Although the chest pain of acute aortic dissection is widely recognised, less consideration has been given to pain associated with other aortic pathologies. In light of contemporary concepts in aortic pathology we would like to present the pathology of a new cardiovascular syndrome—acute aortic syndrome (AAS). 1 This syndrome embraces a heterogeneous group of patients with a similar clinical profile that includes penetrating atherosclerotic aortic ulcer, intramural aortic haematoma, and the classic aortic dissection (fig 1). The physiopathological mechanism that precipitates the appearance of each of these entities is diVerent. However, occasionally some patients exhibit several or all of these lesions, demonstrating the existence of a link between them. In such cases it is diYcult to know which was the initiating event.

AAS is characterised clinically by aortic pain in a patient with a coexisting history of hypertension. In acute coronary syndromes, the existence of a typical chest pain that, since Heberden, has been called angina pectoris is well recognised. Likewise, in AAS chest pain is characteristic and has been called “aortic pain”. The recognition of pain associated with these progressive aortic lesions is of paramount importance. A severely intense, acute, searing or tearing, throbbing, and migratory chest pain denotes that the patient may have an AAS. Anterior chest, neck, throat, and even jaw pain is related to involvement of the ascending aorta, whereas back and abdominal pain more often indicates that the aVected segment is the descending aorta. 2 The chest pain and clinical presentation of patients with penetrating aortic ulcer and intramural aortic haematoma is similar to that of classic aortic dissection. Severe, acute chest pain consistent with AAS may occur in patients with pronounced aortic root dilatation but without histopathologic evidence of aortic lesions. Aortic root stretching and distension are likely mechanisms for the pain experienced by these patients. Aortic pain may be confounded with that of ischaemic syndromes. Laboratory tests (creatine kinase and troponin), electrocardiographic changes, and chest x ray may help to diVerentiate them. It