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Clinical information has low sensitivity for postmortem diagnosis of heart valve disease
  1. Sean Coffey1,2,
  2. Andrew R Harper1,3,4,
  3. Benjamin J Cairns5,6,
  4. Ian SD Roberts7,
  5. Bernard D Prendergast8
  1. 1 National Institute for Health Research (NIHR) Oxford Biomedical Research Centre, Oxford University Hospitals NHS Trust, Oxford, UK
  2. 2 Kolling Institute of Medical Research, University of Sydney, Royal North Shore Hospital, St Leonards, Australia
  3. 3 Royal Brompton and Harefield NHS Foundation Trust, London, UK
  4. 4 Wellcome Trust Centre for Human Genetics, University of Oxford, Oxford, UK
  5. 5 Cancer Epidemiology Unit, University of Oxford, Oxford, UK
  6. 6 British Heart Foundation Centre of Research Excellence, University of Oxford, Oxford, UK
  7. 7 Department of Cellular Pathology, Oxford University Hospitals NHS Trust, Oxford, UK
  8. 8 Department of Cardiology, St Thomas’ Hospital, London, UK
  1. Correspondence to Dr Bernard D Prendergast, Department of Cardiology, St Thomas’ Hospital, London SE1 7EH, UK; bernard.prendergast{at}gstt.nhs.uk

Abstract

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
  • autopsy
  • epidemiology
  • mortality
  • death certificates

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