Inclusion of Multi-Detector CT Angiography (MDCT) in Low to Intermediate Risk Chest Pain Patients Presenting to the Emergency Department; a Randomized Cost Analysis

Background and Significance

Standard-of-care risk-stratification algorithm (SOC):

In the past 20 years since Goldman et al4 described a clinical algorithm to predict MI in ED patients, the clinical ability to decrease the false-negative rate for myocardial events has not improved. Hence, the emergency physician (EP) is compelled to admit to the hospital the majority of patients who present with acute chest pain for further observation and investigation due to inconclusive evidence of ACS or MI during the index ED visit; false-negatives are still sent home with CAD; and false-positives are admitted without CAD; accounting for a significant consumption of resources every year in the US1.

The current state of the art for EPs includes clinical data, electrocardiograms (ECGs) and cardiac biomarkers5 (Fig. 1). The limitations of using the Goldman prediction rule and the ECG is that they are insensitive indicators of myocardial injury in patients with MI4-9. The sensitivity and specificity of cardiac biomarkers is proportional to the time from onset of chest pain. Cardiac troponin begins to rise within 3-4 hours after the onset of myocardial injury and may remain increased for up to 4-7 days for cTnI and 10-14 days for cTnT10. There is enthusiasm for myoglobin as an early marker; however, myoglobin is non-specific11-16 In ED based trials; cardiac biomarkers have performed well but have not changed the cost and admission rate (false-positives). In 1999, McCord et al9 published a single center prospective cohort study that examined point-of-care cardiac biomarkers during the first 90 minutes and if they could help to exclude AMI in the ED chest pain patient. The post-hoc analysis and resultant negative predictive value (NPV) was 98 to 99% at time 0 minutes, 90 minutes, and 3-hours with various combinations of the three biomarkers including Myoglobin, Troponin I and CK-MB. These results demonstrated a consistency of negative predictive values with both combinations of CK-MB with myoglobin equal to Troponin with myoglobin. In 2004, Fesmire, et al17 reported in another prospective ED cohort study that a 2-hour delta CK-MB level outperforms myoglobin level in the early identification and exclusion of acute MI and can effectively risk-stratify patients for 30-day adverse outcomes. In both of these ED based trials, despite the impressive post-hoc NPV in the McCord et al trial, the cost and admission rate (false-positives) remains the same since the rule-out MI process requires admission and 24 hours of serial cardiac enzyme testing.

Patients presenting to the ED with acute chest pain undergo the SOC risk-stratification algorithm to determine the etiology of the complaint (Figure 1). The SOC risk-stratification initially includes the clinical assessment and an ECG. If the ECG reveals an ST elevation MI (STEMI) the patient is treated immediately in the cardiac catheterization laboratory. If the ECG is normal or indeterminate, and there are clinical risk factors, the patient will undergo cardiac biomarker testing. If the cardiac biomarkers are negative, the patient will then be admitted to the hospital for further testing. If the cardiac biomarkers are positive, the patient will be admitted to the cardiac care unit (CCU) for further testing. If the clinical risk factors are absent and the ECG is normal, the patient may be discharged without further testing4-8, however this is practiced in a small percentage (11%) of patients9. This practice risk-stratification algorithm continues to be the SOC. However, the combination of the Goldman predictor risk algorithm (ECG and symptoms) with a Troponin I (cTnI) < 0.3 was not able to identify a group of chest pain patients at <1% risk for the composite outcome of death, AMI or revascularization18. Further demonstrating the need for integration of additional testing that will decrease the false-positive and false-negative rates.