Improved Assessment of Chest pain Trial (IMPACT): assessing patients with possible acute coronary syndromes.

OBJECTIVE: To examine the safety and efficacy of the Improved Assessment of Chest pain Trial (IMPACT) protocol, a strategy for accelerated assessment of patients presenting to emergency departments (EDs) with chest pain. DESIGN, SETTING AND PARTICIPANTS: IMPACT was an intervention trial at a single tertiary referral hospital (Royal Brisbane and Women's Hospital) during February 2011 - March 2014. 1366 prospectively recruited patients presenting to the ED with symptoms of suspected acute coronary syndrome (ACS) were stratified into groups at low, intermediate or high risk of an ACS. INTERVENTION: High risk patients were treated according to NHFA/CSANZ guidelines. Low and intermediate risk patients underwent troponin testing (sensitive assay) 0 and 2 hours after presentation. Intermediate risk patients underwent objective testing after the second troponin test; low risk patients were discharged without further objective testing. MAIN OUTCOME MEASURES: The primary outcome was an ACS within 30 days of presentation. Secondary outcomes were ED and hospital lengths of stay (LOS). RESULTS: The IMPACT protocol stratified 244 (17.9%) patients to low risk, 789 (57.7%) to intermediate risk, and 333 (24.4%) to high risk categories. The overall 30-day ACS rate was 6.6%, but there were no ACS events in the low risk group, and 14 (1.8%) in the intermediate risk group. The median hospital LOS was 5.1 hours (IQR, 4.2-5.6 h) for low risk and 7.7 hours (IQR, 6.1-21 h) for intermediate risk patients. CONCLUSIONS: The IMPACT protocol safely and efficiently allowed a large proportion of patients presenting to EDs with chest pain to undergo accelerated assessment for risk of an ACS. CLINICAL TRIAL REGISTRATION: Australian New Zealand Clinical Trials Registry ACTRN12611000206921.

Comparison of early biomarker strategies with the Heart Foundation of Australia/Cardiac Society of Australia and New Zealand guidelines for risk stratification of emergency department patients with chest pain.

OBJECTIVES: To compare cardiac risk stratification using a 0 and 2 h point-of-care (POC) cardiac troponin (cTn), 0 and 2 h POC multi-biomarkers against the 0 and 6 h laboratory cTn reference standard. METHODS: A prospective observational study of ED patients presenting with chest pain was performed. Patients were risk stratified and treated as per the Heart Foundation of Australia/Cardiac Society of Australia and New Zealand (HF-A/CS-ANZ) guidelines using the 0 and 6 h laboratory cTn (T6). Patients were further stratified using a 0 and 2 h POC cTn (T2) plus 0 and 2 h POC multi-biomarkers (cTn, creatine kinase-MB, myoglobin) (M2). The T6, T2 and M2 strategies were compared using the 30-day major adverse cardiac events as the primary outcome. RESULTS: Seven hundred and four patients (median age 54 years, male 62.1%) were enrolled. Using the T6 reference standard, 2%, 61% and 37% were stratified as low, intermediate and high risk, respectively. The 30-day event rates were 0%, 3.5% and 28.6%, respectively. The T2 strategy stratified 1.5%, 57% and 41% as low, intermediate and high risk, respectively, with 30-day event rates of 0%, 4.2% and 24.8%, respectively. The M2 strategy resulted in significantly different risk distribution with 1%, 40% and 59% stratified as low, intermediate and high risk, respectively, with 30-day event rates of 0%, 3.9% and 18.8%, respectively. CONCLUSION: Using a 2 h POC cTn-only biomarker strategy with the HF-A/CS-ANZ guidelines accurately identified a population at intermediate risk of 30-day events in whom further objective testing might be accelerated, allowing subsequent early discharge of the majority of this cohort. Within 2 h of presentation a high risk population could be identified in whom early management, including admission, was required.