Abstract
Background
Discontinuation of low-dose acetylsalicylic acid (ASA) leads to an increased risk of cardiovascular and cerebrovascular events in patients taking low-dose ASA for secondary cardiovascular prevention. However, little is known about the rate of discontinuation in everyday clinical practice.
Objectives
To assess the rate of low-dose ASA discontinuation in primary care, and identify factors that predict discontinuation.
Methods
The Health Improvement Network, a large UK primary care database, was used to identify patients aged 50–84 years who received at least two consecutive prescriptions for low-dose ASA for secondary cardiovascular or cerebrovascular prevention in 2000–2007 (n = 35,639). Discontinuation was defined as a period of at least 90 days after completion of the last prescribed course of ASA during which no repeat prescription was issued.
Results
During the study, 11,729 patients (32.9%) discontinued ASA therapy (mean follow-up 2.5 years). The discontinuation rate was lower in patients with ASA indicated for myocardial infarction than for other indications. The diagnosis of gastrointestinal disorders during the study (overall odds ratio: 1.74; 95% confidence interval: 1.61–1.88) was associated with increased rates of ASA discontinuation, whereas co-prescription of a proton pump inhibitor from the start of ASA therapy was associated with a decreased rate of discontinuation (odds ratio: 0.80; 95% confidence interval: 0.75–0.86). Co-prescription of several other cardioprotective medications was also associated with a reduced risk of discontinuation, as were increasing age, prior hospitalization and overall number of co-medications.
Conclusion
Continuous co-prescription of a PPI with low-dose ASA may improve adherence and outcomes, particularly in patients at both cardiovascular and gastrointestinal risk.
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Acknowledgments
Elisa Martín-Merino contributed to the study design, data collection, statistical analysis, interpretation of data, and drafting the report; Luis A García Rodríguez contributed to data collection, statistical analysis, and reviewing the report; Saga Johansson and Héctor Bueno contributed to the study design, interpretation of data, and reviewing the report.
Disclosure
This work was supported by an unrestricted research grant from AstraZeneca R&D, Mölndal. Luis A García Rodríguez and Elisa Martín-Merino work for the Spanish Centre for Pharmacoepidemiologic Research, which has received research funding from AstraZeneca R&D, Mölndal. Luis A García Rodríguez has also received honoraria for serving on a scientific advisory board for AstraZeneca. Héctor Bueno has received honoraria for talks and advisory work from Almirall, Bayer, BMS, Daichii-Sankyo, Eli-Lilly, and Sanofi-Aventis, and research grants from AstraZeneca. Saga Johansson is an employee of AstraZeneca R&D, Mölndal. All authors had full access to all of the data (including statistical reports and tables) in the study and can take responsibility for the integrity of the data and the accuracy of the data analysis.
We acknowledge and thank Dr Stephen Sweet and Dr Catherine Hill of Oxford PharmaGenesis™ Ltd, who provided writing assistance also funded by AstraZeneca R&D, Mölndal.