Author + information
- Received April 6, 2017
- Revision received May 30, 2017
- Accepted May 30, 2017
- Published online July 24, 2017.
- Peter Willeit, MD, MPhil, PhDa,b,∗ (, )
- Paul Welsh, PhDc,
- Jonathan D.W. Evans, MBChBb,d,
- Lena Tschiderer, Dipl-Ing, BSca,
- Charles Boachie, BScc,
- J. Wouter Jukema, MD, PhDe,
- Ian Ford, PhDf,
- Stella Trompet, PhDg,
- David J. Stott, MDc,
- Patricia M. Kearney, MD, PhDh,
- Simon P. Mooijaart, MD, PhDg,
- Stefan Kiechl, MDa,
- Emanuele Di Angelantonio, MD, MSc, PhDb,i,j,k and
- Naveed Sattar, MD, PhDc
- aDepartment of Neurology, Medical University of Innsbruck, Innsbruck, Austria
- bDepartment of Public Health and Primary Care, University of Cambridge, Cambridge, United Kingdom
- cInstitute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, United Kingdom
- dTransplant Unit, Papworth Hospital NHS Foundation Trust, Papworth Everard, Cambridge, United Kingdom
- eDepartment of Cardiology, Leiden University Medical Center, Leiden, the Netherlands
- fRobertson Centre for Biostatistics, University of Glasgow, Glasgow, United Kingdom
- gDepartment of Gerontology and Geriatrics, Leiden University Medical Center, Leiden, the Netherlands
- hDepartment of Epidemiology and Public Health, University College Cork, Cork, Ireland
- iNational Institute for Health Research Blood and Transplant Research Unit in Donor Health and Genomics, University of Cambridge, Cambridge, United Kingdom
- jNHS Blood and Transplant, Cambridge, United Kingdom
- kBritish Heart Foundation Cambridge Centre of Excellence, University of Cambridge, Cambridge, United Kingdom
- ↵∗Address for correspondence:
Dr. Peter Willeit, Department of Neurology, Medical University of Innsbruck, Anichstrasse 35, 6020 Innsbruck, Austria.
Background High-sensitivity assays can quantify cardiac troponins I and T (hs-cTnI, hs-cTnT) in individuals with no clinically manifest myocardial injury.
Objectives The goal of this study was to assess associations of cardiac troponin concentration with cardiovascular disease (CVD) outcomes in primary prevention studies.
Methods A search was conducted of PubMed, Web of Science, and EMBASE for prospective studies published up to September 2016, reporting on associations of cardiac troponin concentration with first-ever CVD outcomes (i.e., coronary heart disease [CHD], stroke, or the combination of both). Study-specific estimates, adjusted for conventional risk factors, were extracted by 2 independent reviewers, supplemented with de novo data from PROSPER (Pravastatin in Elderly Individuals at Risk of Vascular Disease Study), then pooled by using random effects meta-analysis.
Results A total of 28 relevant studies were identified involving 154,052 participants. Cardiac troponin was detectable in 80.0% (hs-cTnI: 82.6%; hs-cTnT: 69.7%). In PROSPER, positive associations of log-linear shape were observed between hs-cTnT and CVD outcomes. In the meta-analysis, the relative risks comparing the top versus the bottom troponin third were 1.43 (95% confidence interval [CI]: 1.31 to 1.56) for CVD (11,763 events), 1.67 (95% CI: 1.50 to 1.86) for fatal CVD (7,775 events), 1.59 (95% CI: 1.38 to 1.83) for CHD (7,061 events), and 1.35 (95% CI: 1.23 to 1.48) for stroke (2,526 events). For fatal CVD, associations were stronger in North American studies (p = 0.010) and those measuring hs-cTnT rather than hs-cTnI (p = 0.027).
Conclusions In the general population, high cardiac troponin concentration within the normal range is associated with increased CVD risk. This association is independent of conventional risk factors, strongest for fatal CVD, and applies to both CHD and stroke.
Dr. Willeit was supported by an Erwin-Schrödinger-Fellowship sponsored by the Austrian Science Fund (J-3679-B13). Dr. Willeit, Mrs. Tschiderer, and Dr. Kiechl were supported by the excellence initiative (Competence Centers for Excellent Technologies) of the Austrian Research Promotion Agency FFG: “Research Center of Excellence in Vascular Ageing—Tyrol, VASCage” (K-Project No. 843536) funded by the BMVIT, BMWFW, Wirtschaftsagentur Wien, and Standortagentur Tirol. Dr. Evans was supported by the BHF Cambridge Centre for Research Excellence. Drs. Welsh and Sattar's cardiac biomarker work is supported by a stratified medicine grant from the Chief Scientist Office of the Scottish Government (ASM/14/1). All other authors have reported that they have no relationships relevant to the contents of this paper to disclose. Drs. Willeit, Welsh, and Evans contributed equally to this work as joint first authors. Drs. Di Angelantonio and Sattar contributed equally to this work as joint senior authors.
- Received April 6, 2017.
- Revision received May 30, 2017.
- Accepted May 30, 2017.
- 2017 The Authors