Objectives To characterise peak cardiac troponin levels, in patients presenting with acute myocardial infarction (AMI), according to their comorbid condition and determine the influence of peak cardiac troponin (cTn) levels on mortality.
Methods We included patients with the first admission for AMI in the UK. We used linear regression to estimate the association between eight common comorbidities (diabetes mellitus, previous angina, peripheral arterial disease, previous myocardial infarction (MI), chronic kidney disease (CKD), cerebrovascular disease, chronic heart failure (CHF) and chronic obstructive pulmonary disease (COPD)) and peak cTn. Peak cTn levels were adjusted for age, sex, smoking status and comorbidities. Logistic regression and restricted cubic spline models were employed to investigate the association between peak cTn and 180-day mortality for each comorbidity.
Results 330 367 patients with ST elevation myocardial infarction and non-ST elevation myocardial infarction were identified. Adjusted peak cTn levels were significantly higher in patients with CKD (adjusted % difference in peak cTnT for CKD=42%, 95% CI 13.1 to 78.4) and significantly lower for patients with COPD, previous angina, previous MI and CHF when compared with patients without the respective comorbidities (reference group) (cTnI; COPD=−21.7%, 95% CI −29.1 to −13.4; previous angina=−24.2%, 95% CI −29.6 to −8.3; previous MI=−13.5%, 95% CI −20.6 to −5.9; CHF=−28%, 95% CI −37.2 to −17.6). Risk of 180-day mortality in most of the comorbidities did not change substantially after adjusting for peak cTn. In general, cTnI had a stronger association with mortality than cTnT.
Conclusions In this nationwide analysis of patients presenting with AMI, comorbidities substantially influenced systemic concentrations of peak cTn. Comorbid illness is a significant predictor of mortality regardless of peak cTn levels and should be taken into consideration while interpreting cTn both as a diagnostic and prognostic biomarker.
- acute myocardial infarction
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Contributors VS: study design, analyses, conducting and manuscript preparation. KR: study design, analyses, CB: analyses and manuscript preparation. RZ: manuscript preparation. JS: manuscript preparation. AS: manuscript preparation. TN: planning. JP: analyses. JW: manuscript preparation. LS: design and manuscript preparation. DS: design and manuscript preparation. AT: design and manuscript preparation. SR: study design, conducting and manuscript preparation. JKQ: study design, conducting and manuscript preparation.
Funding This work was funded by an MRC Population Health Scientist Fellowship held by JKQ[G0902135].
Competing interests None declared.
Patient consent for publication Not required.
Provenance and peer review Not commissioned; externally peer reviewed.
Data availability statement Data are available upon reasonable request. We have used a deidentified participant data which is available on request after obtaining specific permissions from the MINAP committee. Additional information on statistical analyses plan and codes (statistical codes and diagnoses codes) are available on request (email address: firstname.lastname@example.org)
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