In this issue, there are two opposing perspectives about testing patients at low risk for acute coronary syndromes (LRACS) in the emergency department (ED). The disagreement between the perspectives is not philosophical; rather, it is a dispute about numbers. The number at the crux of the dispute is as follows: What is the rate of events, that is, the rate of death and myocardial infarction (MI), within 30 days in patients presenting with symptoms suspicious of acute coronary syndrome who are at LRACS and who have negative serial troponins and nonischemic electrocardiograms, when discharged from the ED without further testing? I will call this number the “event rate.” Foy and colleagues believe that the event rate is zero, or no more than the baseline population rate for cardiovascular events, because negative troponin rules out an acute MI. Chang, an emergency physician, disagrees . She quotes event rates around 2%. Who is right? Why do the two sides disagree?
Purpose of Noninvasive Testing in LRACS
Noninvasive testing, such as cardiac computed tomography (CT) or myocardial perfusion imaging, in the ED is done not to diagnose MI but to determine who does not have obstructive coronary artery disease (CAD) which could be responsible for their symptoms. When the cardiac CT is negative, meaning that there is no plaque which causes hemodynamically significant stenosis, typically defined as 50% stenosis in the artery, the patient’s symptoms are deemed not to be from CAD, meaning the patient can safely be discharged .
When the test, anatomical or functional, finds CAD, there are three possibilities. The first is that the finding is incidental, and unrelated to the patient’s symptoms. The second is that the patient has symptoms of stable angina (SA). SA can be managed with either optimal medical therapy (OMT) or percutaneous coronary intervention. Importantly, the treatment need not be commenced urgently. The third possibility is that the patient has unstable angina (UA), and may need a coronary angiogram with a view to intervention. UA is different from SA because, untreated, UA progresses rapidly to MI. In UA, symptoms signal plaque’s instability and vulnerability and herald coronary thrombosis which may cause a fatal MI. In SA, symptoms signal myocardial ischemia. Although prognostically SA and UA are very different, clinically they can be very similar and, as Foy and colleagues reason, may be the same entity .
Does UA Exist?
As Foy and colleagues point out , many cases thought to be UA were reclassified as MI. The reason for the reclassification is that the biomarkers for myocardial injury, notably troponins, are more sensitive for myocardial injury than their predecessors such as Creatine Kinase-MB. In the past, many patients labeled with UA really had biomarker-occult MI. In other words, according to Foy and colleagues , no case of CAD flagged by noninvasive testing and confirmed at catheter angiography, not accompanied by a rise in troponins, is UA. How will we know this assertion is true?
To prove that acute coronary syndrome (ACS) can be excluded with a negative troponin, we must follow many patients with symptoms suspicious for ACS but who are at LRACS and who have a negative troponin, to see if they develop events within 30 days. The time frame for the follow-up is important. If followed for too long, such as 1 year, an event may speak of the baseline event rate for SA, rather than a consequence of untreated UA.
Should Revascularization be an Outcome?
The event rate is not easy to resolve with the present data. This is because in the studies quoted by Chang, while death and myocardial infarction have reasonably been included as events, so has revascularization . Revascularization is not an outcome but it prevents outcomes in UA. Including revascularization as an outcome overestimates the event rate, and excluding it underestimates the event rate, because revascularization reduces MI and death in UA. In other words, to prove whether UA is a true entity, we have to decide whether to use its treatment as a measure, but the treatment assumes that UA is a true entity—this is a catch-22 situation. However, as previously mentioned, a patient at LRACS with CAD may have SA, for which revascularization does not have the same treatment effect as for unstable angina.
Price of Achieving Zero Missed ACS
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Troponins: Trade-off between Sensitivity and Overdiagnosis
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Resolving the Event Rate
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Management of False Positives
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Conclusion
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References
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2. Chang A.M.: Low risk acute coronary syndrome—how high is low?. Acad Radiol 2016;
3. Litt H.I., Gatsonis C., Snyder B., et. al.: CT angiography for safe discharge of patients with possible acute coronary syndromes. N Engl J Med 2012; 366: pp. e1403.
4. Pope J.H., Aufderheide T.P., Ruthazer R., et. al.: Missed diagnoses of acute cardiac ischemia in the emergency department. N Engl J Med 2000; 342: pp. 1163-1170.
5. Foy A.J., Liu G., Davidson W.R., et. al.: Comparative effectiveness of diagnostic testing strategies in emergency department patients with chest pain: an analysis of downstream testing, interventions, and outcomes. JAMA Intern Med 2015; 175: pp. 428-436.
6. Nørgaard B.L., Leipsic J., Gaur S., et. al.: Diagnostic performance of noninvasive fractional flow reserve derived from coronary computed tomography angiography in suspected coronary artery disease: the NXT trial. J Am Coll Cardiol 2014; 63: pp. 1145-1155.
7. Boden W.E., O’Rourke R.A., Teo K.K., et. al.: Optimal medical therapy with or without PCI for stable coronary disease. N Engl J Med 2007; 356: pp. 1503-1516.