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 <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)

scholarly journals Self-reported Morisky 8 item medication adherence scale to statins concords with pill count method and correlates with serum lipid profile parameters and Serum HMGCoA Reductase levels

2019 ◽  
Author(s):  
Abhinav Grover ◽  
Mansi Oberoi ◽  
Harmeet Rehan ◽  
Lalit Gupta ◽  
Madhur Yadav
Keyword(s):  
Medication Adherence ◽  
Lipid Profile ◽  
Density Lipoprotein ◽  
Correlation Coefficients ◽  
Pill Count ◽  
Self Report ◽  
Adherence Score ◽  
Count Method ◽  
High Adherence ◽  
Adherence Scale

ABSTRACTBackgroundIt is imperative that non-compliance to statins be identified and addressed to optimize the clinical benefit of statins. Patient self-reporting methods are convenient to apply in clinical practice but need to be validated.ObjectiveWe studied the concordance of a patient self-report method, MMAS (Morisky eight item medication adherence scale) with pill count method in measuring adherence to statins and their correlation with extended lipid profile parameters and serum HMGCoA-R (hydroxymethylglutaryl coenzyme A reductase) enzyme levels.MethodsMMAS and pill count method were used to measure the adherence to statins in patients on statins for any duration. Patients were subjected to estimation of extended lipid profile and serum HMGCoA-R levels at the end of 3 months follow-up.ResultsOut of a total of 200 patients included in the study, 117 patients had low adherence (score less than 6 on MMAS) whereas 65 and 18 patients had medium (score 6 to less than 8) and high adherence (score of 8) respectively. Majority of patients who had low adherence to statins by MMAS were nonadherent by pill count method yielding concordance of 96.5%. Medium or high adherence to statins by MMAS method had concordance of 89.1% with pill count method. The levels of total cholesterol, low density lipoprotein-cholesterol, apolipoprotein B and HMGCoA-R were significantly negatively correlated with compliance measured by pill count and MMAS with similar correlation coefficients. HMGCoA-R levels demonstrated a plateau phenomenon with levels being 9-10 ng/ml when compliance to statin therapy was greater than 60% by pill count and greater than 6 on Morisky scale.ConclusionIn conclusion, MMAS and pill count methods showed concordance in measuring adherence to statins. These methods need to be explored further for their interchangeability as surrogates for biomarker levels.

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 An expert opinion paper on statin adherence and implementation of new lipid-lowering medications by the ESC Working Group on Cardiovascular Pharmacotherapy: Barriers to be overcome

2019 ◽  
Vol 6 (2) ◽  
pp. 115-121 ◽  
Author(s):  
Heinz Drexel ◽  
Andrew J S Coats ◽  
Ilaria Spoletini ◽  
Claudio Bilato ◽  
Vincenzo Mollace ◽  
...  
Keyword(s):  
Working Group ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Position Paper ◽  
Lipid Lowering ◽  
Low Density ◽  
Low Density Lipoprotein Cholesterol ◽  
Lipid Lowering Drugs ◽  
Cardiovascular Pharmacotherapy ◽  
Statin Adherence

Abstract Benefits and safety on statins have been well-established over 20 years of research. Despite this, the vast majority of patients are not adequately treated and do not achieve the low-density lipoprotein cholesterol target levels. This is mainly due to poor adherence, which is associated with dangerous and sometimes fatal outcomes. To increase adherence and prevent worse outcomes, a combination therapy with lower dosage of statins and new lipid-lowering drugs may be used. However, the implementation of new lipid-lowering drugs in European countries is still at the beginning. For these reasons, the aim of this position paper is to give an up-to-date indication from the ESC Working Group on Cardiovascular Pharmacotherapy in order to discuss the barriers towards statins adherence and new lipid-lowering drugs implementation in Europe.

scholarly journals The Habit Formation trial of behavioral economic interventions to improve statin use and reduce the risk of cardiovascular disease: Rationale, design and methodologies

2019 ◽  
Vol 16 (4) ◽  
pp. 399-409 ◽  
Author(s):  
Mary E Putt ◽  
Peter P Reese ◽  
Kevin G Volpp ◽  
Louise B Russell ◽  
George Loewenstein ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Medication Adherence ◽  
Behavioral Economics ◽  
Health System ◽  
Habit Formation ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Low Density ◽  
Trial Recruitment ◽  
Statin Adherence

BackgroundLow adherence to statin (HMG-CoA reductase inhibitors) medication is common. Here, we report on the design and implementation of the Habit Formation trial. This clinical trial assessed whether the interventions, based on principles from behavioral economics, might improve statin adherence and lipid control in at-risk populations. We describe the rationale and methods for the trial, recruitment, conduct and follow-up. We also report on several barriers we encountered with recruitment and conduct of the trial, solutions we devised and efforts we will make to assess their impact on our study.MethodsHabit Formation is a four-arm randomized controlled trial. Recruitment of 805 participants at elevated risk of atherosclerotic cardiovascular disease with evidence of sub-optimal statin adherence and low-density lipoprotein (LDL) control is complete. Initially, we recruited from large employers (Employers) and a national health insurance company (Insurers) using mailed letters; individuals with a statin Medication Possession Ratio less than 80% were invited to participate. Respondents were enrolled if a laboratory measurement of low-density lipoprotein was >130 mg/dL. Subsequently, we recruited participants from the Penn Medicine Health System; individuals with usual-care low-density lipoprotein of >100 mg/dL in the electronic medical record were recruited using phone, text, email, and regular mail. Eligible participants self-reported incomplete medication adherence. During a 6-month intervention period, all participants received a wireless-enabled pill bottle for their statins and daily reminder messages to take their medication. Principles of behavioral economics were used to design three financial incentives, specifically a Simple Daily Sweepstakes rewarding daily medication adherence, a Deadline Sweepstakes where participants received either a full or reduced incentive depending on whether they took their medication before or after a daily reminder or Sweepstakes Plus Deposit Contract with incentives divided between daily sweepstakes and a monthly deposit. Six months post-incentives, we compared the primary outcome, mean change from baseline low-density lipoprotein, across arms.Results and lessons learnedHealth system recruitment yielded substantially better enrollment and was cost-efficient. Despite unexpected systematic failure and/or poor availability of two wireless pill bottles, we achieved enrollment targets and implemented the interventions. For new trials, we will routinely monitor device function and have contingency plans in the event of systemic failure.ConclusionInterventions used in the Habit Formation trial could be translated into clinical practice. Within a large health system, successful recruitment depended on identification of eligible individuals through their electronic medical record, along with flexible ways of contacting these individuals. Challenges with device failure were manageable. The study will add to our understanding of optimally structuring and implementing incentives to motivate durable behavior change.

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 Clinical Significance of Low Density Lipoprotein Cholesterol Measurements: Direct Versus Indirect Method

2016 ◽  
Vol 15 (1) ◽  
pp. 17-25
Author(s):  
Manushri Sharma ◽  
HS Batra ◽  
Mithu Banerjee ◽  
Arabinda Mohan Bhattarai ◽  
Deeptika Agarwal
Keyword(s):  
Direct Method ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Direct Methods ◽  
Cross Sectional Study ◽  
Lipoprotein Cholesterol ◽  
Low Density ◽  
Low Density Lipoprotein Cholesterol ◽  
Cross Sectional ◽  
Friedewald Formula

Introduction: Estimation of low density lipoprotein cholesterol (LDL-C) is crucial in management of coronary artery disease patients. The management of dyslipidemia is largely based on the concentration of LDL-C. The objective of this study was to compare direct measurement of LDL-C determined by a homogenous method with LDL-C estimation done by Friedewald formula (FF) in heterogeneous populations. Methods: In this cross sectional study, we measured LDL-C by homogenous method (D-LDL-C) in 1,000 fasting samples & compared with FF (F–LDL-C) used for calculation of LDL-C. The measurements of total cholesterol (TC) and triglycerides (TG) were performed using traditional enzymatic methods. The measurements of high density lipoprotein cholesterol (HDL-C) and LDL-C were performed using direct methods with precipitation, and the estimation of the LDL-C fraction was calculated using the FF. Results: Correlation analysis shows that the two methods had significant correlation (p<0.0001). However the FF had positive bias in regard to direct method with TG levels ≤150 mg/dL. No bias was observed between the methods for TG levels from 151-200 mg/dL & from 201-300 mg/dL. Whereas, TG levels from 301-400 mg/dL shows negative bias by FF. Conclusion: The Friedewald’s formula does not shows homogenous performance for estimating LDL-C levels in samples with different TG levels as compared with that of direct method.

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