Dataset Information

Value of genetic testing in the prevention of coronary heart disease events.

ABSTRACT:

Background

The health economic evidence about the value and optimal targeting of genetic testing in the prevention of coronary heart disease (CHD) events has remained limited and ambiguous. The objective of this study is to optimize the population-level use and targeting of genetic testing alongside traditional risk factors in the prevention of CHD events and, thereby, to assess the cost-benefit of genetic testing.

Methods and findings

We compare several strategies for using traditional and genetic testing in the prevention of CHD through statin therapy. The targeting of tests to different patient segments within these strategies is optimized by using a decision-analytic model, in which a patient's estimated risk of CHD is updated based on test results using Bayesian methods. We adopt the perspective of healthcare sector. The data for the model is exceptionally wide and combined from national healthcare registers, the Finnish Institute for Molecular Medicine, and published literature. Our results suggest that targeting genetic testing in an optimal way to those patients about which traditional risk factors do not provide sufficiently accurate information results in the highest expected net benefit. In particular, compared to the use of traditional risk factors only, the optimal use of genetic testing would decrease the expected costs of an average patient aged 45 years or more by 2.54€ in a 10-year follow-up period while maintaining the level of the expected health outcome. Thus, genetic testing is found to be a part of a cost-beneficial testing strategy alongside traditional risk factors. This conclusion is robust to reasonable changes in model inputs.

Conclusions

If targeted optimally, the use of genetic testing alongside traditional risk factors is cost-beneficial in the prevention of CHD.

SUBMITTER: Hynninen Y

PROVIDER: S-EPMC6333335 | biostudies-literature | 2019

REPOSITORIES: biostudies-literature

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Publications

Value of genetic testing in the prevention of coronary heart disease events.

Hynninen Yrjänä Y Linna Miika M Vilkkumaa Eeva E

PloS one 20190115 1

<h4>Background</h4>The health economic evidence about the value and optimal targeting of genetic testing in the prevention of coronary heart disease (CHD) events has remained limited and ambiguous. The objective of this study is to optimize the population-level use and targeting of genetic testing alongside traditional risk factors in the prevention of CHD events and, thereby, to assess the cost-benefit of genetic testing.<h4>Methods and findings</h4>We compare several strategies for using tradi ...[more]

PMID: 30645616

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Project description:Genetic variants have been associated with the risk of coronary heart disease. In this study, we tested whether or not a composite of these variants could ascertain the risk of both incident and recurrent coronary heart disease events and identify those individuals who derive greater clinical benefit from statin therapy.A community-based cohort study (the Malmo Diet and Cancer Study) and four randomised controlled trials of both primary prevention (JUPITER and ASCOT) and secondary prevention (CARE and PROVE IT-TIMI 22) with statin therapy, comprising a total of 48,421 individuals and 3477 events, were included in these analyses. We studied the association of a genetic risk score based on 27 genetic variants with incident or recurrent coronary heart disease, adjusting for traditional clinical risk factors. We then investigated the relative and absolute risk reductions in coronary heart disease events with statin therapy stratified by genetic risk. We combined data from the different studies using a meta-analysis.When individuals were divided into low (quintile 1), intermediate (quintiles 2-4), and high (quintile 5) genetic risk categories, a significant gradient in risk for incident or recurrent coronary heart disease was shown. Compared with the low genetic risk category, the multivariable-adjusted hazard ratio for coronary heart disease for the intermediate genetic risk category was 1·34 (95% CI 1·22-1·47, p<0·0001) and that for the high genetic risk category was 1·72 (1·55-1·92, p<0·0001). In terms of the benefit of statin therapy in the four randomised trials, we noted a significant gradient (p=0·0277) of increasing relative risk reductions across the low (13%), intermediate (29%), and high (48%) genetic risk categories. Similarly, we noted greater absolute risk reductions in those individuals in higher genetic risk categories (p=0·0101), resulting in a roughly threefold decrease in the number needed to treat to prevent one coronary heart disease event in the primary prevention trials. Specifically, in the primary prevention trials, the number needed to treat to prevent one such event in 10 years was 66 in people at low genetic risk, 42 in those at intermediate genetic risk, and 25 in those at high genetic risk in JUPITER, and 57, 47, and 20, respectively, in ASCOT.A genetic risk score identified individuals at increased risk for both incident and recurrent coronary heart disease events. People with the highest burden of genetic risk derived the largest relative and absolute clinical benefit from statin therapy.National Institutes of Health.

Project description:BackgroundGenetic variation at chromosome 9p21 is a recognized risk factor for coronary heart disease (CHD). However, its effect on disease progression and subsequent events is unclear, raising questions about its value for stratification of residual risk.MethodsA variant at chromosome 9p21 (rs1333049) was tested for association with subsequent events during follow-up in 103 357 Europeans with established CHD at baseline from the GENIUS-CHD (Genetics of Subsequent Coronary Heart Disease) Consortium (73.1% male, mean age 62.9 years). The primary outcome, subsequent CHD death or myocardial infarction (CHD death/myocardial infarction), occurred in 13 040 of the 93 115 participants with available outcome data. Effect estimates were compared with case/control risk obtained from the CARDIoGRAMplusC4D consortium (Coronary Artery Disease Genome-wide Replication and Meta-analysis [CARDIoGRAM] plus The Coronary Artery Disease [C4D] Genetics) including 47 222 CHD cases and 122 264 controls free of CHD.ResultsMeta-analyses revealed no significant association between chromosome 9p21 and the primary outcome of CHD death/myocardial infarction among those with established CHD at baseline (GENIUS-CHD odds ratio, 1.02; 95% CI, 0.99-1.05). This contrasted with a strong association in CARDIoGRAMPlusC4D odds ratio 1.20; 95% CI, 1.18-1.22; P for interaction <0.001 compared with the GENIUS-CHD estimate. Similarly, no clear associations were identified for additional subsequent outcomes, including all-cause death, although we found a modest positive association between chromosome 9p21 and subsequent revascularization (odds ratio, 1.07; 95% CI, 1.04-1.09).ConclusionsIn contrast to studies comparing individuals with CHD to disease-free controls, we found no clear association between genetic variation at chromosome 9p21 and risk of subsequent acute CHD events when all individuals had CHD at baseline. However, the association with subsequent revascularization may support the postulated mechanism of chromosome 9p21 for promoting atheroma development.

Project description:BackgroundHighly fragmented ambulatory care (i.e., care spread across many providers without a dominant provider) has been associated with excess tests, procedures, emergency department visits, and hospitalizations. Whether fragmented care is associated with worse health outcomes, or whether any association varies with health status, is unclear.ObjectiveTo determine whether fragmented care is associated with the risk of incident coronary heart disease (CHD) events, overall and stratified by self-rated general health.Design and participantsWe conducted a secondary analysis of the nationwide prospective Reasons for Geographic and Racial Differences in Stroke (REGARDS) cohort study (2003-2016). We included participants who were ≥ 65 years old, had linked Medicare fee-for-service claims, and had no history of CHD (N = 10,556).Main measuresWe measured fragmentation with the reversed Bice-Boxerman Index. We used Cox proportional hazards models to determine the association between fragmentation as a time-varying exposure and adjudicated incident CHD events in the 3 months following each exposure period.Key resultsThe mean age was 70 years; 57% were women, and 34% were African-American. Over 11.8 years of follow-up, 569 participants had CHD events. Overall, the adjusted hazard ratio (HR) for the association between high fragmentation and incident CHD events was 1.14 (95% confidence interval (CI) 0.92, 1.39). Among those with very good or good self-rated health, high fragmentation was associated with an increased hazard of CHD events (adjusted HR 1.35; 95% CI 1.06, 1.73; p = 0.01). Among those with fair or poor self-rated health, high fragmentation was associated with a trend toward a decreased hazard of CHD events (adjusted HR 0.54; 95% CI 0.29, 1.01; p = 0.052). There was no association among those with excellent self-rated health.ConclusionHigh fragmentation was associated with an increased independent risk of incident CHD events among those with very good or good self-rated health.

Dataset Information

Value of genetic testing in the prevention of coronary heart disease events.

Background

Methods and findings

Conclusions

Publications

Value of genetic testing in the prevention of coronary heart disease events.

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