Comparison of QTc and Troponin Levels in ST Elevation MIs Compared with Non-ST Elevation MIs.

OBJECTIVES: ST elevation myocardial infarctions (STEMIs) and non-ST elevation myocardial infarctions (NSTEMIs) have differences that can be important to differentiate. Our primary hypothesis was that corrected QT (QTc) duration and troponin I levels were higher in STEMIs compared with NSTEMIs. The objective of our study was to compare STEMIs with NSTEMIs for QTc duration and troponin levels. METHODS: This was a retrospective case-control study of all STEMIs and a random sample of NSTEMIs during a 1-year period. STEMIs were retrieved by searching our electrocardiogram database for all of the cardiology-diagnosed STEMIs. NSTEMIs were found by selecting a randomized sample of all of the patients with a final discharge diagnosis of NSTEMI. Records and electrocardiograms were reviewed for initial troponin I levels and QTc duration. Data extractors were educated formally and a 5% sample was reevaluated by the other extractor as a reliability measure. Data analysis included χ2 tests and parametric or nonparametric analysis, where appropriate. A logistic regression model was created with variables selected a priori for predictors of STEMIs compared with NSTEMIs. RESULTS: A total of 92 STEMIs and 111 NSTEMIs were evaluated, and interrater reliability showed 90% agreement. Patients with NSTEMIs had significantly longer QTc. Troponin I did not differ on univariate analysis. In a logistic model, Hispanics were more likely than whites to have a STEMI (adjusted odds ratio [AOR] 2.2, 95% confidence interval [CI] 1.09-4.5). An increase in troponin I of 1 was associated with a 7% increase in the AOR of a STEMI (AOR 1.7, 95% CI 1.03-1.12) and an increase in QTc by 10 was associated with a 13% decrease in the AOR of a STEMI (AOR 0.87, 95% CI 0.78-0.93). CONCLUSIONS: Patients with NSTEMIs had longer QTc intervals and lower troponin I levels than those with STEMIs.

The meaning of elevated troponin I levels: not always acute coronary syndromes.

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.

Head CT Guidelines Following Concussion among the Youngest Trauma Patients: Can We Limit Radiation Exposure Following Traumatic Brain Injury?

INTRODUCTION: Recent studies have provided guidelines on the use of head computed tomography (CT) scans in pediatric trauma patients. The purpose of this study was to identify the prevalence of these guidelines among concussed pediatric patients. METHODS: A retrospective review was conducted of patients four years or younger with a concussion from blunt trauma. Demographics, head injury characteristics, clinical indicators for head CT scan (severe mechanism, physical exam findings of basilar skull fracture, non-frontal scalp hematoma, Glasgow Coma Scale score, loss of consciousness, neurologic deficit, altered mental status, vomiting, headache, amnesia, irritability, behavioral changes, seizures, lethargy), CT results, and hospital course were collected. RESULTS: One-hundred thirty-three patients (78.2%) received a head CT scan, 7 (5.3%) of which demonstrated fractures and/or bleeds. All patients with skull fractures and/or bleeds had at least one clinical indicator present on arrival. Clinical indicators that were observed more commonly in patients with positive CT findings than in those with negative CT findings included severe mechanism (100% vs. 54.8%, respectively, p = 0.020) and signs of a basilar skull fracture (28.6% vs. 0.8%, respectively, p = 0.007). Severe mechanism alone was found to be sensitive, but not specific, whereas signs of a basilar skull fracture, headache, behavioral changes, and vomiting were specific, but not sensitive. No neurosurgical procedures were necessary, and there were no deaths. CONCLUSION: Clinical indicators were present in patients with positive and negative CT findings. However, severe mechanism of injury and signs of basilar skull fracture were more common for patients with positive CT findings.