Background: Non-steroidal anti-inflammatory drugs (NSAIDs) are commonly used to treat pain, but have potential side effects in patients with cardiovascular disease (CVD).
Objectives: To determine trends in NSAIDs prescribing between 2002 and 2010 in patients with CVD, and ascertain whether prescribing patterns changed following publication of major national (the Medicines and Healthcare products Regulatory Agency (MHRA) and the National Institute for Health and Clinical Excellence (NICE)) guidance to GPs.
Methods: This was an observational database study of adult patients in 11 practices (Staffordshire, England). NSAIDs were categorised into basic, COX-2 and topical. Study duration was divided on a quarterly basis from 2002-quarter-1 to 2010q4. CVD patients were identified using pre-defined Read Codes recorded in the two years prior to each quarter. Quarterly prevalence was determined. Times of significant changes in prescribing trends were determined using Joinpoint Regression, and compared to dates of the five major guidelines (in 2004q4, 2005q1, 2005q3, 2006q4, 2008q1).
Results: In CVD patients, the prescription of basic NSAIDs showed a decreasing trend throughout the study period, from 774 (95% CI, 691-863) per 10000 patients in 2002q1 to 245 (204-291) in 2010q4. COX-2 prescribing increased from 232/10000 (187-286) in 2002q1 to 403/10000 (348-464) in 2004q3. Prescribing then fell sharply to 102/10000 (76-134) in 2005q2 before stabilising around 55/10000. Topical NSAIDs prescribing showed a steady increase, starting at 115/10000 (108-123) in 2002q1 and ending at 270/10000 (258-281) in 2010q4. Similar trends were observed in patients without CVD, particularly a sharp drop in COX-2 prescribing also occurred from 2004q4 when initial MHRA guidance was issued.
Conclusion: Despite guidelines and a trend toward decreased prescribing, the use of potentially harmful NSAIDs continued in CVD patients. The MHRA directives potentially might have affected patients without CVD who may have inappropriately restricted their use of COX-2.