Troponin elevations only detected with a high-sensitivity assay: clinical correlations and prognostic significance
Frederick K Korley1, Steven P Schulman, Lori J Sokoll
1The Department of Emergency Medicine, Baltimore, MD.
Insights
Elevated high-sensitivity troponin I (hsTnI) in patients without current troponin elevation indicates a higher risk for mortality and cardiac events. This finding is crucial for understanding the implications of hsTnI in acute coronary syndrome evaluations.
Area of Science:
- Cardiology
- Clinical Diagnostics
Background:
- The clinical utility of high-sensitivity troponin I (hsTnI) assays is increasing, leading to more frequent troponin elevations.
- The clinical significance and implications of these elevations, particularly when traditional assays do not detect them, remain incompletely understood.
Purpose of the Study:
- To quantify the prevalence of elevated hsTnI in patients presenting with possible acute coronary syndrome (ACS) but without elevated troponin on a current-generation assay (cardiac troponin I [cTnI]).
- To determine the association between these newly detected hsTnI elevations and a composite outcome of all-cause mortality and subsequent cardiac hospitalization.
Main Methods:
- A prospective observational study involving 808 patients evaluated for possible ACS, with follow-up for up to 1 year.
- Troponin levels were measured using both hsTnI and cTnI assays.
- Cardiac hospitalization was defined as admission for ACS, revascularization, acute heart failure, or tachy/bradyarrhythmia.
Main Results:
- Approximately 9-11% of subjects without cTnI elevation showed elevated hsTnI on initial sampling.
- Among those with elevated hsTnI but not cTnI, diagnoses included ACS (4.6%), acute heart failure (23.1%), and other cardiac or non-cardiac conditions.
- Elevated initial hsTnI (with nonelevated cTnI) was associated with a nearly twofold increased risk of all-cause mortality and subsequent cardiac hospitalization (HR = 1.91).
Conclusions:
- A significant proportion of patients evaluated for ACS exhibit hsTnI elevations even when cTnI levels are not elevated.
- These hsTnI elevations, though often not indicative of ACS, identify a patient group at higher risk for adverse outcomes, including mortality and cardiac hospitalizations.
Objectives:
With clinical use of high-sensitivity troponin I (hsTnI), more frequent troponin elevations will occur. However, the burden and implications of these elevations are not well understood. The authors quantified the prevalence of elevated hsTnI in patients presenting with possible acute coronary syndrome (ACS) who do not have elevated troponin with a current generation assay (cardiac troponin I [cTnI]) and determined the association of these newly detected elevations with a composite of all-cause mortality and subsequent cardiac hospitalization.
Methods:
This was a prospective observational study of 808 subjects evaluated for possible ACS and followed for up to 1 year. Troponin values were measured with hsTnI (Abbott Laboratories) and cTnI (Abbott and Beckman Coulter). Cardiac hospitalization was defined as hospitalization for ACS, revascularization, acute heart failure (AHF), or tachy/brady arrhythmia that occurred after the index emergency department (ED) visit or hospital discharge.
Results:
Forty subjects (5%) were diagnosed with ACS (26 myocardial infarction and 14 unstable angina). On the initial sample, the prevalence of elevated hsTnI among subjects with nonelevated cTnI was 9.2% using a gender-neutral cutoff (95% confidence interval [CI] = 7.1% to 11.4%) and 11.1% using a gender-specific cutoff (95% CI = 8.8% to 13.4%). Adjudicated diagnoses for subjects whose initial samples had elevated hsTnI but nonelevated cTnI (gender-neutral cutoff) were as follows: three (4.6%) ACS, 15 (23.1%) AHF, three (4.6%) volume overload etiology unclear/noncardiac, three (4.6%) cardiac (non-ACS), and 41 (63.1%) other. Of the 65 patients whose initial samples had hsTnI but nonelevated cTnI, eight developed cTnI elevation on subsequent serial sampling. After traditional cardiovascular risk factors and renal function were adjusted for, subjects with elevated initial hsTnI but nonelevated cTnI (initial and serial sampling) had a higher risk of all-cause mortality and subsequent cardiac hospitalization than subjects with both nonelevated hsTnI and nonelevated cTnI (hazard ratio [HR] = 1.91, 95% CI = 1.14 to 3.19).
Conclusions:
On the initial sample, 9% to 11% of subjects without cTnI elevation had hsTnI elevation. Although the majority of the patients with these newly detected hsTnI elevations did not have ACS, they had a higher risk for all-cause mortality and subsequent cardiac hospitalization.
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