Low Risk Chest Pain- Accelerated Rule-out

Do you hate chest pain, or is it easy if you have a chest and you have pain you get admitted. Or if you are ultra-low risk (usually 0 risk) you just send them home, no testing. But what about people with a decent story? Is it safe to send someone home, or do these people need further testing as recommended by the AHA (stress within 72 hours?) 

Chest pain represents about 10% of ED visits and a diagnostic strategy to safely identify and discharge low risk patients in a rapid fashion has been debated. A quarter of all hospital admissions are secondary to chest pain, and about 85% do not leave the hospital with a diagnosis of acute coronary syndrome.

Today’s mini JC focuses on the safety of a rapid identification of the “low risk” patient who can be safely discharged from the hospital with a 2 hour-accelerated diagnostic protocol.

1.  Why is this topic important?

Rapid evaluation and discharge of low risk chest pain may substantially reduce both outpatient and inpatient LOS, cost to the patient and health care system, and reduce physician liability. A rapid diagnostic protocol that can discharge patients within two hours of being evaluated represents a superior alternative to admission for serial enzymes, and possible a stress test (which more and more seems to be of limited utility.)

2.  What does this study attempt to show?

The study attempts to demonstrate that in patients whom are low risk defined as two negative troponins, 2 hours apart, a TIMI risk score of 0 (see below) and no new EKG changes (see manuscript, but a LBBB if it was old did not preclude them from enrollment in the study) can be safely discharged home with a 30 day event rate < 1%.  Major adverse cardiac events (MACE) were identified as: death, cardiac arrest, emergent revascularization procedure, high degree AV block, and acute MI. AMI is defined as having ischemic symptoms + a rising biomarker (troponin). In this protocol no physician judgment including (patients whom the provider deemed to be low risk) was included to provide more generalizable results.  It is important to note this a prospective observational study, not an intervention study.

 3.  What are the essential findings?

1,975 patients were prospectively enrolled, and ultimately 302 patients (15.3%) developed MACE within 30 days. The accelerated diagnostic protocol (ADP) classified 392 patients (20%) as low risk. One lone patient who was ADP negative developed MACE at 30 days giving the ADP a sensitivity of 99.7%, (95% CI 98.1%-99.9%), and a specificity of 23.4% (95% CI 21.4% to 35.4%).  The lone patient that was missed by the ADP was previously healthy with no risk factors, a normal EKG, and first trop of <0.01, and 2nd of 0.03, with the 3rd troponin being 16.8. Angiography showed right coronary artery and circumflex artery stenosis and he had stenting in both vessels. No cardiac problems at one year follow-up.

In addition, the supplemental data from table’s 2A/B suggests that 75% of ADP negative patients underwent further diagnostic evaluation with stress testing.  7 ultimately had “non-emergent cardiac catheterization with revascularization.” Many patients were exposed to potentially dangerous anti-coagulants. 

Table 2a Use of further investigations in ADP negative patients within 30 days


Median # of days post presentation



CT Coronary Angiogram




Stress Radionuclide




Stress Echo




Stress ECG









Table 2b Acute treatments on ADP negative patients within 30 days

In-patient Therapy 




LMW Heparin


G2b3a inhibitor


Heparin + G2b3a inhibitor


LMW Heparin + G2b3a inhibitor


Non-emergency Revascularization


ADP = Accelerated Diagnostic Protocol, LMW = Low Molecular Weight.


4.  How is patient care impacted?

Although this study is not an intervention study, it is strong food for thought. Using a TIMI risk score of 0, no new EKG changes, and 2 negative troponins, (<99%ile for your lab) 2 hours apart suggest these patients are low risk for MACE at 30 days. This study suggests that about 1/5th of our chest pain patients, who make up approximately 10,000 patients visits a year, can be safely discharged within a few hours of their initial ED evaluation. That’s 2,000 patients annually that could avoid admission and further diagnostic testing as an inpatient.

5.  Is this an area of controversy?

Of course. The study is prospective observational, and 75% of ADP negative patients ultimately had further diagnostic testing. In order for us to believe that an accelerated diagnostic protocol is useful the protocol needs to be used on patients in a prospective fashion (patients actually getting assigned the ADP vs. traditional care), and followed for 30-day outcomes.

Others may state that although only one lone patient in the ADP negative group developed MACE at 30 days, many more ADP negative patients received further diagnostic testing (CTCA, stress echo/EKG/radio nucleotide, and angiography with 7 patients ultimately getting non-emergent revascularization.) 

What do I think about this? Well if you were to take a cohort of patients walking around who developed chest pain > 50, many may have coronary artery disease, and if cathed may have a >70% lesion. However, what we have learned from prior mini JC’s is that stable coronary artery disease can be managed medically with equivalent if not superior results to invasively. Therefore, the benefit of an invasive strategy in these patients with NO EKG changes, negative biomarkers and perhaps a positive stress test must be questioned.

6.  Major Limitations of the study?

As stated previously this is a prospective observational study, not an intervention study, although not a limitation of the study itself, it may limit the applicability to your daily practice. However, other studies have suggested similar results including 30 day outcomes in “low risk patients” when evaluating CCTA. Therefore if you have a low risk patient by history, EKG, and a delta troponin at 2 hours it is reasonable to discharge those patients home with follow-up with their primary medical doctor.

The argument against this strategy is that you are missing the “unstable angina people”.  One important factor to remember is that likely the old “unstable angina patient” who came in 20 years ago before ultrasensitive troponins likely was having some trop leak as they exerted themselves with a partially occluded coronary artery. Those patients are likely called NSTEMI nowadays. In addition, plaques that are about 70-80% lesions are much less likely to rupture than are plaques that are say 20,30,40% as these plaques are much more unstable. These type of lesions will not be picked up by a stress test, and wouldn’t get a stent if they were cathed, and maximal medical therapy would be undertaken. Therefore the utility of identifying a plaque that may rupture is inherently flawed.

I reference you to an alternative approach, used at the mayo clinic, for placing the power of decision making back into the patients hands.  

I know two articles in one mini JC, but try using it next time you have a patient with chest pain, and let me know how it works for you! Essentially it is a protocol that after initial evaluation patients are given a pamphlet with 4 options to help them decide what they ultimately want to do. See chest pain decision aid I attached for you. 

Hess E et al. The chest pain choice Decision Aid. Circ Cardiovasc Qual Outcomes. 2012;5:251-259.

Ultimately I think an ADP is useful, and that patients who meet the aforementioned ADP negative criteria can be safely discharged home, and that further diagnostic testing is not warranted from the emergency department. I would recommend having that discussion using the decision aid with your patients so that they can be part of the medical decision making process. 

Until next time!




2-Hour accelerated diagnostic protocol to assess patients with chest pain symptoms using contemporary troponins as the only biomarker: the ADAPT trial. Than M, Cullen L, Aldous S, Parsonage WA, Reid CM, Greenslade J, Flaws D, Hammett CJ, Beam DM, Ardagh MW, Troughton R, Brown AF, George P, Florkowski CM, Kline JA, Peacock WF, Maisel AS, Lim SH, Lamanna A, Richards AM. J Am Coll Cardiol. 2012 Jun 5;59(23):2091-8