OBJECTIVES: Guidelines recommend a 0-hour/1-hour high-sensitivity cardiac troponin T (hs-cTnT) diagnostic strategy in acute chest pain patients. There are, however, little data on the performance of this strategy when combined with clinical risk stratification. We aimed to evaluate the diagnostic accuracy of an accelerated diagnostic protocol (ADP) using the 0-hour/1-hour hs-cTnT strategy together with an adapted Thrombolysis In Myocardial Infarction (TIMI) score and electrocardiogram (ECG) for ruling out major adverse cardiac events (MACE) within 30 days.
METHODS: This prospective observational study enrolled consecutive emergency department (ED) chest pain patients. TIMI score variables, ED physicians' assessments of the ECG, and 0- and 1-hour hs-cTnT were collected. Thirty-day MACE was defined as acute myocardial infarction (AMI), unstable angina (UA), cardiogenic shock, ventricular arrhythmia, atrioventricular block, cardiac arrest, or death of cardiac or unknown cause.
RESULTS: A total of 1,020 patients were included in the final analysis. The combination of an adapted TIMI score =1, a nonischemic ECG, and either a 0-hour hs-cTnT < 5 ng/L or a 0-hour hs-cTnT < 12 ng/L combined with a 1-hour increase < 3 ng/L identified 432 (42.4%) patients as very low risk with a negative predictive value of 99.5% (95% confidence interval [CI] = 98.3%-99.9%) and a negative likelihood ratio of 0.04 (95% CI = 0.01-0.14) for 30-day MACE. The ADP missed only two patients with UA and no patients with AMI or other forms of MACE.
CONCLUSION: An ADP using the guideline recommended 0-hour/1-hour hs-cTnT strategy rapidly identified patients with a very low risk of 30-day MACE including UA where no further cardiac testing would be needed. This could potentially allow safe early discharge of about 40% of ED chest pain patients.
Interesting data from a small single-center observational study - needs to be replicated with a larger cohort of low-risk patients.
Not new with respect to news. I doubt it will be used by most given our legal environment and will take time before it becomes adopted.
This is a secondary analysis of a prospective cohort study and so really adds nothing to the multiple similar studies. We need RCTs to determine which, if any, of these protocols is as safe and more effective than current standard care.
A large number of observational studies (which are Tier 2 of diagnostic evidence hierarchy - see http://onlinelibrary.wiley.com/doi/10.1111/acem.12832/full) imply that high-sensitivity cardiac troponin (hsTrop) improves the diagnostic standard of care for ED chest pain risk stratification. The current observational study is a secondary analysis of prospective observational data, very much like several other recent hsTrop studies. However, observational studies of diagnostic evidence do not prove patient - or societal - level benefit. To advance our understanding of the benefits and harms of hsTrop, researchers now need to focus on diagnostic RCTs that highlight patient-oriented outcomes (http://pmid.us/28063913). One early RCT of hsTrop does not demonstrate such benefits (http://circoutcomes.ahajournals.org/content/9/5/542.long).
This article contributes to the growing body of literature utilizing advances in diagnostic testing to improve our ability to risk-stratify chest pain in the Emergency Room. Nearly half of their cohort were stratified as low risk, and MACE rates in this group were very low.
The word of caution necessary here is that this decision cannot be made based only on the troponin. It only works if you also use the clinical criteria. In practice, it appears to me that too many people fail to take an adequate history and, in many instances, dismiss the risk factors when the troponin comes back as negative.