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Original research article
Troponin and BNP are markers for subsequent non-ischaemic congestive heart failure: the Caerphilly Prospective Study (CaPS)
  1. Christopher C Patterson1,
  2. Stefan Blankenberg2,3,
  3. Yoav Ben-Shlomo4,
  4. Luke Heslop5,
  5. Anthony Bayer5,
  6. Gordon Lowe6,
  7. Tanja Zeller2,3,
  8. John Gallacher7,
  9. Ian Young1 and
  10. John W G Yarnell1
  1. 1Centre for Public Health, Queen’s University Belfast, Belfast, UK
  2. 2Department of General and Interventional Cardiology, University Heart Centre Hamburg, Hamburg, Germany
  3. 3DZHK German Center for Cardiovascular Research, Partner Sites Hamburg, Lubeck, Kiel, Hamburg, Germany
  4. 4School of Social and Community Medicine, University of Bristol, Bristol, UK
  5. 5Division of Population Medicine, Cardiff University School of Medicine, Cardiff, UK
  6. 6Institute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, UK
  7. 7Department of Psychiatry, University of Oxford, Warneford Hospital, Oxford, UK
  1. Correspondence to Prof Christopher C Patterson; c.patterson{at}qub.ac.uk
  • Dr John W G Yarnell deceased, 13 Jul 2017

Abstract

Objective To examine the long-term predictive value of 28 biomarkers for subsequent non-ischaemic congestive heart failure (CHF) and separately for other cardiovascular outcomes (myocardial infarction (MI) and stroke).

Methods The Caerphilly Prospective Study recruited 2171 men aged 55–69 years from the general population in 1989–1993; men were screened for evidence of cardiovascular disease (CVD) and followed for clinical cardiovascular events. Fasting blood samples were stored at −70°C until assayed for novel biomarkers in 2010–2013. A competing risks proportional hazards regression analysis was used to estimate subhazard ratios (SHRs) for each biomarker for each cardiovascular outcome.

Results During follow-up (average 13 years), only new, initial events were evaluated in the whole cohort: 584 MIs, 313 strokes and 261 episodes of CHF (not associated with acute MI). In a subcohort of men who had no clinical history or evidence of CVD at baseline examination (n=1279) those in the top third of the distributions of troponin and B-type natriuretic peptide (BNP) showed a threefold increase in risk for subsequent CHF as a first event after adjustment for all conventional risk factors (SHRs 3.37, 95% CI 1.39 to 8.14 and 3.23, 95% CI 1.45 to 7.23), respectively, in contrast to moderate elevations in risk for acute MI (troponin SHR 1.63, 95% CI 1.10 to 2.41) and for stroke (BNP SHR 1.75 95% CI 1.06 to 2.88).

Conclusion Troponin and BNP could be considered as potentially useful screening tools to detect subjects without prior CVD at increased risk of developing CHF in subsequent years in addition to having lesser roles for predicting subsequent MI (troponin) or stroke (BNP).

  • heart failure
  • epidemiology
  • stroke
  • atherosclerosis

This is an Open Access article distributed in accordance with the terms of the Creative Commons Attribution (CC BY 4.0) license, which permits others to distribute, remix, adapt and build upon this work, for commercial use, provided the original work is properly cited. See: http://creativecommons.org/licenses/by/4.0/

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Footnotes

  • Contributors CCP advised on the statistical design of the study, compiled the data, conducted the data analysis and coauthored the manuscript. SB participated in the study as principal investigator of BiomarCaRE and read and approved the final manuscript. YB-S helped devise the project, assisted in the data collection, validated the clinical events and read and approved the final manuscript. LH was responsible for collecting and compiling the outcome data and convening the validation committee, and he read and approved the final manuscript. AB helped devise the project, participated in the data collection and validation committee and read and approved the final manuscript. GL helped devise the project, was responsible for the Glasgow biomarker assays and read and approved the final manuscript. TZ responsible for the assays conducted within BiomarCaRE and read and approved the final manuscript. JG helped devise the project and read and approved the final manuscript. IY helped devise the project, had overall responsibility for the Belfast assays and read and approved the final manuscript. JWGY devised the study, obtained the funding, assisted in the data collection, compilation and analysis, and wrote the manuscript in conjunction with CCP.

  • Funding The work was principally supported by the British Heart Foundation (PG/09/002/26056). Biomarker assays performed in Germany were funded by the BiomarCaRE Project (EU 7th Framework: Health- F2-2011-278913).

  • Competing interests Abbott Diagnostics provided reagents for troponin-I determination. SB reports investigator-initiated grants from Siemens, Abbott Diagnostics and Thermofisher. JWGY, IY, YB-S, JG and GL were the grant holders from the British Heart Foundation.

  • Patient consent Obtained.

  • Ethics approval This project was approved by the South East Wales Research Ethics Committee in July 2009 (reference 09/WSE04/32).

  • Provenance and peer review Not commissioned; internally peer reviewed.

  • Data sharing statement Data will be shared with the BiomarCaRE Project (EU 7th Framework: Health-F2-2011-278913) in the first instance.