Rapid Rule Out for Patients with Chest Pain
Rapid Rule Out for Patients with Chest Pain
Abstract & Commentary
By Andrew J. Boyle, MBBS, PhD
Assistant Professor of Medicine, Interventional Cardiology, University of California, San Francisco
Dr. Boyle reports no financial relationships relevant to this field of study.
This article originally appeared in the August 2012 issue of Clinical Cardiology Alert. It was edited by Michael H. Crawford, MD, and peer reviewed by Ethan Weiss, MD. Dr. Crawford is Professor of Medicine, Chief of Clinical Cardiology, University of California, San Francisco, and Dr. Weiss is Assistant Professor of Medicine, Division of Cardiology and CVRI, University of California, San Francisco. Dr. Crawford reports no financial relationships relevant to this field of study, and Dr. Weiss is a scientific advisory board member for Bionovo.
Source: Than M, et al. 2-hour accelerated diagnostic protocol to assess patients with chest pain symptoms using contemporary troponins as the only biomarker: The ADAPT trial. J Am Coll Cardiol 2012;59:2091-2098.
Chest pain presentations to the emergency department (ED) are common and very costly to the health care system. Although the event rates are low in patients with a low clinical risk profile, the price of a missed diagnosis is high. Some low-risk patients who are discharged from the ED may suffer a myocardial infarction (MI) and potentially even die. Our ability to predict who will go on to suffer an acute coronary syndrome (ACS) is imperfect. Thus, many patients are unnecessarily admitted to the hospital for observation. A more rapid means to assess low-risk chest pain (i.e., rule out MI) in the ED may facilitate earlier discharge and lead to substantial savings for the health care system.
Than and colleagues developed an accelerated diagnostic protocol (ADP) to rapidly rule out MI in low-risk patients presenting to the emergency room with chest pain. Their aim is to facilitate early discharge from the ED in these patients, and the ADAPT (2-Hour Accelerated Diagnostic Protocol to Assess Patients With Chest Pain Symptoms Using Contemporary Troponins as the Only Biomarker) trial is a prospective, observational study performed at two urban EDs. Their protocol identified low-risk chest pain patients as those with a Trials In Myocardial Infarction (TIMI) risk score of 0, no ischemic ECG changes, and negative cardiac troponin I (cTnI) upon arrival and at 2 hours. The TIMI risk score applies 1 point for each of the following parameters: age > 65 years, ≥ three cardiac risk factors, aspirin use in the preceding 7 days, known coronary stenosis ≥ 50%, ≥ two episodes of chest pain in the preceding 24 hours or ongoing pain, ST segment changes on the ECG, and elevation of biomarkers. All patients had cTnI drawn at 0 and 2 hours after arrival. Importantly, the 2-hour cTnI was not communicated to the physicians, so usual care was performed (which usually entailed a 6-12 hour cTnI measurement). The primary endpoint of the study was major adverse cardiac events (MACE) occurring within 30 days of presentation (including during the initial hospitalization). MACE included: death (unless clearly non-cardiac), MI, cardiac arrest, emergency revascularization procedure, cardiogenic shock, ventricular arrhythmia needing intervention, and high-degree atrioventricular block needing intervention. Follow-up was by review of hospital records, national death index, and telephone contact.
Of the total 1975 patients enrolled, 302 (15.3%) had a MACE within 30 days. The ADP classified 392 patients (20%) as low risk. No patients were lost to follow-up. One (0.25%) of these patients had a MACE, giving the ADP a sensitivity of 99.7% (95% confidence interval [CI]: 98.1% to 99.9%), negative-predictive value of 99.7% (95% CI: 98.6% to 100.0%), specificity of 23.4% (95% CI: 21.4% to 25.4%), and positive-predictive value of 19.0% (95% CI: 17.2% to 21.0%). Because the results of the cTnI were not communicated to the treating physician, most ADP-negative patients had further investigations (74.1%), and therapeutic (18.3%) or procedural (2.0%) interventions during the initial hospital attendance and/or 30-day follow-up. The authors performed a post-hoc analysis to determine the sensitivity and specificity of each parameter of the ADP using combinations of two parameters. They found that using all three parameters of the ADP (TIMI risk score of 0, non-ischemic ECG, and negative cTnI) performed best.
The authors conclude that when using the ADP, a large group of patients was successfully identified as having low short-term risk of a MACE and therefore suitable for rapid discharge from the ED with early follow-up. This approach could decrease the observation period required for some patients with chest pain.
Commentary
Any strategy that can safely facilitate the more rapid discharge of patients from the ED would be most welcome. This study from Than and colleagues represents a step in that direction. The identification of low-risk patients who may be suitable for early discharge by simple clinical risk features, ECG, and a 2-hour cTnI measurement may help alleviate ED crowding. The rate of MACE in their low-risk cohort (one patient with a missed MI; 0.25%) was low, and is in the range that many ED physicians would call “acceptable.” However, exactly what one considers an acceptable rate of missed MI remains the subject of considerable debate.
This study has several strengths that should be noted. First, they used a current fourth-generation troponin assay that is similar to those widely used in the United States today. Second, this was a prospective, two-center study performed in two countries (but not in the United States). These features add weight to the conclusions that can be drawn. However, several limitations should also be noted. First, by not allowing the physicians access to the 2-hour troponin result, these patients were not actually discharged early. They all underwent 6- to 12-hour follow-up troponin and the majority underwent stress testing or invasive treatments. The MACE endpoint included emergency revascularization, but not elective treatment/revascularization. It is possible that some of the treatments received may have reduced the MACE rate. I would like to have seen data on what treatments these patients received. Second, the patients were predominantly Caucasian males, so the results may not be generalizable to women and non-Caucasian populations. This study is exciting in that it may lead to earlier discharge of these low-risk patients from the ED. However, until the strategy of discharge is actually tested prospectively, this study should be considered hypothesis generating rather than practice changing.
Where this approach will fit in the evolving world of chest pain assessment is not clear. Computed tomography coronary angiography is increasingly being used to rule out MI in low-intermediate risk groups. In addition, highly sensitive troponin assays are emerging and show potential to diagnose or rule out MI earlier, albeit with a trade-off of more “false” positives. Dedicated chest pain centers with after hours stress testing facilities are appearing. Future studies will define the best use of all of these new approaches, and will hopefully reduce ED crowding and the economic burden of chest pain presentations on the health care system.
Chest pain presentations to the emergency department (ED) are common and very costly to the health care system. Although the event rates are low in patients with a low clinical risk profile, the price of a missed diagnosis is high.Subscribe Now for Access
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