Diagnostic imaging studies in the setting of clinical suspicion of dissection have important primary goals such as confirmation of clinical suspicion, classification of dissection, localization of tears and assessment of both extent of dissection and indicators of urgency (e.g. pericardial, mediastinal, or pleural hemorrhage); in addition, biomarkers (such as myocardial markers, D-dimer elevation >500 μg/L and smooth muscle myosin heavy chain) may be used strategically in concert with swift aortic imaging, although an ideal algorithm has yet to be determined [12, 14–17]. Selection of imaging is often hospital-specific, but CT angiography is most readily available and accurate (Table 5.3). Clinical suspicion of acute aortic syndrome is high with abrupt or severe retrosternal or interscapular chest pain often migrating down the back; associated findings can produce signs of acute aortic insufficiency, pericardial effusion or occluded aortic sidebranches causing ischemia or pulse differential [4]. With predisposing factors such as hypertension, connective tissue disorders, bicuspid aortic valve, coarctation and previous cardiac surgery or recent percutaneous instrumentation, undelayed diagnostic imaging is required for any of the above symptoms and suspected acute aortic syndrome (Table 5.4) [13]. While transthoracic ultrasound provides vital information (new-onset aortic insufficiency, pericardial effusion or even visualisation of proximal dissection), additional transoesophageal (TEE) interrogation of the thoracic aorta is the logical next step, or MD-CT scanning of the entire aorta if considered safe [5, 10, 11, 17]. Both imaging modalities provide further detail beyond classification as type A and B (or distal) dissection and allow for strategic planning; ultrasound technology is portable, avoids transport of a critically-ill patient and may even be held in the operating theatre [17]. MRI has no place in the urgent diagnostic work-up of acutely symptomatic patients. Additional information not essential for immediate management decisions such as coronary, arch vessel and side-branch involvement is usually depicted on CT-angiograms without the need for invasive angiography, even in the presence of ST-changes [5, 11].

All patients must receive the best medical treatment available at admission [5, 13]. Initial management of AAS is directed at limiting propagation of diseased wall components by control of blood pressure and reduction in dP/dt. Reduction in pulse pressure with a target systolic pressure of 100–120 mmHg and a heart rate of 60–80 bpm to just maintain sufficient end-organ perfusion is a priority with the use of intravenous ß-blockade as first-line therapy. Often multiple agents are required, with patients ideally managed in an intensive care setting. Opiate analgesia should be prescribed to attenuate the sympathetic release of catecholamines to pain with resultant tachycardia and hypertension (Table 5.5). High-risk but asymptomatic patients with AAS, with the exception of type A aortic dissection, can probably be followed up without urgent intervention if they do not reveal any early complications [2, 18, 19]. All symptomatic patients will need surgical or interventional treatment, since the evolution is unpredictable with a high likelihood of severe complications. Moreover, it is clearly necessary to distinguish IMH and PAU from classic acute aortic dissection. The site of lesion and evidence of complications, as well as evidence of disease progression on serial imaging dictate the management strategy besides the initial medical management.