Which chest pain patients can be discharged?

Ryan Radecki from EM Lit of Note is here to deconstruct the HEART score, utility of stress tests in low risk patients, and his approach to low risk chest pain. As a bonus, Ryan is also the wordsmith for the show notes.


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Important stuff mentioned on this show

The Show notes…

There is no such thing as “zero-risk” chest pain:

Once you learn to stop worrying and love again, where are we going with “low-risk” chest pain?

Simply put, most of our observation chest pain evaluations represent low-value care:

  • In a study comparing CCTA and rapid stress-testing for rule-out of “low-risk” patients, only a handful had positive results.
  • In a study reviewing two years of chest pain rule-outs, again, just 1.7% of stress tests performed were positive, and 1/3rd of those were false positives. No “low-risk” patients had a positive stress.
  • A study reviewing stress test outcomes in an intermediate risk cohort (mean age 60) resulted in ~25% positive of indeterminate results, with a third of those referred for angiography – half of which received an intervention.At the micro level, why should we care? Patients make their free choice to come for comprehensive evaluation.However, on a macro level, it’s unsustainable. And, as more and more patients are shifted to HMO and ACO care and payment models – the Kaisers, Geisengers, Intermountains, Partners of the world – there will be, essentially, mandates to reduce such low-value care.So, how do we do this safely?Step 1: Highly-sensitive troponin assays.
    The evidence, of which there is ample, is of reasonable quality. Much of it, unfortunately, is sponsored by the manufactures of the assays involved, which degrades some confidence in the results. But, there are a few main summary points:
  • Sensitivity for nSTEMI is about 90% at ED presentation.
  • Specificity of any troponin elevation, however, is 50-60%.
  • The longer the time from onset of symptoms, the more reliable the sensitivity.
  • Repeating a troponin 1- or 2-hours after presentation, particularly for thosepresenting early in symptoms, will increase sensitivity for late rise – and likewise improve specificity by ruling out AMI for patients’ whose troponins do not increase.

Step 2: Shared decision-making.
After making a diagnosis regarding acute MI in the Emergency Department – or, at least, to the extent hs-Troponin permits such an answer – outcome prognostication begins.

Most folks are familiar with TIMI for risk-stratification, despite not being derived in the Emergency Department. While it is still a reasonable to assess overall risk with TIMI, most folks are moving to the HEART score, while a few other protocols/algorihtms – EDACS, MACS, Vancouver, modified Goldman – are also vying for use.

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There’s a lovely synergy between identifying a patient as “low risk” and the negative predictive value of negative troponin testing in the Emergency Department. Patients discharged with negative – particularly undetectable troponins – will have event rates at a fraction of a percent, and even lower if only AMI or cardiac-death are included. This is why HEART is described, primarily, as a single-troponin strategy.

These are the sorts of numbers to present to patients in the context of shared decision-making as part of changing the routine conversation about admission into one about discharge. Returning autonomy to the patient to make an informed choice about further care – and documenting such – allows the patient to assume the risks of their self-determination. Adding mention of the frequency of false- positives in a low-risk population – roughly as frequent as the true positives – is also valuable.

There are still quirks with HEART – mostly that patients, in theory, can have ischemic EKGs or elevated troponins and still remain “low risk”. These instances ought to be extremely rare in practice – and clinicians will have to make prudent individualized decisions given the clinical context. The fantastic Stephen Smith, of Hennepin County, also frequently reminds me true unstable angina is still an important troponin-negative. These are near-critical occlusions of the coronary circulation, and the key to diagnosis – and missed diagnosis – is correctly interpreting the EKG and performing serial EKGs in the Emergency Department.

Lastly, it is important to note the AHA Guidelines, as well as prudent longitudinal medical care, recommend patients still have follow-up for additional diagnostics or management, as indicated. Patients at low-risk and with negative biomarkers are at profoundly low-risk for events in, at least, the very short term. Of 11,230 patients observed and with negative biomarkers in Ohio community hospitals, only 20 had a potentially preventable poor outcome related to hospitalization. Narrowed down to the 7,266 patients with entirely normal EKGs and vital signs, 4 had poor outcomes – 2 of which were noncardiac, and 2 of which were iatrogenic. Patients, particularly low-risk, are almost certainly safer outside the hospital than in!

Stress Test Utility Citations:
“Safety of a rapid diagnostic protocol with accelerated stress testing” 

“The Association Between Pretest Probability of Coronary Artery Disease and Stress Test Utilization and Outcomes in a Chest Pain Observation Unit” 

“The incremental value of stress testing in patients with acute chest pain beyond serial cardiac troponin testing

hs-Troponin Citations:
“Multicenter Evaluation of a 0-Hour/1-Hour Algorithm in the Diagnosis of Myocardial Infarction With High-Sensitivity Cardiac Troponin T”

“High-sensitivity cardiac troponin I at presentation in patients with suspected acute coronary syndrome: a cohort study”

“Implications of Introducing High-Sensitivity Cardiac Troponin T Into Clinical Practice

“Prospective validation of a 1-hour algorithm to rule-out and rule-in acute myocardial infarction using a high-sensitivity cardiac troponin T assay

“Does undetectable troponin I at presentation using a contemporary sensitive assay rule out myocardial infarction? A cohort study”

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