Background Accuracy of routinely collected information concerning cause of death is essential for public health and health systems planning. Since clinical examination has relatively low sensitivity for detection of valvular heart disease (VHD), mortality data based on clinical information alone might routinely underestimate the number of deaths due to VHD.
Methods We compared autopsy findings against premortem clinical information for 8198 consecutive adult postmortems (mean age 69.1 years, 61.3% men), performed in a single UK tertiary referral centre with on-site cardiac surgical facilities over a 10-year period (2004–2013) during which 21% of the adult population underwent postmortem examination.
Results Following postmortem, VHD was the principal cause of death in 165 individuals (2.0%), a principal or contributory cause (‘any cause’) of death in 326 (4.0%) and an incidental (ie, non-causal) finding in a further 346 (4.2%). Clinical documentation of VHD before death was highly specific but relatively insensitive for postmortem identification of VHD as the principal (specificity 96.8%; 95% CI 96.4% to 97.2%; sensitivity 69.7%, 95% CI 62.1% to 76.6%) or any (specificity 98.1%; 95% CI 97.8% to 98.4%; sensitivity 68.4%, 95% CI 63.1% to 73.4%) cause of death. VHD (principally aortic stenosis, endocarditis and rheumatic heart disease) was newly noted at postmortem and listed as a cause of death in 142 individuals (1.7%).
Conclusions Clinical information recorded premortem is highly specific but relatively insensitive for the cause of death established at autopsy. Population-based mortality statistics that depend on premortem clinical information are likely to routinely underestimate the mortality burden of VHD.
- valvular heart disease
- death certificates
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Contributors SC, ISDR and BDP conceived and designed the study. SC and ARH acquired the data. SC performed data analysis. ARH wrote the first draft. All authors were responsible for interpreting the data and critically revising the paper. All authors approved the final version of the paper.
Funding SC and BDP were supported by the National Institute for Health Research Oxford Biomedical Research Centre. ARH was supported through the National Institute for Health Research Academic Foundation Programme, and BJC by the BHF Centre of Research Excellence, Oxford (British Heart Foundation, grant RE/13/1/30181). The views expressed here are the authors’ and not necessarily those of the UK Department of Health.
Competing interests None declared.
Provenance and peer review Not commissioned; externally peer reviewed.
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