VCU EM Journal Club – Chest pain in the ED
Capital Ale House – 6pm - Wednesday August 20th 2014
Articles:
Keller et al Serial High Sensitivity Trop for MI JAMA 2011
Kontos et al MPI Sensitivity for MI Nuc Card 2004
Udelson et al MPI Eval Triage ACS 2002 JAMA
PICOT Sheet:
VCU Emergency Medicine Journal Club – PICOT sheet – Fill one out for each article!
Questions:
Keller et al - Serial Changes in Highly Sensitive Troponin I Assay and Early
Diagnosis of Myocardial Infarction - JAMA Dec. 2011
1. How was the 99th percentile cutoff value determined? How might this cutoff value
change based on demographic and geographic factors? Do you think it would be
applicable to the population we treat at VCU? How do the authors address this in the
study?
2. What percentage of enrolled patients had non-detectable troponin values on
admission? What was the sensitivity and NPV as reported by the authors? What was
the specificity? How does increasing the cutoff threshold to 99% percentile affect
the sensitivity and specificity?
3. Using the hsTnI assay there are detectable levels of troponin in up to 90% of the
general “healthy” population and there is discussion that these values can be used to
prognosticate future risk of cardiac events and other diseases. What are the
implications of this as it pertains to
a. Overall cost benefit analysis of switching to high sensitivity assays
b. Medicolegal implications in the ED
4. The authors imply that a minority of patients can be rule out immediately at the
time of presentation with a single highly sensitive troponin. In practice, do you
agree with this? What else would you want to know about the patient?
5. What do the authors say are limitations to the study? What other limitations can you
think of?
Kontos et al - Sensitivity of acute rest myocardial perfusion imaging for identifying
patients with myocardial infarction based on a troponin definition - J Nuc Card 2004
1.
What is the relationship between sensitivity, specificity, PPV, and NPV? What
do you think of the sensitivity of MPI for MI? The NPV?
2.
MPI has a relatively poor sensitivity for MI by elevation of troponin. Were
there clinically significant outcomes for patients with elevated troponin but
negative MPI?
3.
What are the limitations of the study? How might have MPI results influenced
the outcomes and work ups the patients had? What was the timing of the
positive troponins?
4.
How should we interpret a negative resting MPI study in low and moderate
risk patients with chest pain?
5.
Though not explicitly reported by the authors, MPI had a very low specificity
and PPV. How does it compare to the PPV and specificity reported for cTi in
this paper?
6.
What can we infer about utility of CK MB? Were there patient oriented
specific outcomes that were missed by CK MB but found by troponin?
7.
What percentage of patients with positive troponin but negative MPI were
judged to have a true MI? What other causes were found for troponinemia?
8.
Do you agree with the authors’ conclusion that MPI has a high sensitivity for
predicting troponin elevation?
Udelson et al, Myocardial Perfusion Imaging for Evaluation and Triage of Patients
With Suspected Acute Cardiac Ischemia – JAMA Dec 2002
1. In this paper, the two comparison groups used to evaluate ED triage decisions
regarding chest pain in low risk individuals were the usual care strategy and the
usual care plus the perfusion scan. The authors do not go into great detail about the
“usual care strategy” and note that the standard of care may be different at differing
hospitals. Is there a better way to account for these differences in standard of care?
2. The author’s looked at the “appropriateness of the ED triage decision” as their main
outcome. Is this patient centered? Is there another outcome they could have used?
3. Which group (standard treatment or perfusion) had better ED triage decision
making in patients with acute cardiac ischemia? Which group had better decision
making in those without acute cardiac ischemia?
4. What was difference in outcome of the standard care group versus the perfusion
scan group at 30 days? What does this mean in terms of the decision to discharge
more patients from the ED with the use of the perfusion scan?
5. The authors state that there was no final decision tree made for any of the ED
providers and that the decision to admit or discharge was made based on the
provider’s clinical judgment given all of the data. The group with the perfusion scan
just had another piece of data. Given the negative predictive value of the perfusion
scan as we have discussed with the previous papers, would a negative scan change
your disposition in a low risk patient with chest pain?