Models for Describing Relations Among the Various Statin Drugs, Low-Density Lipoprotein Cholesterol Lowering, Pleiotropic Effects, and Cardiovascular Risk††Conflicts of interest: In the past 2 years, Dr. Robinson has received grants from Abbott Laboratories, Abbott Park, Illinois, Astra-Zeneca, Wilmington, Delaware, Bristol-Myers Squibb, Princeton, New Jersey, GlaxoSmithKline, Pittsburgh, Pennsylvania, Hoffman La Roche, Basel, Switzerland, Merck & Company, West Point, Pennsylvania, Pfizer, New York, New York, Procter & Gamble, Cinncinnati, Ohio, Sankyo, Parsippany, New Jersey, Schering-Plough, Kenilworth, New Jersey, and Takeda Pharmaceuticals, Lincolnshire, Illinois and honoraria for education programs from Merck & Company, and has been a consultant and advisory board member for Merck Schering Plough.

2008 ◽  
Vol 101 (7) ◽  
pp. 1009-1015 ◽  
Author(s):  
Jennifer G. Robinson
Keyword(s):  
New York ◽  
New Jersey ◽  
Conflicts Of Interest ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Advisory Board ◽  
West Point ◽  
Low Density Lipoprotein Cholesterol ◽  
The Past ◽  
Statin Drugs

Safety and Efficacy of Atorvastatin-Induced Very Low-Density Lipoprotein Cholesterol Levels in Patients With Coronary Heart Disease (a Post Hoc Analysis of the Treating to New Targets [TNT] Study)††Conflicts of interest: Dr. LaRosa has served as a consultant to Pfizer, Inc., New York, New York; Merck Whitehouse Station, New Jersey; Bristol-Myers Squibb, New York, New York; and AstraZeneca, Wilmington, Delaware; and has received lecture fees from Pfizer. Dr. Grundy has consulted with Abbott, Chicago, Illinois; GlaxoSmithKline, Durham, North Carolina, Pfizer, AstraZeneca, and Sanofi-Aventis, Bridgewater, New Jersey; received lecture fees from Merck Schering Plough, Kenilworth, New Jersey; Kos, Edison, New Jersey, Pfizer, GlaxoSmithKline, Lilly, and Bristol-Myers Squibb; and received research support from Abbott and GlaxoSmithKline. Dr. Kastelein has received consulting fees, lecture fees, and grant support from Pfizer, Merck Schering Plough, Bristol-Myers Squibb, and Sankyo, Munich, Germany; Dr. Kostis has served as a consultant to Pfizer, Schering Plough, Berlex, Montville, New Jersey; Taisho, Tokyo, Japan; Forest Laboratories, New York, New York; and Sankyo; received lecture fees from Pfizer, Merck, Bristol-Myers Squibb, AstraZeneca, Sanofi Aventis, and Otsuka, Rockville, Maryland; and received grant support from Pfizer and Schering Plough. Dr. Greten has received consulting and lecturing fees from Pfizer, Merck, Schering Plough, and Kowa Company, Nagoya, Japan.

2007 ◽  
Vol 100 (5) ◽  
pp. 747-752 ◽  
Author(s):  
John C. LaRosa ◽  
Scott M. Grundy ◽  
John J.P. Kastelein ◽  
John B. Kostis ◽  
Heiner Greten
Keyword(s):  
New York ◽  
North Carolina ◽  
New Jersey ◽  
Conflicts Of Interest ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Research Support ◽  
Cholesterol Levels ◽  
Grant Support ◽  
Post Hoc

scholarly journals Next-generation sequencing to confirm clinical familial hypercholesterolemia

2020 ◽  
pp. 204748732094299
Author(s):  
Laurens F Reeskamp ◽  
Tycho R Tromp ◽  
Joep C Defesche ◽  
Aldo Grefhorst ◽  
Erik SG Stroes ◽  
...  
Keyword(s):  
Next Generation Sequencing ◽  
Familial Hypercholesterolemia ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Pathogenic Variant ◽  
Low Density ◽  
Low Density Lipoprotein Cholesterol ◽  
The Past ◽  
Cholesterol Levels ◽  
Generation Sequencing

Background Familial hypercholesterolemia is characterised by high low-density lipoprotein-cholesterol levels and is caused by a pathogenic variant in LDLR, APOB or PCSK9. We investigated which proportion of suspected familial hypercholesterolemia patients was genetically confirmed, and whether this has changed over the past 20 years in The Netherlands. Methods Targeted next-generation sequencing of 27 genes involved in lipid metabolism was performed in patients with low-density lipoprotein-cholesterol levels greater than 5 mmol/L who were referred to our centre between May 2016 and July 2018. The proportion of patients carrying likely pathogenic or pathogenic variants in LDLR, APOB or PCSK9, or the minor familial hypercholesterolemia genes LDLRAP1, ABCG5, ABCG8, LIPA and APOE were investigated. This was compared with the yield of Sanger sequencing between 1999 and 2016. Results A total of 227 out of the 1528 referred patients (14.9%) were heterozygous carriers of a pathogenic variant in LDLR (80.2%), APOB (14.5%) or PCSK9 (5.3%). More than 50% of patients with a Dutch Lipid Clinic Network score of ‘probable’ or ‘definite’ familial hypercholesterolemia were familial hypercholesterolemia mutation-positive; 4.8% of the familial hypercholesterolemia mutation-negative patients carried a variant in one of the minor familial hypercholesterolemia genes. The mutation detection rate has decreased over the past two decades, especially in younger patients in which it dropped from 45% in 1999 to 30% in 2018. Conclusions A rare pathogenic variant in LDLR, APOB or PCSK9 was identified in 14.9% of suspected familial hypercholesterolemia patients and this rate has decreased in the past two decades. Stringent use of clinical criteria algorithms is warranted to increase this yield. Variants in the minor familial hypercholesterolemia genes provide a possible explanation for the familial hypercholesterolemia phenotype in a minority of patients.

scholarly journals Next-generation sequencing to confirm clinical familial hypercholesterolemia

2020 ◽  
Vol 28 (8) ◽  
pp. 875-883 ◽  
Author(s):  
Laurens F Reeskamp ◽  
Tycho R Tromp ◽  
Joep C Defesche ◽  
Aldo Grefhorst ◽  
Erik S G Stroes ◽  
...  
Keyword(s):  
Next Generation Sequencing ◽  
Familial Hypercholesterolemia ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Pathogenic Variant ◽  
Low Density ◽  
Low Density Lipoprotein Cholesterol ◽  
The Past ◽  
Cholesterol Levels ◽  
Generation Sequencing

Abstract Background Familial hypercholesterolemia is characterised by high low-density lipoprotein-cholesterol levels and is caused by a pathogenic variant in LDLR, APOB or PCSK9. We investigated which proportion of suspected familial hypercholesterolemia patients was genetically confirmed, and whether this has changed over the past 20 years in The Netherlands. Methods Targeted next-generation sequencing of 27 genes involved in lipid metabolism was performed in patients with low-density lipoprotein-cholesterol levels greater than 5 mmol/L who were referred to our centre between May 2016 and July 2018. The proportion of patients carrying likely pathogenic or pathogenic variants in LDLR, APOB or PCSK9, or the minor familial hypercholesterolemia genes LDLRAP1, ABCG5, ABCG8, LIPA and APOE were investigated. This was compared with the yield of Sanger sequencing between 1999 and 2016. Results A total of 227 out of the 1528 referred patients (14.9%) were heterozygous carriers of a pathogenic variant in LDLR (80.2%), APOB (14.5%) or PCSK9 (5.3%). More than 50% of patients with a Dutch Lipid Clinic Network score of ‘probable’ or ‘definite’ familial hypercholesterolemia were familial hypercholesterolemia mutation-positive; 4.8% of the familial hypercholesterolemia mutation-negative patients carried a variant in one of the minor familial hypercholesterolemia genes. The mutation detection rate has decreased over the past two decades, especially in younger patients in which it dropped from 45% in 1999 to 30% in 2018. Conclusions A rare pathogenic variant in LDLR, APOB or PCSK9 was identified in 14.9% of suspected familial hypercholesterolemia patients and this rate has decreased in the past two decades. Stringent use of clinical criteria algorithms is warranted to increase this yield. Variants in the minor familial hypercholesterolemia genes provide a possible explanation for the familial hypercholesterolemia phenotype in a minority of patients.

scholarly journals Safety of Prescribing Statins in Childhood Dyslipidemia

2020 ◽  
Vol 10 (01) ◽  
pp. e119-e125
Author(s):  
Mohammed Khaled Al-Alaili ◽  
Abdikarim Mohamed Abdi ◽  
Bilgen Basgut
Keyword(s):  
Randomized Clinical Trials ◽  
Drug Class ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Heart Association ◽  
Cochrane Library ◽  
Low Density Lipoprotein Cholesterol ◽  
The Past ◽  
Artery Disease ◽  
Age Range

AbstractHyperlipidemia is on the rise in pediatrics, leading to early coronary artery disease complications. Familial hypercholesterolemia is an important risk factor, with the homozygous subtype being more dangerous, yet less prevalent than the heterozygous subtype. Statins are shown to be an effective treatment in this population. This systematic review will emphasize the safety of such drug class in pediatrics, while taking into consideration the latest cholesterol guideline. Cochrane Library, Clinicaltrials.gov, and PubMed were reviewed systematically in June 2019 and rechecked in November 2019 for the past 5 years with keywords like child, safety, hyperlipidemia, and statins, which resulted in nine randomized clinical trials. In short, statins are shown to be intermediately effective—median decrease of low-density lipoprotein cholesterol was 32% achieving the target of < 160 mg/dL in 67% of patients—in lowering lipid levels yet preventing early complications. They are also considered safely tolerated in most cases, even when taken for extended periods, but still not evidently permissible for children below 8 years old, which was the average age of all participants in the trials. Statins should not be given generally for pediatrics of less than 8 years old, in contrast to what was mentioned in the American Heart Association guideline (0–19 age range), since there is no evidence supporting their safety within this age group.

High but not low self-reported statin adherence was confirmed by a novel method based on plasma-statin measurements in coronary outpatients

2021 ◽  
Vol 28 (Supplement_1) ◽  
Author(s):  
O Kristiansen ◽  
E Sverre ◽  
K Peersen ◽  
MW Fagerland ◽  
E Gjertsen ◽  
...  
Keyword(s):  
Medication Adherence ◽  
Direct Method ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Low Density Lipoprotein Cholesterol ◽  
The Past ◽  
High Adherence ◽  
Adherence Scale ◽  
Statin Adherence ◽  
Reduced Adherence

Abstract Funding Acknowledgements Type of funding sources: Public hospital(s). Main funding source(s): Helse Sør-Øst Background To what extent self-reported adherence measures correspond with directly measured statin adherence is unknown. Purpose  To determine the relationship between, self-reported adherence measures, low density lipoprotein-cholesterol (LDL-C) and directly measured statin adherence in coronary outpatients. Methods Patients on atorvastatin (N = 373) participated in a cross-sectional study median 16 months after a coronary event. Adherence to statins the past 7 days, general medication adherence assessed by the 8-item Morisky medication adherence scale (MMAS-8), and the Gehi adherence question was obtained by a self-report questionnaire. Atorvastatin was determined in spot blood plasma samples by a novel liquid-chromatography tandem mass-spectrometry method discriminating between adherence (0-1 doses omitted) and reduced (≥2 doses omitted) adherence. Participants were unaware of the atorvastatin analyses at study participation.  Results Mean age was 63 (SD 9) years and 19% were females. Mean atorvastatin dose was 64 (SD 21) mg. The number with reduced adherence by the different measurement methods, Cohens kappa agreement score between the self-reported and direct adherence measures, and LDL-C are shown in the Table. Statin adherence was confirmed by the direct method among 96% reporting high statin adherence the past 7 days, among 95% reporting high adherence on the MMAS-8 and among 94% reporting high adherence on the Gehi adherence question. In contrast, among patients classified with reduced statin adherence by the direct method, only 40% reported reduced statin adherence the past week, 32% reported reduced adherence with the MMAS-8 and 22% with the Gehi adherence question. Conclusions The direct method confirmed high, but not low, self-reported statin adherence in this selected sample of coronary outpatients. In patients with elevated LDL-cholesterol, plasma-statin measurements emerges as a potential improvement for clinical statin management. Adherence measures and LDL cholesterol Directly measured atorvastatin adherence Self-reported statin adherence past 7 days Self-reported medication adherence past month (Gehi) 8-item Morisky medication adherence scale Number with reduced adherence, % 7.8 5.5 3.0 8.4 Cohen"s kappa (95% CI) Reference 0.4 (0.2 to 0.6) 0.3 (0.1 to 0.5) 0.2 (0.1 to 0.4) LDL-C, Adherent, mean (95% CI) 1.9 (1.8 to 1.9) 1.9 (1.8 to 2.0) 1.9 (1.8 to 2.0) 1.9 (1.8 to 1.9) LDL-C, Reduced adherence, mean (95% CI) 2.8 (2.4 to 3.2) 2.8 (2.3 to 3.2) 3.2 (2.5 to 3.8) 2.1 (1.9 to 2.4) LDL-C, Adherent versus reduced adherence P &lt;0.001 P = 0.001 P = 0.004 P = 0.07 Agreement between directly measured atorvastatin adherence, self-reported measures of adherence, and mean low density lipoprotein-cholesterol (LDL-C)

Effect of Plant Stanol Tablets on Low-Density Lipoprotein Cholesterol Lowering in Patients on Statin Drugs

2006 ◽  
Vol 97 (3) ◽  
pp. 376-379 ◽  
Author(s):  
Anne C. Goldberg ◽  
Richard E. Ostlund ◽  
Joyce H. Bateman ◽  
Linda Schimmoeller ◽  
Timothy B. McPherson ◽  
...  
Keyword(s):  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Lipoprotein Cholesterol ◽  
Low Density ◽  
Low Density Lipoprotein Cholesterol ◽  
Cholesterol Lowering ◽  
Plant Stanol ◽  
Statin Drugs

Moving beyond the “LDL hypothesis”

VASA ◽  
2015 ◽  
Vol 44 (5) ◽  
pp. 333-340 ◽  
Author(s):  
Christian Werner ◽  
Ulrich Laufs
Keyword(s):  
Ldl Cholesterol ◽  
Causal Relation ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Clinical Trial Data ◽  
Randomised Clinical Trial ◽  
Trial Data ◽  
Low Density Lipoprotein Cholesterol ◽  
Genetic Studies ◽  
Statin Drug

Abstract. Summary: The term “LDL hypothesis” is frequently used to describe the association of low-density lipoprotein cholesterol (LDL-cholesterol, LDL-C) and cardiovascular (CV) events. Recent data from genetic studies prove a causal relation between serum LDL-C and CV events. These data are in agreement with mechanistic molecular studies and epidemiology. New randomised clinical trial data show that LDL-C lowering with statins and a non-statin drug, ezetimibe, reduces CV events. We therefore believe that the “LDL-hypothesis” has been proven; the term appears to be outdated and should be replaced by “LDL causality”.

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