There are only a few things I know about the world. Sunrise in the east, sunset in the west. Death and taxes. Black Friday at one time referred to a SINGLE day that came immediately after Thanksgiving.

TL:DR – HEART score and pathway are awesome. EDACS may be better. Also, reconsider whether inpatient/outpatient stress testing is good for anybody already risk stratified to less than 1% risk of MACE in 1-2months (sorry cardiology and echo techs). You (and I) probably need to use a clinical decision guide to better risk stratify our ED chest pain patients.

I’ve been known to talk about cocaine chest pain in the ED. Let’s spread our wings a bit and talk about risk stratifying all CP we suspect may be ACS.

For those of us who haven’t been practicing for 25 years, leaning on clinical decision guides can be helpful with disposition decisions. These ED chest pain guides are really an attempt to risk stratify the patient with suspected low risk chest pain and a negative initial troponin. Very few ED docs will discharge a patient with newly positive troponin. For these low risk patients: Is it safe to discharge them? Do they need admission? If so, what do we expect the inpatient team to do? Does admission “help”?

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Since I started training, there has been a rapid evolution in (but still not universal adoption of) how to workup these patients. As an intern, there really weren’t any ED derived/validated tools, and it was either use TIMI/GRACE ‘out of context’ in the ED (vs. inpatient), or good old fashioned clinical gestalt. Then Backus (2008), gave us the APGAR score for ED chest pain: History, ECG, Age, Risk Factors, Troponin – HEART score. Low score = Low risk.  For the Dutch (where it was derived), the risk (2.5% of MACE) was low enough to justify discharge.

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Barbra Backus validated it in 2010 and 2013, with slightly ‘better’ numbers. These made sense to everybody but Americans. We have ‘decided’ AMI is a 1% problem.

Simon Mahler studied the HEART pathway (HEART + 3hr troponin) in ‘Merica at an Academic ED. It has been validated several times, including by a team that included our own Dr. Maksimenko in Texas, and it does not get more American than Texas. Using the HEART pathway, ED docs safely
doubled the number of early discharges, and shortened overall length of stay.

captureI love the HEART Score and Pathway.  I think you should love it too. It’s not perfect but neither are you. In a clinical sense, I grew up with the HEART Score, and it helped me with my own risk tolerance. It is easily used to justify an admission to inpatient team using an ‘objective’ validated tool.

[start: movie announcer voice]But, in a world of scores, and 8-10 million ED Chest Pain visits a year in the US, a new challenger is rising up from the “land down under.” EDACS may give you a HEART attack.[/end]

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You may not have heard of EDACS, but you’ve probably seen it on the side of the MDCALC HEART score calculator. It’s not quite as ‘do it in your head’ as the HEART score. It has positive and negative points to calculate, but ‘eliminates’ the subjective History part of the ‘objective’ HEART score.

In EDACS, the Emergency Department Assessment of Chest Pain Score, there are negative points for pleuritic and reproducible pain. Score positive points for age, male sex, risk factors, and characteristics of the pain history. Calculate a low score below 16, in the setting of non-ischemic ECG, and negative troponin at 0 and 2 hours, and you can often classify 40-50% of the patients as low risk for MACE and can be discharged to close follow up with their PCP (not cards, not stress testing, lets revisit in a minute).

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EDACS, was created and validated in Australia and New Zealand, from 2014-2016, and this last year, Kaiser Permanente used their considerable access to Big Data, they compared the performance of the HEART and EDACS decision tools.

Both performed well in terms of correctly identifying patients with low likelihood of MACE in the short term (60d),  essentially not missing any bad outcomes. NPV all >99%.

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EDACS has the added benefit of identifying more patients as low risk (up to 66% in the Kaiser population).

Finally, the HEART pathway was often interpreted to include short-term cardiology follow up for provocative testing. Distinguish that from the EDACS protocol, which recommended PCP not cardiology follow-up.

This is key. There is some question as to the value of stress testing in this population. When the scores themselves get you to a risk of <1% MACE in 4-8 weeks, there can be little additional risk stratification by any test.  Also, stress testing was designed to identify patients with clinically important obstructions in the coronary arteries. We know that a plaque today may not be clinically obstructive, but when it becomes unstable, occlusive myocardial infarction could happen tomorrow.

So, the value in observation admissions for, or 72-hour appointments for, stress tests is likely a costly and unnecessary burden to the patient and the health care system.

Since EDACS shows that it is safe to forego this step in population that is larger than would be identified by HEART score/pathway, I suggest it may be the Clinical Decision Guide you ‘grow up with’.

Faculty Author: Steve McGuire, DO


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LONG, B AND KOYFMAN, A, HTTP://WWW.EMDOCS.NET/CHEST-PAIN-CONTROVERSIES-RISK-STRATIFICATION-STRESS-TEST-UTILITY-PART-1/ EMDOCS.NET – EMERGENCY MEDICINE EDUCATION, CHEST PAIN CONTROVERSIES: RISK STRATIFICATION AND STRESS TEST UTILITY (PART 1), PUBLISHED JANUARY 23, 2018, ACCESSED NOVEMBER 20, 2018