Elsevier

American Heart Journal

Volume 169, Issue 2, February 2015, Pages 257-265.e1
American Heart Journal

Clinical Investigation
Acute Ischemic Heart Disease
Cardiac troponin I for prediction of clinical outcomes and cardiac function through 3-month follow-up after primary percutaneous coronary intervention for ST-segment elevation myocardial infarction

https://doi.org/10.1016/j.ahj.2014.10.015Get rights and content

Background

Circulating levels of cardiac troponin I (cTnI) after ST-segment elevation myocardial infarction (STEMI) are associated with infarct size and chronic left ventricular dysfunction, but the relation to clinical end points and biochemical measures of global cardiac function remains less well defined.

Methods

One thousand sixty-six patients receiving primary percutaneous coronary intervention (PCI) in the PROTECTION AMI trial were studied in a post hoc analysis. Cardiac troponin I was measured at several time points during the index hospitalization, and patients were followed up for 3 months before reassessment including N-terminal pro-B-type natriuretic peptide (NT-proBNP) and left ventricular ejection fraction (LVEF) measurements.

Results

The median (quartile 1-3) cTnI levels were 0.4 (0.1-0.4) μg/L at admission, 33.1 (12.8-72.1) μg/L after 16 to 24 hours, and 9.1 (3.9-17.5) μg/L after 70 to 80 hours. In adjusted models, all post-PCI single points, peak, and area under curve were found to be independently associated with clinical events, NT-proBNP >118 pmol/L, or LVEF <40% (P for all <.001). When cTnI was added to a baseline risk model for prediction of clinical events, the C statistic improved from 0.779 to 0.846 (16-24 hours) and 0.859 (70-80 hours). Quantified by integrated discrimination improvement, the addition of cTnI significantly augmented prediction ability (relative integrated discrimination improvement 44%-154%; P for all ≤.001). Consistent improvements in discrimination of NT-proBNP >118 pmol/L and LVEF <40% were observed.

Conclusions

Cardiac troponin I measured after primary PCI for STEMI is independently associated with clinical outcomes and cardiac function through 3-month follow-up. These results suggest that cTnI levels are a useful risk stratification tool in STEMI patients.

Section snippets

Study design and population

This was a post hoc analysis of data from patients receiving PCI in the PROTECTION AMI (http://clinicaltrials.gov, NCT00785954) trial. The rationale, design, and main results have been published previously.9, 10 Briefly, PROTECTION AMI was a prospective, international, multicenter, phase II, randomized placebo-controlled trial that included individuals with suspected STEMI presenting within 6 hours of pain onset in 114 hospitals in 18 different countries between December 2008 and June 2010.

Baseline characteristics

In the PROTECTION AMI trial, 1,176 patients were included; and the present analyses consisted of 1,066 individuals all receiving primary PCI within 6 hours. The most common reasons for exclusion were no significant atherosclerotic stenosis (49 patients), anatomy unsuitable for revascularization (18 patients), or referral for coronary bypass surgery (11 patients). Median age was 61 years, and approximately 80% were males. Median time from symptom onset to PCI was 190 (143-265) minutes (Table I).

Discussion

In the present study, we evaluated the relation of cTnI to clinical outcomes and cardiac function in a large, well-described population of STEMI patients followed up for 3 months after primary PCI. The main findings were strong associations of single-point, peak, and cumulative cTnI with clinical events, NT-proBNP, and LVEF after MI. When added to clinical risk factors in multivariable regression models, cTnI significantly improved model discrimination for prediction of these end points. Thus,

Conclusions

Cardiac troponin I measured after primary PCI for STEMI is associated with clinical outcomes and cardiac function through 3-month follow-up. These results suggest that cTnI may be a useful risk stratification tool in STEMI patients.

Conflict of interest disclosures

Dr Hallén is an employee of Pronova BioPharma, Norway, with the company not being involved in this study. Dr Krucoff has received research funding from Abbott Vascular Business and has consulted for or received honoraria from Abbott Vascular Business, Angel Medical Systems, Cappella, Ischemix, KAI Pharmaceuticals, Medtronic, Merck, OrbusNeich, Svelte Medical, St Jude Medical, and Terumo. Dr Roe has received research funding from Eli Lilly, Sanofi-Aventis, Daiichi-Sanko, American College of

Acknowledgements

We thank all investigators and staff involved in the PROTECTION AMI trial. We also thank the statistical department at Cleveland Clinic Coordinating Center for Clinical Research for their assistance throughout the study and Øystein H. Horgmo at the University of Oslo for graphic processing of figures.

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    Deepak L. Bhatt, MD, MPH, served as guest editor for this article.

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