Article Text
Abstract
Objective International studies report a decline in mortality following ST-elevation myocardial infarction (STEMI). The extent to which the observed improvements in STEMI survival are explained by temporal changes in patient characteristics and utilisation of treatments is unknown.
Methods Cohort study using national registry data from the Myocardial Ischaemia National Audit Project between first January 2004 and 30th June 2013. 232 353 survivors of hospitalisation with STEMI as recorded in 247 hospitals in England and Wales. Flexible parametric survival modelling and causal mediation analysis were used to estimate the relative contribution of temporal changes in treatments and patient characteristics on improved STEMI survival.
Results Over the study period, unadjusted survival at 6 months and 1 year improved by 0.9% and 1.0% on average per year (HR: 0.991, 95% CI: 0.988 to 0.994 and HR: 0.990, 95% CI: 0.987 to 0.993, respectively). The uptake of primary percutaneous coronary intervention (PCI) (HR: 1.025, 95% CI: 1.021 to 1.028) and increased prescription of P2Y12 inhibitors (HR: 1.035, 95% CI: 1.031 to 1.039) were significantly associated with improvements in 1-year survival. Primary PCI explained 16.8% (95% CI: 10.8% to 31.6%) and 13.2% (9.2% to 21.9%) of the temporal survival improvements at 6 months and 1 year, respectively, whereas P2Y12 inhibitor prescription explained 5.3% (3.6% to 8.8%) of the temporal improvements at 6 months but not at 1 year.
Conclusions For STEMI in England and Wales, improvements in survival between 2004 and 2013 were significantly explained by the uptake of primary PCI and increased use of P2Y12 inhibitors at 6 months and primary PCI only at 1 year.
Trial registration number NCT03749694
- acute myocardial infarction
- epidemiology
- electronic medical records
- quality and outcomes of care
- acute coronary syndromes
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Footnotes
Twitter @bernadetteTDond, @cpgale3
Contributors TBD analysed the data and drafted the manuscript. TBD, MH, TM and MEY provided scientific and statistical input. ADT, PDB, TJ, KAAF and CPG provided expert clinical opinion and interpretation of the data. All authors made critical revisions and provided intellectual content to the manuscript, approved the final version to be published and agreed to be accountable for all aspects of the work. CPG is the guarantor for this study.
Funding This work was supported by the British Heart Foundation (Project Grant PG/13/81/30474) and by the Wellcome Trust, Sir Henry Wellcome Postdoctoral Fellowship (206470/Z/17/Z). The Myocardial Ischaemia National Audit Project (MINAP) is commissioned by the Health Quality Improvement Partnership as part of the National Clinical Audit and Patient Outcomes Programme. The funding organisations for this study had no involvement in the design and conduct of the study; collection, management, analysis and interpretation of the data; preparation, review or approval of the manuscript; or the decision to submit the manuscript for publication.
Competing interests CPG reports personal fees and non-financial support from AstraZeneca, non-financial support from BMS-Pfizer, personal fees from Bayer, personal fees from Novartis, personal fees from Vifor Pharma, outside the submitted work. KAAF reports grants and personal fees from Bayer/Janssen, grants from AstraZeneca, personal fees from Sanofi/Regeneron, personal fees from Verseon, outside the submitted work.
Patient consent for publication Not required.
Ethics approval Ethical approval was not required under NHS research governance arrangements. The National Institute for Cardiovascular Outcomes Research (NICOR) which includes the Myocardial Ischaemia National Audit Project (MINAP) database (Ref: NIGB: ECC 1-06 (d)/2011) has support under section 251 of the National Health Service (NHS) Act 2006 to use patient information for medical research without consent.
Provenance and peer review Not commissioned; externally peer reviewed.
Data availability statement No data are available.