Abstract
Introduction: Cardiac troponin I (TnI) is a sensitive and specific marker of acute myocardial infarction (AMI). However, a wide range of non-AMI conditions can also cause significant elevations in cardiac troponins. Given the deleterious impact of misdiagnosis, the ability to risk stratify patients who present with an elevated troponin is paramount. Hypothesis: We hypothesized that maximum TnI would be more predictive of mortality and the diagnosis of AMI than the initial or change in TnI. Methods: Records of 30,173 patients from a nine-hospital system in Texas were reviewed over a 24-month period 2016-2018. Data were collected on patients > 40 years of age and included international classification of disease (ICD-10) diagnoses, TnI, demographic data (age, sex, race, smoking status, chronic medical conditions), death during hospitalization, and readmission within 30 days. Results: Notable finding include TnI as a significant predictor of death with odds of death increased by 0.9% (1.009, 95% CI 1.004-1.013) for initial, and 0.7% (1.007, 95% CI 1.005-1.009) for delta and maximum TnI. An ROC curve demonstrated a statistically significant predictive ability of death for the maximum TnI level (0.6782, 95% CI (0.6576, 0.6989)) when compared to the initial and change in TnI. We analyzed the initial TnI as a significant predictor of AMI demonstrating the odds of AMI increased by 7.4% as initial TnI values increased (1.074, 95% CI 1.063-1.085), and 3.1% for delta and maximum TnI (1.031, 95% CI 1.028-1.034). A separate ROC curve demonstrated that the maximum TnI level 0.9401, 95% CI (0.9353, 0.9449) showed a statistically significant predictive ability to predict an AMI compared to initial change in TnI. Conclusions: Regardless of TnI level, a detectable TnI results in an increased risk of in-hospital mortality. Our study demonstrates that the maximum TnI level is a more sensitive and specific predictor of mortality when compared to delta or initial TnI. Similarly, the maximum TnI is the most predictive of an AMI versus other causes of TnI elevation. Further studies are needed to correlate TnI levels and clinical manifestations, which may be helpful in redefining AMI to better distinguish AMI from non-AMI diagnoses.
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