Rapid Evaluation of Chest Pain in the Emergency Department

Chestpain is responsible formore than8millionvisits toemergency departments (EDs) each year in the United States. This diagnosis presents a large burden on the ED, acute care hospitals, andoverall resources dedicated tomedical care. In this eraof shrinking resources, increasedefficiencyof initial evaluationandsafedischargedirectly fromtheEDofpatientsatvery low risk has the potential of reducing unnecessary admissions, thereby reducing significant costs.1 Inadvertent dischargeof patients presentingwith chest pain is a constant fear of EDphysicians, and thedire consequences of an acute coronary event drives the desire for substantial testing to achieve a high level of certainty for a negative diagnosis. Current guidelines2 emphasize (1) rapid determination of the likelihood that the presentation represents acute coronary artery disease and (2) rapid assessment of the immediate risk for amajor adverse cardiac event (MACE). The cornerstone of treatment is a rapid history, focused physical examination, 12-leadelectrocardiogram (ECG), and laboratory tests forbiomarkers.This strategyquicklydetectsongoing ST-elevation myocardial infarction, for which highly sophisticated triageand interventionsystemsexist, andongoingnon– ST-elevation myocardial infarction presenting with ECG signatures of ischemia and/or immediately positive biomarkers. These are the straightforward cases; unfortunately, theymay account foronly 25%ofacute chestpainpresentations toEDs.3 The dilemma is what to do with the other 75% of acute chest pain presentations. Contemporary studies1 have shown thatmanypatients at very low risk (<5%probability ofMACE) whoare identifiable by symptoms, physical examination, and an ECG demonstrating no abnormalities can be safely discharged from the ED and continue their evaluation as outpatients,with anexpected riskofMACEof 2.5%over 30days. Patients perceived to be at intermediate risk require more intensive scrutiny. Current guidelines4 suggest that these patientsarecandidates forongoingobservation inchestpainunits or hospital admission to rule out myocardial infarction. The guidelines are based on use of fourth-generation troponin T levels,whichwhenusedalone seemtowork just aswell as troponinT levels combinedwitholdermarkers, such as themyocardial band isoenzyme of creatine kinase and myoglobin. It is suggested thatpatientswhopresent to theEDwithin6hours of theonsetof symptomsbeplaced inobservationuntil at least 8 to 12 hours from the onset of initial symptoms, when a follow-up ECG and biomarker tests can be obtained to maximize thechancethat thetest resultsbecamepositive.Thisstrategy is then followed at the end of the observation periodwith some type of confirmatory stress test, the purpose being to lower the risk to a level at which it is safe to discharge the patient. Althoughvery safe, the strategy is time and resource intensive. This has led to a search for alternative strategies to speed theevaluationandcareofpatientswithchestpainwhile maintaining the same level of patient safety fromMACE. Investigators fromChristchurch,NewZealand, reporta randomized clinical trial of an accelerated 2-hour diagnostic protocol (ADP) for evaluation of possible cardiac chest pain. This study is a natural continuation of information acquired in the 2-HourAcceleratedDiagnosticProtocol toAssessPatientsWith Chest Pain Symptoms Using Contemporary Troponins as the OnlyBiomarker (ADAPT) trial.5 TheADAPTwas a prospective observational study of 1975 patients that used the modified Thrombolysis inMyocardial Infarctionscore tohelp riskstratify the history, a 12-lead ECG at 0 and 2 hours, and troponin levels at 0 and 2 hours. Patients were monitored for 30 days for MACE.Theprotocol identified392patientsas lowrisk,andonly 1 individual had a MACE during the next 30 days, for a negative predictive value of 99.7%.However, thiswas an observational study; the investigators could not control interventions,and74%oftheexperimentalgrouphadfurtherdiagnostic testing, with some having therapeutic (18.3%) or procedural (2.0%) interventions during the follow-up. The authors hypothesized that their ADP could rapidly triage perhaps 20%of patients presenting toEDswith chest pain, avoidinghospitalization or prolonged observation. The present study6 used a similar strategy. The investigators identifiedpatientswith amodifiedThrombolysis inMyocardial Infarction score of 0 and used immediate and 2-hour ECGs and laboratory troponin I levels for their ADP. Patients were randomized to the ADP or conventional guidelinedriven therapy of more prolonged observation and a second ECG and troponin 6 to 12 hours after symptom onset. Criteria for successwere discharging the patient homewithin 6 hours of presentation and no MACE for the next 30 days. Of a total of 542 randomizedpatients, 19.3%of theADPgroupand 11.0% of the standard-caregroupweredischargedwithin6hours. Interestingly,anadditional35patients in theADPgroupwereclassified as low risk and couldhavebeendischargedbutwere admitted to the hospital by their attending physician (who apparently did not trust the ADP). None of these patients had a MACE. A unique part of this trial was that patients were required to return for a confirmatory stress test, generallywithin 24hours, as a separate visit. Onepatient in theADPgroup and nopatients in the standard-caregroupdevelopedaMACEover the next 30 days. The patient who developed aMACE should havebeen identifiedby theprotocol as higher risk butwasnot because of a clinical error. Taken together, the ADAPT observational trial and the present trial suggest that a successful strategy can be devised to rapidly identify and process patients at low risk for an acute coronary syndrome. If followed, this strategy might empower more clinicians to discharge low-risk patients home rapidly from the ED. In my institution, the ADP would reduce charges by 50% compared with a convenRelated article page 51 2-Hour Diagnostic Protocol for Cardiac Chest Pain Original Investigation Research