BACKGROUND: Troponin elevation can be caused by etiologies other than acute coronary syndromes (ACS). Our hypothesis was that elevated troponins occur more frequently in non-ACS cases but that ACS cases (type 1 ST-elevation myocardial infarction [STEMI] and type 1 non-STEMI [NSTEMI]) have significantly higher troponin elevations. METHODS: This was a cross-sectional cohort analysis of a random subset of all patients with elevated troponins (defined as ≥0.06 ng/mL) over a 1-year period from July 2013 to June 2014. The first positive troponin I and the peak were used in this study. All included patients had medical record reviews looking for whether our cardiologists or hospitalists attributed the elevated troponin to an ACS (NSTEMI or STEMI) or non-ACS cause. Non-ACS causes were categorized as infection, cancer, renal diseases, cardiovascular disease, pulmonary disease, trauma, cardiac arrest, neurologic disease, hypertension, or other. Data were extracted by 2 investigators on the cause of the elevated troponin. Three sessions to educate data extractors were arranged and methods of data extraction discussed, then a 5% sample was reevaluated by the other extractor to determine interrater agreement measures. Parametric data were evaluated with t test and analysis of variance. Dichotomous variables were compared using χ(2) test. Troponin data were evaluated using nonparametric Kruskal-Wallis or Mann-Whitney U. A logistic regression model was created with variables selected a priori to evaluate the predictive ability of these variables in differentiating ACS vs non-ACS causes of elevated troponin. RESULTS: We evaluated 458 randomly selected patients from 1317 unique cases of all patients with initial elevated troponins at least 0.06 mg/mL during the study period. There was 84% interrater agreement in the 5% sampling. Seventy-nine percent had a non-ACS cause of elevated troponin, and the average initial positive troponin I level was significantly lower in the non-ACS cases (0.14; 95% confidence interval [CI], 0.08-0.37) than those with documented STEMI (10.2; 95% CI, 0.75-20.1) or NSTEMIs (0.4; 95% CI, 0.13-1.7). In the non-ACS group, the median initial troponin was 0.14 ng/mL (0.08-0.37 ng/mL). Peak troponin levels were highest in STEMI, next NSTEMI, and lowest in non ACS causes. The most frequent subgroups in the non-ACS group were non-ACS cardiovascular, infectious, renal, or hypertensive causes. In a linear regression model adjusting for age and sex, higher troponin levels had higher odds of being related to ACS causes (adjusted odds ratio, 1.4; 95% CI, 1.2-1.6) than non-ACS causes. CONCLUSION: The etiology for most initial elevated troponin I levels in a randomly selected population is the result of non-ACS causes. As initial + troponin levels increased, they were more likely associated with ACS causes than with non-ACS causes. Average initial + and peak troponin values were highest in STEMIs, next highest in NSTEMIs, and lowest overall in non-ACS causes.
BACKGROUND: Troponin elevation can be caused by etiologies other than acute coronary syndromes (ACS). Our hypothesis was that elevated troponins occur more frequently in non-ACS cases but that ACS cases (type 1 ST-elevation myocardial infarction [STEMI] and type 1 non-STEMI [NSTEMI]) have significantly higher troponin elevations. METHODS: This was a cross-sectional cohort analysis of a random subset of all patients with elevated troponins (defined as ≥0.06 ng/mL) over a 1-year period from July 2013 to June 2014. The first positive troponin I and the peak were used in this study. All included patients had medical record reviews looking for whether our cardiologists or hospitalists attributed the elevated troponin to an ACS (NSTEMI or STEMI) or non-ACS cause. Non-ACS causes were categorized as infection, cancer, renal diseases, cardiovascular disease, pulmonary disease, trauma, cardiac arrest, neurologic disease, hypertension, or other. Data were extracted by 2 investigators on the cause of the elevated troponin. Three sessions to educate data extractors were arranged and methods of data extraction discussed, then a 5% sample was reevaluated by the other extractor to determine interrater agreement measures. Parametric data were evaluated with t test and analysis of variance. Dichotomous variables were compared using χ(2) test. Troponin data were evaluated using nonparametric Kruskal-Wallis or Mann-Whitney U. A logistic regression model was created with variables selected a priori to evaluate the predictive ability of these variables in differentiating ACS vs non-ACS causes of elevated troponin. RESULTS: We evaluated 458 randomly selected patients from 1317 unique cases of all patients with initial elevated troponins at least 0.06 mg/mL during the study period. There was 84% interrater agreement in the 5% sampling. Seventy-nine percent had a non-ACS cause of elevated troponin, and the average initial positive troponin I level was significantly lower in the non-ACS cases (0.14; 95% confidence interval [CI], 0.08-0.37) than those with documented STEMI (10.2; 95% CI, 0.75-20.1) or NSTEMIs (0.4; 95% CI, 0.13-1.7). In the non-ACS group, the median initial troponin was 0.14 ng/mL (0.08-0.37 ng/mL). Peak troponin levels were highest in STEMI, next NSTEMI, and lowest in non ACS causes. The most frequent subgroups in the non-ACS group were non-ACS cardiovascular, infectious, renal, or hypertensive causes. In a linear regression model adjusting for age and sex, higher troponin levels had higher odds of being related to ACS causes (adjusted odds ratio, 1.4; 95% CI, 1.2-1.6) than non-ACS causes. CONCLUSION: The etiology for most initial elevated troponin I levels in a randomly selected population is the result of non-ACS causes. As initial + troponin levels increased, they were more likely associated with ACS causes than with non-ACS causes. Average initial + and peak troponin values were highest in STEMIs, next highest in NSTEMIs, and lowest overall in non-ACS causes.
Authors: Alexander A Fokin; Joanna Wycech Knight; Kai Yoshinaga; Ayesha T Abid; Robert Grady; Amaris L Alayon; Ivan Puente Journal: Cureus Date: 2022-03-04