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The association of financial incentives for low density lipoprotein cholesterol reduction with patient activation and motivation.

ABSTRACT: There is growing interest in using financial incentives for patients to improve medication adherence, but few studies have evaluated whether financial incentives are associated with patients' activation and motivation. We analyzed survey data collected as part of a randomized clinical trial conducted from 2011 to 2014 of four financial incentive interventions to reduce low density lipoprotein cholesterol (LDL-C) among patients at risk for atherosclerotic cardiovascular disease. The main trial included 1503 patients aged 18-80 and recruited from primary care practices affiliated with three health systems. Participants were randomized into four groups: patient financial incentives, primary care physicians (PCPs) incentives, patients and PCPs shared incentives, or no incentives for LDL-C control. Patient Activation Measure (PAM) and Treatment Self Regulation Questionnaire (TSRQ) surveys were administered at baseline and 12?months. Clinical outcomes were change in LDL-C at 12 and 15?months and average medication adherence as measured by electronic pill bottle opening. Mean changes in PAM and TSRQ scores were compared between patients eligible and not eligible for incentives. Clinical outcomes were tested against baseline and change in psychosocial measures using bivariate and multivariate regression. Change in PAM score and TSRQ autonomous subscore did not differ significantly between patients eligible and not eligible for incentives. Lower baseline and greater increase in TSRQ autonomous subscore were predictive of greater 15-month decrease in LDL-C. A financial incentive intervention to improve LDL-C control was not associated with changes in patients' activation or autonomous motivation. Increases in patient autonomous motivation are predictive of long-term LDL-C control.

SUBMITTER: Liu T

PROVIDER: S-EPMC6416647 | biostudies-literature | 2019 Jun

REPOSITORIES: biostudies-literature

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The association of financial incentives for low density lipoprotein cholesterol reduction with patient activation and motivation.

Liu Tianyu T Volpp Kevin G KG Asch David A DA Zhu Jingsan J Wang Wenli W Wu Ruoming R Troxel Andrea B AB Finnerty Darra D DD Hoffer Karen K Shea Judy A JA

Preventive medicine reports 20190309

There is growing interest in using financial incentives for patients to improve medication adherence, but few studies have evaluated whether financial incentives are associated with patients' activation and motivation. We analyzed survey data collected as part of a randomized clinical trial conducted from 2011 to 2014 of four financial incentive interventions to reduce low density lipoprotein cholesterol (LDL-C) among patients at risk for atherosclerotic cardiovascular disease. The main trial in ...[more]

PMID: 30911461

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Project description:ImportanceFinancial incentives shared between physicians and patients were shown to significantly reduce low-density lipoprotein cholesterol (LDL-C) levels in a randomized clinical trial, but it is not known whether these health benefits are worth the added incentive and utilization costs required to achieve them.ObjectiveTo evaluate the long-term cost-effectiveness of financial incentives on LDL-C level control.Design, setting, and participantsIn this economic evaluation, a previously validated microsimulation computer model was parameterized using individual-level data from the randomized clinical trial on financial incentives, National Health and Nutrition Examination Surveys for model population inputs, and other published sources. The study was conducted from April 15, 2016, to March 29, 2018.InterventionsThe following interventions were used: (1) usual care, (2) trial control strategy (increased cholesterol level monitoring and use of electronic pill bottles), (3) financial incentives for physicians, (4) financial incentives for patients, and (5) incentives shared between physicians and patients.Main outcomes and measuresDiscounted costs (2017 US dollars), lifetime cardiovascular disease risk, quality-adjusted life-years (QALYs), and incremental cost-effectiveness ratios (ICERs).ResultsThe model population (n?=?1?000?000 [30.7% women]) had similar mean (SD) age (61.5 [11.9] years) and LDL-C level (153.9 mg/dL) as the observed trial population (n?=?1503 [42.7% women]; age, 62.0 [8.7] years; and LDL-C level, 160.6 mg/dL). Using base-case assumptions (including a 10-year waning period of LDL-C level reductions), the usual-care strategy was dominated (higher costs and lower QALYs) by all other strategies. Strategies for physician- or patient-only incentives were dominated by the shared-incentives strategy, which had an ICER of $60?000/QALY compared with the trial control strategy. In a sensitivity analysis regarding the duration of LDL-C level reductions, the shared-incentives strategy remained cost-effective (ICERs <$100?000/QALY and <$150?000/QALY) for scenarios with LDL-C level reductions lasting, with linear waning, at least 7 and 5 years, respectively. In the 1-way sensitivity analysis for the time horizon of the analysis, the ICER of the shared-incentives strategy exceeded $100?000/QALY at 11 years and $150?000/QALY at 8 years. In probabilistic sensitivity analysis, the shared-incentives intervention was cost-effective in 69% to 77% of iterations using cost-effectiveness thresholds of $100?000 to $150?000/QALY. Cost-effectiveness results were also sensitive to the duration of intervention costs.Conclusions and relevanceThis study suggests that the financial incentives shared between patients and physicians for LDL-C level control meet conventional standards of cost-effectiveness, but these results appeared to be sensitive to assumptions about the durations of LDL-C level reductions and years of intervention costs included, as well as to the choice of time horizon.

Project description:Low-density lipoprotein cholesterol (LDL-C) is an important modifiable risk factor for atherosclerotic cardiovascular disease. It is unclear whether the percentage LDL-C lowering with pharmacotherapies differs on the basis of baseline LDL-C levels. To evaluate the association between baseline LDL-C levels and the percentage LDL-C reduction with a statin, ezetimibe, and a PCSK9 inhibitor. This secondary exploratory study analyzed data from 3 randomized placebo-controlled clinical trials (Aggrastat to Zocor-Thrombolysis in Myocardial Infarction 21 [A to Z-TIMI 21], Improved Reduction of Outcomes: Vytorin Efficacy International Trial [IMPROVE-IT], and Further Cardiovascular Outcomes Research With PCSK9 Inhibition in Subjects With Elevated Risk [FOURIER]) of lipid-lowering therapies (statin, ezetimibe, and a PCSK9 inhibitor) and included participants with atherosclerotic cardiovascular disease. Analyses took place form April to October 2020. In A to Z-TIMI 21, 1:1 randomization to simvastatin, 40 mg, daily for 30 days followed by 80 mg daily thereafter vs placebo for 4 months followed by simvastatin, 20 mg, daily thereafter. In IMPROVE-IT, 1:1 randomization to ezetimibe, 10 mg, daily plus simvastatin, 40 mg, daily vs placebo plus simvastatin, 40 mg, daily. In FOURIER, 1:1 randomization to evolocumab, 140 mg, every 2 weeks or 420 mg monthly vs matching placebo. The percentage LDL-C reduction at either 1 month (A to Z-TIMI 21, IMPROVE-IT) or 3 months (FOURIER) as a function of baseline LDL-C level. Data were modeled using a generalized linear regression model. A total of 3187 patients from A to Z-TIMI 21, 10 680 patients from IMPROVE-IT, and 25 847 patients from FOURIER were analyzed. There was a higher percentage reduction in LDL-C levels with evolocumab in patients with lower baseline LDL-C levels, ranging from 59.4% (95% CI, 59.1%-59.8%) in patients with a baseline LDL-C level of 130 mg/dL to 66.1% (95% CI, 65.6%-66.6%) in patients with a baseline LDL-C level of 70 mg/dL (P < .001). In contrast, across the same range of baseline LDL-C level, there was a more modest difference for simvastatin (44.6% [95% CI, 43.9%-45.2%] vs 47.8% [95% CI, 46.4%-49.2%]; P < .001) and minimal difference with ezetimibe (25.0% [95% CI, 23.3%-26.6%] vs 26.2% [95% CI, 24.2%-28.1%]; P = .007). The percentage LDL-C reduction with statins, ezetimibe, and PCSK9 inhibition is not attenuated in patients starting with lower baseline LDL-C levels and is 6.6% greater for PCSK9 inhibition. These data are encouraging for the use of intensive LDL-C-lowering therapy even for patients with lower LDL-C levels.

Project description:Background Conventional "low-density lipoprotein cholesterol (LDL-C)" assays measure cholesterol content in both low-density lipoprotein and lipoprotein(a) particles. To clarify the consequences of this methodological limitation for clinical care, our study aimed to compare associations of "LDL-C" and corrected LDL-C with risk of cardiovascular disease and to assess the impact of this correction on the classification of patients into guideline-recommended LDL-C categories. Methods and Results Lipoprotein(a) cholesterol content was estimated as 30% of lipoprotein(a) mass and subtracted from "LDL-C" to obtain corrected LDL-C values (LDL-Ccorr30). Hazard ratios for cardiovascular disease (defined as coronary heart disease, stroke, or coronary revascularization) were quantified by individual-patient-data meta-analysis of 5 statin landmark trials from the Lipoprotein(a) Studies Collaboration (18 043 patients; 5390 events; 4.7 years median follow-up). When comparing top versus bottom quartiles, the multivariable-adjusted hazard ratio for cardiovascular disease was significant for "LDL-C" (1.17; 95% CI, 1.05-1.31; P=0.005) but not for LDL-Ccorr30 (1.07; 95% CI, 0.93-1.22; P=0.362). In a routine laboratory database involving 531 144 patients, reclassification of patients across guideline-recommended LDL-C categories when using LDL-Ccorr30 was assessed. In "LDL-C" categories of 70 to <100, 100 to <130, 130 to <190, and ?190 mg/dL, significant proportions (95% CI) of participants were reassigned to lower LDL-C categories when LDL-Ccorr30 was used: 30.2% (30.0%-30.4%), 35.1% (34.9%-35.4%), 32.9% (32.6%-33.1%), and 41.1% (40.0%-42.2%), respectively. Conclusions "LDL-C" was associated with incident cardiovascular disease only when lipoprotein(a) cholesterol content was included in its measurement. Refinement in techniques to accurately measure LDL-C, particularly in patients with elevated lipoprotein(a) levels, is warranted to assign risk to the responsible lipoproteins.

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The association of financial incentives for low density lipoprotein cholesterol reduction with patient activation and motivation.

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The association of financial incentives for low density lipoprotein cholesterol reduction with patient activation and motivation.

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