Background: The objective of this study was to assess the cost-effectiveness of pravastatin therapy in survivors of myocardial infarction with average cholesterol levels.
Methods: We performed a cost-effectiveness analysis based on actual clinical, cost, and health-related quality-of-life data from the Cholesterol and Recurrent Events (CARE) trial. Survival and recurrent coronary heart disease events were modeled from trial data in Markov models, with the use of different assumptions regarding the long-term benefit of therapy.
Results: Pravastatin therapy increased quality-adjusted life expectancy at an incremental cost of $16,000 to $32,000 per quality-adjusted life-year gained. In subgroup analyses, the cost-effectiveness of pravastatin therapy was more favorable for patients >60 years of age and for patients with pretreatment low-density lipoprotein cholesterol levels >125 mg/dL. Results were sensitive to the cost of pravastatin and to assumptions about long-term survival benefits from pravastatin therapy.
Conclusions: The cost-effectiveness of pravastatin therapy in survivors of myocardial infarction with average cholesterol levels compares favorably with other interventions.
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Dutch Pharmacogenetics Working Group (DPWG) guideline for the gene-drug interaction between SLCO1B1 and statins and CYP2C9 and sulfonylureas.
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Article Synopsis
- - Familial hypercholesterolemia is a common condition that can lead to early heart disease and stroke, with statins being the primary treatment, but they might also increase the risk of type 2 diabetes due to effects on β-cells.
- - The study used a mouse insulinoma model to analyze the effects of simvastatin and pravastatin on β-cells in the presence of fatty acids, revealing that simvastatin reduced cholesterol more effectively but was also more cytotoxic and suppressed insulin levels.
- - While simvastatin lowered insulin content significantly, this effect was reversible and not dependent on its main action, indicating that it may impact insulin secretion through mechanisms beyond just blocking HMG-CoA reductase. *
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