 to January 13, 2008 (n = 8,813,674) and January 14, 2008 to July 13, 2008 (n = 9,131,030), 6 months before and after reporting of the results of The Ezetimibe and Simvastatin in Hypercholesterolemia Enhances Atherosclerosis Regression trial (ENHANCE) trial on January 14, 2008. Expected LDL-C reductions were estimated using data from previous controlled clinical trials.

Results

During 6 months post-ENHANCE, greater proportions of patients were switched from ezetimibe/simvastatin and ezetimibe plus statins to other lipid-lowering therapies by health care providers than 6 months pre-ENHANCE (21.1% vs 6.0% and 46.9% vs 38.5%, differences: −15.06% [95% confidence interval −15.14%, −14.97%] and −8.43% [95% confidence interval −8.70%, −8.17%], respectively). Greater proportions of these patients switched to statin monotherapy in the later than earlier period. Prescription patterns were similar for statins during both time periods, although fewer patients switched to ezetimibe/simvastatin and ezetimibe plus statin therapies post-ENHANCE. In both time periods, greater proportions of patients on ezetimibe/simvastatin and ezetimibe plus statins switched to less-than-equivalent LDL-C lowering efficacy doses of statins than those on statin therapy. On the basis of previous clinical data for these therapies, smaller LDL-C reductions would be expected in patients who switched from ezetimibe/simvastatin and ezetimibe plus statins to statins, despite a trend toward switching to greater statin doses in the later time period.

Conclusions

More patients switched from ezetimibe/simvastatin and ezetimibe plus statin to statin monotherapy 6 months after the reporting of the ENHANCE trial, the majority of which were prescribed less potent, LDL-C-lowering therapies. On the basis of the known LDL-C lowering efficacies for these therapies, such changes would be expected to increase LDL-C levels in these patients and may reduce the proportion of patients who achieve guideline-recommended LDL-C goals.

  Robert J. Simko , Peter P. Toth , S. R. Palli and R. A. Quimbo
  Type II diabetes mellitus (T2DM) patients have increased risk for atherosclerotic cardiovascular disease (CVD), which is partly attributable to dyslipidemia. Although statins are the recommended therapeutic strategy, fenofibrate (FFB)-known to decrease TG levels, increase HDL-C, and shift the distribution of LDL subfractions towards larger, less atherogenic particles-has been recommended as adjuvant therapy with statins.
  Elaine Chiquette , Gilbert Ramirez , Peter P. Toth , Michael Cobble , Brandon Walsh and Robert Chilton
  The Reynolds Risk Score best-fitting model (RRS) estimates 10-year coronary heart disease (CHD) risk by incorporating an expanded number of risk markers, including A1C, systolic blood pressure, C-reactive protein (hsCRP), apolipoproteins, and the interaction of lipoprotein(a) and ApoB. Treatment of type 2 diabetes (T2DM) with the GLP-1 receptor agonist exenatide has been reported to improve A1C, body weight, blood pressure, and lipid profiles; however, evidence regarding the impact of exenatide on other apolipoproteins is limited.
  Peter P. Toth , Danielle Potter and Eileen E. Ming
 

Background

The association between increased low-density lipoprotein cholesterol (LDL-C) and increased risk for cardiovascular events is well established, with treatment focusing on LDL-C lowering. Other lipid abnormalities are also associated with increased cardiovascular risk (eg, low high-density lipoprotein cholesterol [HDL-C], high triglycerides [TG], and high non-HDL-C). Despite national lipid guidelines, the prevalence of these abnormal lipid parameters alone or in combination (mixed dyslipidemia) is not well recognized.

Objective

We assessed the prevalence of high LDL-C, low HDL-C, high TG, high non-HDL-C, and mixed dyslipidemia by using National Health and Nutrition Examination Survey (NHANES) data to estimate the proportions of U.S. adults not at guideline-recommended lipid goals.

Methods

NHANES 2003-2006 fasting blood serum data were used to categorize adults aged ≥20 years by LDL-C (risk stratum-specific), HDL-C (men, <40 mg/dL; women, <50 mg/dL), non-HDL-C (in subjects with TG ≥200 mg/dL), and TG (≥150 mg/dL) target levels with use of the NCEP ATP III definitions based on coronary heart disease (CHD) risk.

Results

An estimated 53% (105.3M) of U.S. adults have lipid abnormalities: 27% (53.5M) have high LDL-C, 23% (46.4M) have low HDL-C, and 30% (58.9M) have high TG. Among patients with serum TG levels ≥200 mg/dL, approximately 13% (25.7M) of adults have non-HDL-C levels ≥130 mg/dL. Also, 21% (42.0M) of U.S. adults have mixed dyslipidemia (high LDL-C with either low HDL-C and/or high TG), with nearly 6% (11.6M) having all three lipid abnormalities. For LDL-C, an estimated 23M adults with CHD or a CHD risk equivalent and 17M with ≥2 risk factors but a Framingham risk ≤20% are not at goals of <100 and <130 mg/dL, respectively.

Conclusion

Prevalence of dyslipidemia in the United States continues to be high, with the majority of U.S. adults now affected by some form of lipid abnormality. Efforts to promote screening, risk stratification, and initiating appropriate treatment should be intensified.

  Harold E. Bays , Peter P. Toth , Penny M. Kris-Etherton , Nicola Abate , Louis J. Aronne , W. Virgil Brown , J. Michael Gonzalez-Campoy , Steven R. Jones , Rekha Kumar , Ralph La Forge and Varman T. Samuel
  The term “fat” may refer to lipids as well as the cells and tissue that store lipid (ie, adipocytes and adipose tissue). “Lipid” is derived from “lipos,” which refers to animal fat or vegetable oil. Adiposity refers to body fat and is derived from “adipo,” referring to fat. Adipocytes and adipose tissue store the greatest amount of body lipids, including triglycerides and free cholesterol. Adipocytes and adipose tissue are active from an endocrine and immune standpoint. Adipocyte hypertrophy and excessive adipose tissue accumulation can promote pathogenic adipocyte and adipose tissue effects (adiposopathy), resulting in abnormal levels of circulating lipids, with dyslipidemia being a major atherosclerotic coronary heart disease risk factor. It is therefore incumbent upon lipidologists to be among the most knowledgeable in the understanding of the relationship between excessive body fat and dyslipidemia. On September 16, 2012, the National Lipid Association held a Consensus Conference with the goal of better defining the effect of adiposity on lipoproteins, how the pathos of excessive body fat (adiposopathy) contributes to dyslipidemia, and how therapies such as appropriate nutrition, increased physical activity, weight-management drugs, and bariatric surgery might be expected to impact dyslipidemia. It is hoped that the information derived from these proceedings will promote a greater appreciation among clinicians of the impact of excess adiposity and its treatment on dyslipidemia and prompt more research on the effects of interventions for improving dyslipidemia and reducing cardiovascular disease risk in overweight and obese patients.
  Peter P. Toth , Philip J. Barter , Robert S. Rosenson , William E. Boden , M. John Chapman and Marina Cuchel
  For >4 decades it has been recognized that elevated serum levels of high-density lipoprotein cholesterol (HDL-C) are associated with reduced risk of cardiovascular disease (CVD) and its sequelae. Many prospective observational studies performed around the world have confirmed an inverse relationship between HDL-C and cardiovascular risk in people irrespective of sex, race, or ethnicity. Consequently, it was assumed that, by extension, raising HDL-C through lifestyle modification and pharmacologic intervention would reduce risk of CVD. Animal studies are consistent with this assumption. Lipid treatment guidelines around the world promoted the recognition of HDL-C as a therapeutic target, especially in high-risk patients. Some post hoc analyses from randomized controlled trials also suggest that raising HDL-C beneficially affects the risk of CVD. However, a number of recent randomized studies putatively designed to test the “HDL hypothesis” have failed to show benefit. The results of these trials have caused many clinicians to question whether HDL-C is a legitimate therapeutic target. In response to the many questions and uncertainties raised by the results of these trials, the National Lipid Association convened an expert panel to evaluate the current status of HDL-C as a therapeutic target; to review the current state of knowledge of HDL particle structure, composition, and function; and to identify the salient questions yet to be answered about the role of HDL in either preventing or contributing to atherosclerotic disease. The expert panel's conclusions and clinical recommendations are summarized herein. The panel concludes that, although low HDL-C identifies patients at elevated risk, and much investigation suggests that HDL may play a variety of antiatherogenic roles, HDL-C is not a therapeutic target at the present time. Risk stratified atherogenic lipoprotein burden (low-density lipoprotein cholesterol and non-HDL-C) should remain the primary and secondary targets of therapy in patients at risk, as described by established guidelines. The National Lipid Association emphasizes that rigorous research into the biology and clinical significance of low HDL-C should continue. The development of novel drugs designed to modulate the serum levels and functionality of HDL particles should also continue. On the basis of an enormous amount of basic scientific and clinical investigation, a considerable number of reasons support the need to continue to investigate the therapeutic effect of modulating HDL structure and function.
  Maciej Banach , Michael Davidson and Peter P. Toth
  Not available
  Matthew Konerman , Krishnaji Kulkarni , Peter P. Toth and Steven R. Jones
  There is little known about the relative predictive value of different lipoprotein(a) [Lp(a)] assays in clinical use, although each has been shown to predict similar incremental risk over conventional clinical and lipid risk factors. Thus, we examined the classification behavior of two commonly used Lp(a) assays and their associations with other lipid parameters. Serum lipid and Lp(a) concentrations were measured in 144 primary and secondary prevention patients. Lp(a) cholesterol [Lp(a)-C] was measured with the Vertical Auto Profile (upper limit of normal, 10 mg/dL). Lp(a) particle concentrations [Lp(a)-P] were measured with an isoform-independent molar assay (upper limit of normal, 70 nmol/L). The subjects were divided into the following four groups on the basis of their Lp(a)-C and Lp(a)-P levels: normal Lp(a)-P and Lp(a)-C; high Lp(a)-P and normal Lp(a)-C; normal Lp(a)-P and high Lp(a)-C; and high Lp(a)-P and Lp(a)-C. The proportion of subjects with values above the upper limit of normal was similar with both assays (P = .15). However, the Lp(a)-C and Lp(a)-P assays discordantly classified 23% of the study's subjects. In addition, the four Lp(a)-defined groups displayed differences in their relationships with other lipoproteins. The two groups with elevated Lp(a)-C showed significant associations with higher high-density lipoprotein cholesterol, apolipoprotein AI, and high-density lipoprotein cholesterol/apolipoprotein AI ratios. Triglycerides were also noted to be above normal in discordant and normal within concordant Lp(a) groups. Finally, the amount of cholesterol per Lp(a) particle [Lp(a)-C/Lp(a)-P] varied widely across the four groups. These findings suggest that the four Lp(a)-defined groups are physiologically discrete. Further investigation is warranted to assess which parameters among Lp(a)-P, Lp(a)-C, and Lp(a)-C/Lp(a)-P can be used to more accurately characterize Lp(a)-associated cardiovascular risk.
  Peter P. Toth , JoAnne M. Foody , Joanne E. Tomassini , Shiva G. Sajjan , Dena R. Ramey , David R. Neff , Andrew M. Tershakovec , X. Henry Hu and Kaan Tunceli
 

Background

Statin combination therapy and statin uptitration have been shown to be efficacious in low-density lipoprotein cholesterol (LDL-C) lowering and are recommended for patients with high-risk coronary heart disease (CHD) who do not reach guideline-endorsed LDL-C goals on statin monotherapy.

Objective

This analysis evaluated treatment practice patterns and LDL-C lowering for patients with CHD/CHD risk equivalent on statin monotherapy in a real-world practice setting in the United States.

Methods

In this retrospective, observational study, patients with CHD/CHD risk equivalent on statin therapy were identified during 2004 to 2008 in a US managed care database. Prescribing patterns and effect of switching from statin monotherapy to combination ezetimibe/simvastatin therapy vs uptitration to higher statin dose/potency level and no change from initial statin potency on LDL-C lowering were assessed. Percentage of change from baseline in LDL-C levels and odds ratios for LDL-C goal attainment were estimated with analyses of covariance and logistic regression.

Results

Of 27,919 eligible patients on statin therapy, 2671 (9.6%) switched to ezetimibe/simvastatin therapy, 11,035 (39.5%) uptitrated statins, and 14,213 (50.9%) remained on the same statin monotherapy. LDL-C reduction from baseline and attainment of LDL-C <100 and <70 mg/dL were substantially greater for patients who switched to ezetimibe/simvastatin therapy (−24.0%, 81.2%, and 35.2%, respectively) than for patients who titrated (−9.6%, 68.0%, and 18.4%, respectively) or remained on initial statin therapy (4.9%, 72.2%, and 23.7%, respectively). The odds ratios for attainment of LDL-C <100 and <70 mg/dL were also higher for patients who switched than for patients who uptitrated and had no therapy change than for patients who titrated vs no therapy change. Similarly, among a subgroup of patients not at LDL-C <100 mg/dL on baseline therapy, attainment of LDL-C <100 and <70 mg/dL was greater for patients who switched than for statin uptitration vs no change, as well as for patients who uptritrated statins vs no therapy change.

Conclusion

In this study, LDL-C lowering and goal attainment rates improved substantially for patients with high-risk CHD on statin monotherapy who switched to combination ezetimibe/statin or uptitrated their statin therapies; however, approximately one-third of these patients still did not attain the optional recommended LDL-C goal of <70 mg/dL. Moreover, these higher efficacy lipid-lowering therapies were infrequently prescribed, indicating the need for further assessment of barriers to LDL-C goal attainment in actual practice settings.

  Gerald F. Watts , Samuel Gidding , Anthony S. Wierzbicki , Peter P. Toth , Rodrigo Alonso , W. Virgil Brown , Eric Bruckert , Joep Defesche , Khoo Kah Lin , Michael Livingston , Pedro Mata , Klaus G. Parhofer , Frederick J. Raal , Raul D. Santos , Eric J.G. Sijbrands , William G. Simpson , David R. Sullivan , Andrey V. Susekov , Brian Tomlinson , Albert Wiegman , Shizuya Yamashita and John J.P. Kastelein
  Familial hypercholesterolemia (FH) is a dominantly inherited disorder present from birth that markedly elevates plasma low-density lipoprotein cholesterol and causes premature coronary heart disease. There are at least 20 million people with FH worldwide, but the majority remains undetected, and current treatment is often suboptimal. To address this major gap in coronary prevention we present, from an international perspective, consensus-based guidance on the care of FH. The guidance was generated from seminars and workshops held at an international symposium. The recommendations focus on the detection, diagnosis, assessment, and management of FH in adults and children and set guidelines for clinical purposes. They also refer to best practice for cascade screening and risk notifying and testing families for FH, including use of genetic testing. Guidance on treatment is based on risk stratification, management of noncholesterol risk factors, and the safe and effective use of low-density lipoprotein-lowering therapies. Recommendations are given on lipoprotein apheresis. The use of emerging therapies for FH is also foreshadowed. This international guidance acknowledges evidence gaps but aims to make the best use of contemporary practice and technology to achieve the best outcomes for the care of FH. It should accordingly be used to inform clinical judgment and be adjusted for country-specific and local healthcare needs and resources.
  W. Virgil Brown , Benjamin J. Ansell , Rachel H. Mackey and Peter P. Toth
  One of the most difficult and confusing issues for clinical lipidologists and physicians in general has been the management of low concentrations of high-density lipoprotein cholesterol. We know this to be a very powerful predictor of risk in scores of community-based and clinical trial cohorts. Raising this number in many patients would seem to provide a great therapeutic opportunity, but so far this concept has been very difficult to prove. I have been joined for this discussion by a cardiovascular epidemiologist, Dr. Rachel Mackey, from the University of Pittsburgh and two clinical lipidologists who have studied and written in depth about this problem. These are Dr. Benjamin Ansell from the University of California in Los Angeles and Dr. Peter Toth from Johns Hopkins University School of Medicine. Our objective in this discussion is to give primary care clinicians our thoughts about the recent research findings and the implications of these data on the best clinical practice.
  Fahri Bayram , Derya Kocer , Kursat Gundogan , Ahmet Kaya , Ozgur Demir , Ramazan Coskun , Tevfik Sabuncu , Ahmet Karaman , Mustafa Cesur , Manfredi Rizzo , Peter P. Toth and Vedia Gedik
 

Background and Objectives

Dyslipidemia is a modifiable major risk factor for coronary heart disease. The objective of this study was to determine the prevalence of dyslipidemia among Turkish adults and its associations with other cardiovascular risk factors.

Methods

This study included 4309 people ages 20 to 83 years old from 7 provinces of Turkey. People from the city centers, districts, and villages were selected by a stratified sampling method. Weight, height, and waist and hip circumferences were measured. Blood samples were obtained to determine glucose, total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), and triglycerides (TG); these parameters were measured with an autoanalyzer. Dyslipidemia was defined according to National Cholesterol Education Program Adult Treatment Panel III diagnostic criteria.

Results

Of 4309 subjects, 43% had high TC, 41.5% had low HDL-C, 36.2% had high LDL-C, and 35.7% had high TG. Of these measures, at least 1 lipid abnormality was diagnosed in 78.7% of men and 80.4% of women. The prevalence of high TC, LDL-C, and TG increased with age, with the highest prevalence in the 46-to-65-year-old age group. The mean values (mg/dL) of TC, LDL-C, HDL-C, and TG were 194.2 ± 47.7, 117.7 ± 41.1, 50.3 ± 16.3, and 145.4 ± 96.3, respectively. Dyslipidemia was positively associated with age, body mass index, waist circumference, fasting blood glucose, and blood pressure, and negatively associated with altitude.

Conclusions

The high prevalence of dyslipidemia in Turkey is an important public health problem. Enhanced public health preventive measures should be implemented to better diagnose and comprehensively treat dyslipidemia in Turkey.

 
 
 
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