Chest pain constitutes 10% of all presentations to the emergency department (ED), with 85% eventually discharged as being non-cardiac in origin1-2. Of those admitted with chest pain, 25% receive a diagnosis of an acute coronary syndrome (ACS). 2% of patients with chest pain due to ACS are erroneously discharged, which is associated with a twofold increase in 30-day mortality and morbidity.

Absence of chest pain does not preclude ACS, so considering it as part of your differential can help reduce erroneous discharge. Current best practice care involves obtaining a 12 lead ECG alongside careful history-taking, clinical examination, and judicious use of investigations3. Clinical risk stratification using diagnostic pathways may help determine the likelihood of ACS and help reduce mortality from such presentations3-4.

Many scoring systems exist for chest pain. The HEART score was developed as a chest pain scoring system for non-differentiated chest pain and predicts the risk of developing major adverse cardiovascular events (MACE) within 6 weeks of presentation5. It enables stratification for chest pain relative to risk according to a points-based risk score6. Other scores including GRACE and TIMI rely on already established acute ACS diagnosis for chest pain, and thereby estimates mortality post-diagnosis7. Improved high sensitivity (hs)-troponin assays alongside chest pain algorithms have helped in improving detection of underlying myocardial injury, ruling out MI with normal and serial low troponins8.

Many other conditions can result in an elevated troponin level, including pulmonary embolism, end-stage renal disease, sepsis, amongst others. For patients presenting with suspected cardiac chest pain with no ischaemic changes on an ECG, they may fall into an intermediate risk category. These patients are a heterogeneous group and may have normal or elevated hs-troponins or normal or indeterminate ECG findings. Only 30-40% of these patients will ultimately be found to have experienced a myocardial infarction. Many of these patients will require admission for observation, further blood tests, and potential invasive angiography.

Coronary computed tomography angiography (CCTA) has increasingly been examined for its role in assessing coronary vasculature in the presence of low-to-intermediate risk chest pain through coronary visualization, calcium scoring and identifying high-risk vascular plaques9. Its non-invasive strategy may provide more information which could reduce the number of patients proceeding to invasive angiography which carries its own risks4.

CCTA has been studied for low-to-intermediate risk chest pain in the ED setting10-11, with at least 6 randomized control trials (RCTs) examining its utility. The ROMICAT-II trial studied the use of CCTA in patients aged between 40-74 presenting with symptoms suggestive of ACS, comparing it to standard ED evaluation for determining ACS. This cohort of low-risk patients (>80% of patients had a TIMI score 0 or 1 (a mortality rate of <4% for MACE)) found more patients had a reduced length of stay and were able to be discharged from the ED but found no difference in MACE at 28 days11.

However, the study was underpowered to determine if CCTA could provide a statistically significant reduction in MACE during follow-up between groups. 8 events were recorded: 4 myocardial infarctions (MI) and 2 unstable anginas (US) in the standard evaluation group, with one MI and one US in the CCTA group)12. A follow-up of ROMICAT II found that those patients receiving standard care endured shortened stays but had lower diagnostic rates of ACS and invasive angiography. With negative troponins, non-ischaemic ECG and non-invasive-testing in the form of CCTA, patients endured longer length of stay and further investigations without differences in MACE recorded at 28-day follow-up12.  

A second study, CT-COMPARE, was a randomized, non-blinded trial examining CCTA against exercise stress testing (ExECG) in patients with low-risk chest pain presenting to the ED. The incidence of ACS was 4.2% overall, with 5.2% in the CCTA group and 2.9% in the ExECG group. There was a demonstrated improved diagnostic turnaround, no demonstrable missed MACE on follow-up but an increased rate of invasive investigations13.  

Finally, BEACON, an open-label randomized trial compared CCTA to current standard practice on the effect of revascularization at 30 days. No difference was demonstrated in the primary endpoint (patients undergoing coronary revascularization within 30 days) (9% vs. 7%, p=0.5), the incidence of undetected ACS, discharge from the ED (65% vs. 59%, p=0.16), length of stay (6.3h, p=0.8), with similar rates of MACE (10% vs. 9%, p=0.54). The CCTA group demonstrated less outpatient testing after the index visit (4% vs. 10%, p<0.01) and lower costs (€337 vs €511, p<0.01)10

As a conclusion, the improved assays and role of hs-troponins, alongside incorporated chest pain pathways may mitigate the utility of CCTA in low-risk chest pain. However, benefits are minimized when considering that the patients studied are low risk for ACS at presentation. Therefore, the role for CCTA in those patients with intermediate-risk chest pain may benefit from non-invasive imaging, particularly where they have indeterminate cardiac markers, non-ischaemic ECGs and have risk factors that may enable CCTA to deliver benefits not seen in those at lower risk of developing ACS14.

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