Objective To determine the frequency of biochemical monitoring after initiation of aldosterone antagonists(AA) in patients also using angiotensin-converting enzyme inhibitors/angiotensin receptor blockers (ACEI/ARB).
Setting UK primary care.
Participants ACEI/ARB users who initiated AA between 2004 and 2014.
Outcomes We calculated the proportions with: (1) biochemical monitoring ≤2 weeks post initiation of AA, (2) adverse biochemical values ≤2 months (potassium ≥6 mmol/L, creatinine ≥220 µmol/L and ≥30% increase in creatinine from baseline) and (3) discontinuers of AA in those with an adverse biochemical value. We used logistic regression to study patient characteristics associated with monitoring and adverse biochemical values.
Results In 10 546 initiators of AA, 3291 (31.2%) had a record of biochemical monitoring ≤2 weeks post initiation. A total of 2.0% and 2.7% of those with follow-up monitoring within 2 months of initiation experienced potassium ≥6 mmol/L and creatinine ≥220 µmol/L, respectively, whereas 13.5% had a ≥30% increase in creatinine. Baseline potassium (OR 3.59, 95% CI 2.43 to 5.32 for 5.0–5.5 mmol/L compared with <5.0 mmol/L) and estimated glomerular filtration rate 45-59 ml/min/1.73 m2 (OR 2.06, 95% CI 1.26 to 3.35 compared with ≥60 ml/min/1.73 m2) were independently predictive of potassium ≥6 mmol/L. Women and people with diabetes had higher odds of ≥30% increase in creatinine.
Conclusion Less than one-third of patients taking ACEI/ARB had biochemical monitoring within 2 weeks of initiating AAs. Higher levels of monitoring may reduce adverse biochemical events.
- drug monitoring
- heart failure
- electronic health records
- health care delivery
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Contributors LAT had the idea for the study and acquired data permissions. S-JS, KEM, MS, DN and LAT designed the study. S-JS, KEM and MS managed the data and established the cohort. S-JS did the analyses. All authors participated in the discussion and interpretation of the results. S-JS organised the writing and wrote the initial drafts. All authors critically revised the manuscript for intellectual content and approved the final version. S-JS is the guarantor.
Funding S-JS is supported by the Wellcome Trust Sir Henry Wellcome Fellowship (107340/Z/15/Z). LS is supported by the Wellcome Trust Senior Research Fellowship in Clinical Science (098504/Z/12/Z). LAT is supported by the Wellcome Trust Intermediate Clinical Fellowship (101143/Z/13/Z) which also funded KEM. KB is supported by the Sir Henry Dale Fellowship jointly funded by the Wellcome Trust and the Royal Society (107731/Z/15/Z). MS is supported by the AP Møller Foundation for the Advancement of Medical Science, Snedkermester Sophus Jacobsen og Hustru Astrid Jacobsens Fond and Christian og Ottilia Brorsons Rejselegat for yngre videnskabsmænd og-kvinder.
Competing interests S-JS, KEM, MS, DN and LAT have nothing to declare. LS reports grants from the Wellcome Trust and British Heart Foundation during the conduct of the study; grants from the Wellcome Trust, Medical Research Council, National Institute for Health Research and European Union outside the submitted work; personal fees from GSK for advisory work unrelated to the submitted work; grant funding from GSK for academic research unrelated to the submitted work; acts as an unpaid steering committee chair for AstraZeneca for a randomised trial unrelated to the submitted work and is a trustee of the British Heart Foundation. KB declares grants from the Wellcome Trust, Royal Society, MRC, NIHR and BHF outside the submitted work.
Ethics approval The protocol for this study was approved by the London School of Hygiene and Tropical Medicine Ethics Committee (no 6536) and the Independent Scientific Advisory Committee (ISAC) for Medicines and Healthcare Products Regulatory Agency (no 16_025A).
Provenance and peer review Not commissioned; externally peer reviewed.
Data sharing statement No additional data available.
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