• Cardiovascular Diseases
• Diagnostic Tests
• diagnosis
• clinical assessment

McLatchie and colleagues present observational data on the prevalence of acute aortic syndromes (AAS) in 27 emergency departments (ED) in the UK, over 2–55 days.1 They found that the prevalence of AAS was around 1 in 300 patients presenting to ED with chest, back or abdominal pain; or ‘malperfusion’ (defined as stroke, myocardial infarction, bowel or limb ischaemia), while the CT aortogram rate was 7%. In a separate study, the same group of authors present national survey data showing inconsistency in the approach to diagnosing AAS in EDs across the UK.2

The observational study is important, as the authors attempted to identify AAS cases prospectively from an undifferentiated patient cohort. Despite being the most relevant to clinical practice in the ED, this methodology is rarely used in diagnostic accuracy studies due to logistic and cost issues. Prospective identification of cases from an undifferentiated cohort enables a more reliable estimate of the accuracy of our diagnostic armamentarium than retrospective case identification, especially when only selected patients are included in the latter (such as those going for CT or having a D-Dimer test). That fewer than half of patients were prospectively identified despite a highly engaged stakeholder group undertaking the present study speaks volumes to the need for dedicated research staff embedded within ED, rather than hoping that busy clinical staff will be able to undertake extra tasks for research. The good intentions that clinicians express to help with research are soon dissipated by the clinical workload in a crowded ED. Limitations in the authors’ ability to adjudicate final diagnoses, validate the data collected and follow all patients with respect to 30-day mortality reflect the need to build these important quality checks into the research design and funding applications for such research. An important piece of information also missing from the present study is the level of training and experience of the clinicians assessing the likelihood of AAS.

Notwithstanding these limitations, the study findings are an important step in the journey towards an evidence-based consensus on approaching the diagnostic workup of possible AAS in the ED. With respect to diagnosing AAS, clinical acumen outperformed the current clinical decision tools (CDT), with an Area Under the Curve of the Reciever Operator Curve (AUC ROC) of 0.96. This level of accuracy is rarely seen with common diagnostic tests and highlights the importance of including clinical gestalt when assessing the potential added value of any diagnostic test or CDT.

Of the CDTs, only the Canadian clinical practice guideline score reached the threshold as a good diagnostic test (AUC ROC > 0.8), which likely reflects the extensive research and gold-standard method underpinning the development of the guideline (and the inclusion of clinical gestalt in the score).3 All diagnostic methods explored in this study had high Negative Predictive Values (NPV) simply reflects the extremely low prevalence of AAS in this undifferentiated ED cohort.

None of the current AAS CDTs includes ethnicity in their risk assessment, when it is known that different ethnic groups have different incidences of AAS. Future studies should explore ethnicity as a potential risk factor for AAS when developing or validating CDTs in a local context.4 5

Although only a minority of patients in this study had a D-Dimer, D-Dimer alone was found to be a poor test for AAS (barely better than flipping a coin) due to its very low specificity and less than desired sensitivity in this setting. Adding D-Dimer to clinical acumen in this study reduced diagnostic accuracy, most likely because of reduced specificity with no great improvement in sensitivity compared with clinical gestalt. This has important implications for clinical practice as increased use of D-Dimer in ‘all comers’ with possible AAS is likely to lead to more use of CTA without improving diagnostic accuracy for those with very low pretest probability of AAS and increases the chance of delaying or not requesting a CTA in those with a high pretest probability of AAS. Given the time-sensitive nature of mortality with AAS, delaying CTA waiting for a D-Dimer result in the ED may be disastrous.

However, there may still be a place for D-Dimer in the diagnosis of AAS. The Canadian clinical practice guideline proposes using D-Dimer only when there is between 0.5% and 5% pretest probability of AAS (score of 1). When there is a lower risk (score of 0), then no further testing is required; and when there is higher risk (score of 2 or more) CTA should be done. The present study supports this approach, with a similar diagnostic accuracy found for the Canadian practice guideline including D-Dimer only when score=1, to when the clinicians thought the likelihood of AAS was more than 2 on an 11-point ordinal scale.

In their survey study,2 the authors advocate for a standard diagnostic pathway for detection of AAS, which is a laudable goal. However, as AAS is a very rare condition, the key first step is that clinicians recognise the potential for AAS. If that threshold is not crossed, then a pathway will not be used even if it was available. So simply mandating a pathway may not lead to fewer missed AAS. Furthermore, clinician gestalt outperformed all CDTs in the observational study, due to a higher specificity. This raises the possibility that a standard pathway using a CDT may lead to more CT scanning without increasing the diagnostic yield for AAS compared with clinical gestalt. This may have significant resource implications, expose patients to unnecessary radiation and contribute to ED crowding by prolonging length of stay for low-risk chest pain patients and reducing access to the CT scanner for other patients.

The observational study demonstrates that large-scale multicentre prospective studies for diagnosis of AAS in the ED are possible and still needed.1 Such studies should focus on comparing clinical gestalt on an 11-point scale with the Canadian clinical practice guideline, using D-Dimer in only those with an intermediate risk of AAS and addressing ethnicity as a potential risk factor for ASS (where relevant in the local context). Future studies need to be adequately funded and resourced to address the limitations of the present study.1