Author + information
- Received March 7, 2016
- Revision received September 28, 2016
- Accepted October 4, 2016
- Published online December 19, 2016.
- Ian Ford, PhDa,
- Anoop S.V. Shah, MDb,
- Ruiqi Zhang, MSca,
- David A. McAllister, MDc,
- Fiona E. Strachan, PhDb,
- Muriel Caslake, PhDd,
- David E. Newby, MDb,
- Chris J. Packard, DScd and
- Nicholas L. Mills, MDb,∗ ()
- aRobertson Centre for Biostatistics, University of Glasgow, Glasgow, United Kingdom
- bBHF Centre for Cardiovascular Science, University of Edinburgh, Edinburgh, United Kingdom
- cCentre for Population Health Sciences, University of Edinburgh, Edinburgh, United Kingdom
- dInstitute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, United Kingdom
- ↵∗Reprint requests and correspondence:
Dr. Nicholas L. Mills, BHF/University Centre for Cardiovascular Science, Chancellor’s Building, University of Edinburgh, Edinburgh EH16 4SB, United Kingdom.
Background Cardiac troponin is an independent predictor of cardiovascular mortality in individuals without symptoms or signs of cardiovascular disease. The mechanisms for this association are uncertain, and a role for troponin testing in the prevention of coronary heart disease has yet to be established.
Objectives This study sought to determine whether troponin concentration could predict coronary events, be modified by statins, and reflect response to therapy in a primary prevention population.
Methods WOSCOPS (West of Scotland Coronary Prevention Study) randomized men with raised low-density lipoprotein cholesterol and no history of myocardial infarction to pravastatin 40 mg once daily or placebo for 5 years. Plasma cardiac troponin I concentration was measured with a high-sensitivity assay at baseline and at 1 year in 3,318 participants.
Results Baseline troponin was an independent predictor of myocardial infarction or death from coronary heart disease (hazard ratio [HR]: 2.3; 95% confidence interval [CI]: 1.4 to 3.7) for the highest (≥5.2 ng/l) versus lowest (≤3.1 ng/l) quarter of troponin (p < 0.001). There was a 5-fold greater reduction in coronary events when troponin concentrations decreased by more than a quarter, rather than increased by more than a quarter, for both placebo (HR: 0.29; 95% CI: 0.12 to 0.72 vs. HR: 1.95; 95% CI: 1.09 to 3.49; p < 0.001 for trend) and pravastatin (HR: 0.23; 95% CI: 0.10 to 0.53 vs. HR: 1.08; 95% CI: 0.53 to 2.21; p < 0.001 for trend). Pravastatin reduced troponin concentration by 13% (10% to 15%; placebo adjusted, p < 0.001) and doubled the number of men whose troponin fell more than a quarter (p < 0.001), which identified them as having the lowest risk for future coronary events (1.4% over 5 years).
Conclusions Troponin concentration predicts coronary events, is reduced by statin therapy, and change at 1 year is associated with future coronary risk independent of cholesterol lowering. Serial troponin measurements have major potential to assess cardiovascular risk and monitor the impact of therapeutic interventions.
This research was supported by a Special Project Grant from the British Heart Foundation (SP/12/10/29922) and by an investigator initiated research grant from Abbott Laboratories. Drs. Mills and Newby are supported by the Butler Senior Clinical Research Fellowship (FS/16/14/32023) and Chair (CH/09/002) awards from the British Heart Foundation. Dr. Shah has acted as a consultant for Abbott Laboratories. Dr. McAllister has been a paid lecturer for Roche; and has served as an advisor for the GSK-COPD trial and for Galecto. Dr. Packard has received grants from Merck Sharp & Dohme and Roche; and has received honoraria from Merck Sharp & Dohme, Pfizer, and Sanofi. Dr. Mills has acted as a consultant for Abbott Laboratories, Beckman-Coulter, Roche Diagnostics, and Singulex. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- Received March 7, 2016.
- Revision received September 28, 2016.
- Accepted October 4, 2016.
- The Authors