The number of chest pain presentations you see in a week or a month can be overwhelming. They crowd your emergency department and claim scarce inpatient beds. But your ED can achieve relief as several advancements converge. Better risk stratification models can identify low-risk ED patients, and improved troponin assays allow us to rule out myocardial infarction.
You can safely and quickly discharge patients when the ED has accelerated diagnostic protocols in place, too, which means that all that is left is updating your low-risk chest pain protocol.
Risk models designed to predict adverse outcomes in chest pain patients are not new; many have been developed over the decades. They usually incorporate features of the patient's presentation, medical history, ECG, and initial troponin. TIMI is the most widely known and used, but was originally developed to predict in-hospital mortality and has poor predictive capability.
Newer models developed specifically for ED patients include the HEART score, Manchester ACS (MACS), the Vancouver Chest Pain Rule, and the Emergency Department Assessment of Chest Pain Score (ED-ACS). Physicians developed the risk scores using patients just like you see every day in your ED — the undifferentiated patient with chest pain. Patients scored as low risk with these models have 30-day adverse outcomes of less than two percent, and the HEART score and ED-ACS have been validated in follow-up studies.
Our troponin assays are also getting better. No high-sensitivity troponin test is approved for use in the United States, but our contemporary assays have continually improved. Sensitive contemporary assays are available with lower detection limits (though not as good as high-sensitivity assays) and improved precision. Detecting smaller amounts of troponin allows for earlier detection of infarction (higher MI sensitivity), with the tradeoff being increased detection of false-positives such as chronic kidney disease or heart failure.
This increased precision means the troponin measurement has less variability, and the change between troponin measurements can be measured reliably, especially at low levels of troponin, which is important for ruling out myocardial infarction. You can use a shorter interval of two hours — instead of four to six — and still get an accurate measurement of the troponin change. It is the increased precision, which the assay manufacturers refer to as coefficient of variance, that is most important for rapid chest pain assessment in the ED. (Read more about troponins at http://emn.online/Feb15SponCric.)
Troponin level was detectable only above the 99 percent upper limit of normal (ULN) in older assays. This fit with the definition of myocardial infarction, which is a rise or fall in cardiac troponin with at least one value above this 99 percent level. Troponins, with these more sensitive assays, may be reported above the level of detection (the absolute minimum amount of troponin detectable with the assay) but lower than the 99 percent level required for an MI.
Within this range, a delta troponin that is less than 99 percent ULN or is a change of 20 percent or 9 ng/mL from the initial level indicates a myocardial infarction. A negative troponin with these assays imply a much lower troponin level than with the older assays and reduced risk.
Using these new tools, researchers developed accelerated diagnostic protocols for rapid disposition of chest pain patients. A group of Australian researchers developed a two-hour rule-out protocol studied with a large cohort of patients using the TIMI risk score and high-sensitivity troponins published in a series of studies such as RATPAC and ASPECT. Using a subset of the same patients along with new subjects, the authors' ADAPT study substituted a contemporary troponin, which showed low-adverse events in low-risk patients with a two-hour delta troponin that was negative. (Detailed discussion at http://emn.online/Aug15SponCirc.)
This is being incorporated across Queensland, Australia, with the ACRE project. The same group of researchers also developed the ED-ACS risk score and validated it using a similar two-hour protocol. Independently, Simon A. Mahler, MD, at Wake Forest validated a pathway that used the HEART score (developed by Dr. Backus in the Netherlands) and a three-hour delta troponin measurement for early discharge of chest pain patients. This has been implemented with great success at the University of Maryland along with a risk visualization tool and shared decision-making.
How can you adapt these protocols to your emergency department? After the history and physical, ECG, and initial troponin, risk-stratify your patient as low, moderate, or high risk. Risk models such as TIMI, the HEART score, ED-ACS, or the Vancouver Chest Pain Rule can assist the physician's judgment. If the outcome is low risk, discuss with the patient the concerning features of history and exam, evaluation results, risk stratification, and assessment of 30-day risk of major adverse cardiac events.
You should offer the patient hospital observation for further evaluation (including a realistic expectation of duration), the opportunity to remain in the emergency department for a second troponin measurement in two to three hours, or no further testing and follow-up. Visual aids are useful in these circumstances to assist the patient in understanding the risks. This shared decision-making process and patient choice should be documented. If the patient remains in the ED for a second troponin and it is negative or unchanged from the initial level, then you can reasonably exclude myocardial infarction and discharge him.
For low-risk patients able to be discharged from the ED, it is unclear if provocative stress testing adds value to their diagnosis, risk stratification, or treatment. It remains recommended in the AHA 2015 guidelines, but has very low sensitivity and specificity and adds to the patient's burden and health care cost. This is another situation where shared decision-making with the patient, perhaps with the patient's primary physician, can lead to fruitful reduction in our health care system's pattern of overtesting.
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