Article Text
Abstract
Objective In patients with acute chest pain who have had myocardial infarction excluded, plasma cardiac troponin I concentrations ≥5 ng/L are associated with risk of future adverse cardiovascular events. We aim to evaluate the association between cardiac troponin and coronary plaque composition in such patients.
Methods In a prespecified secondary analysis of a prospective cohort study, blinded quantitative plaque analysis was performed on 242 CT coronary angiograms of patients with acute chest pain in whom myocardial infarction was excluded. Patients were stratified by peak plasma cardiac troponin I concentration ≥5 ng/L or <5 ng/L. Associations were assessed using univariable and multivariable logistic regression analyses.
Results The cohort was predominantly middle-aged (62±12 years) men (69%). Patients with plasma cardiac troponin I concentration ≥5 ng/L (n=161) had a higher total (median 33% (IQR 0–47) vs 0% (IQR 0–33)), non-calcified (27% (IQR 0–37) vs 0% (IQR 0–28)), calcified (2% (IQR 0–8) vs 0% (IQR 0–3)) and low-attenuation (1% (IQR 0–3) vs 0% (IQR 0–1)) coronary plaque burden compared with those with concentrations <5 ng/L (n=81; p≤0.001 for all). Low-attenuation plaque burden was independently associated with plasma cardiac troponin I concentration ≥5 ng/L after adjustment for clinical characteristics (adjusted OR per doubling 1.62 (95% CI 1.17 to 2.32), p=0.005) or presence of any visible coronary artery disease (adjusted OR per doubling 1.57 (95% CI 1.07 to 2.37), p=0.026).
Conclusion In patients with acute chest pain but without myocardial infarction, plasma cardiac troponin I concentrations ≥5 ng/L are associated with greater burden of low-attenuation coronary plaque.
- computed tomography angiography
- chest pain
- biomarkers
- atherosclerosis
Data availability statement
Data are available upon reasonable request.
Statistics from Altmetric.com
Data availability statement
Data are available upon reasonable request.
Footnotes
Twitter @RyanWereski, @imagingmedsci
Contributors All persons who meet the authorship criteria are listed as authors, and all authors certify that they have participated sufficiently in the work to take public responsibility for the content, including participation in the concept, design, analysis, writing or revision of the manuscript. MNM designed the study, analysed the scans and wrote the initial draft. RW, MRD, AB, MCW, EJRvB, NLM, DD and DEN helped with concepts and revision of the manuscript. KKL helped with the design of the study and assisted with manuscript preparation and revision. MNM acts as guarantor.
Funding MNM (FS/19/46/34445), MCW (FS/ICRF/20/26002, FS/11/014, CH/09/002), NLM (CH/F/21/90010, RG/20/10/34966, RE/18/5/34216) and DEN (FS/19/15/34155, CH/09/002, RG/16/10/32375, RE/18/5/34216) are supported by the British Heart Foundation. DEN is also a recipient of a Wellcome Trust Senior Investigator Award (WT103782AIA). DD is supported by National Institutes of Health/National Heart, Lung, and Blood Institute grants (1R01HL148787-01A1 and 1R01HL151266). KKL is supported by a British Heart Foundation (BHF) Clinical Research Training Fellowship (FS/18/25/33454).
Competing interests Outside the current study, DD received software royalties from Cedars-Sinai Medical Center and has a patent. MCW has spoken at meetings sponsored by Canon Medical Systems and Siemens Healthineers. DEN is on the Editorial Board of Heart. MRD, MCW and KKL are members of Heart’s Editorial Board.
Patient and public involvement Patients and/or the public were not involved in the design, or conduct, or reporting, or dissemination plans of this research.
Provenance and peer review Not commissioned; externally peer reviewed.