Abstract
Background: Cardiac troponins I and T are highly sensitive and specific markers for 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 of AMI, the ability to risk-stratify patients who present with an elevated troponin is paramount. We hypothesized that the maximum troponin level would be more predictive of mortality and the diagnosis of AMI than the initial troponin level or change in troponin level.Methods: Patient records from a 9-hospital system (n=30,173) in Texas were reviewed during a 24-month period in 2016-2017. Data collected for patients aged ≥40 years included International Classification of Diseases, Tenth Revision diagnoses, troponin I, demographic data (age, sex, smoking history, and chronic medical conditions), and death during hospitalization. We used logistic regression with the Firth penalized likelihood approach to determine the predictive ability of initial, maximum, and change in troponin level for mortality and the diagnosis of AMI.Results: Demographic characteristics of our cohort included a median age of 70 years, with 48.05% male and 51.95% female. The most common preexisting risk factor was hypertension in 78.81% of the cohort. Notable findings from the logistic regression include the predictive ability of maximum troponin on the odds of death by 0.7% for each unit of increase in troponin value. Also, the odds of AMI increased by 3.1% for each unit of increase in the maximum troponin value.Conclusion: Regardless of the level, a detectable amount of troponin in the serum results in a significantly elevated risk of mortality. Many patients with elevated troponin levels leave the hospital without a specific diagnosis, which can lead to poor outcomes because a detectable troponin does not represent a no-risk population. Our study demonstrates that maximum troponin level is a more sensitive and specific predictor of mortality than initial or change in troponin. Similarly, maximum troponin is the most predictive of AMI vs other causes of troponin elevation, likely because of the correlation between rising troponin levels and cardiomyocyte damage. Further studies are needed to correlate maximum troponin levels and clinical manifestations, which may be helpful in redefining AMI so that AMI can be distinguished more easily from non-AMI diagnoses.
Highlights
Studies have suggested that an increase of 20% for conventional or 30% for sensitive cardiac troponin assays should be added to the Fourth Universal Definition of Myocardial Infarction criteria because these increases separate an acute elevation from background elevations, thereby allowing for further discrimination between acute and chronic causes of troponin elevation.[7,8]
We attempted to determine if the initial troponin, change in troponin, or maximum troponin level is diagnostic of acute myocardial infarction (AMI) and mortality
A receiver operating characteristic (ROC) curve demonstrated that the area under the curve (AUC) for maximum troponin level is 0.6782, which represented a statistically significant ability to predict death when compared to the AUC for the initial 0.6547 and the AUC for the change in troponin 0.6113 levels (Table 3, Figure 1)
Summary
Cardiac troponins I and T are highly sensitive and specific markers for acute myocardial infarction (AMI). We hypothesized that the maximum troponin level would be more predictive of mortality and the diagnosis of AMI than the initial troponin level or change in troponin level. We used logistic regression with the Firth penalized likelihood approach to determine the predictive ability of initial, maximum, and change in troponin level for mortality and the diagnosis of AMI. Notable findings from the logistic regression include the predictive ability of maximum troponin on the odds of death by 0.7% for each unit of increase in troponin value. Many patients with elevated troponin levels leave the hospital without a specific diagnosis, which can lead to poor outcomes because a detectable troponin does not represent a no-risk population. Our study demonstrates that maximum troponin level is a more sensitive and specific predictor of mortality than initial or change in troponin. Further studies are needed to correlate maximum troponin levels and clinical manifestations, which may be helpful in redefining AMI so that AMI can be distinguished more from non-AMI diagnoses
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