Introduction

Acute aortic dissection (AAD) is a relatively rare but much-feared clinical presentation which has a high mortality, particularly if definitive treatment is delayed. A combination of aortic wall stress and abnormalities of the medial layer of the aortic wall leads to disruption of the media and an intimal tear with subsequent penetration of blood, which splits the aortic wall layers. This creates a cavity within the medial layer, the so-called false lumen (FL), which is separated from the native true lumen (TL) by the dissection membrane.1 This process can result in disruption of the adventitia (aortic rupture) or in a second tear in the dissection membrane, which allows blood to re-enter the TL. If AAD occurs within the ascending aorta (AA), 40% of patients die immediately and mortality is 1%–2% for each hour afterwards resulting in a 48-hour mortality of approximately 50% (see figure 1).2

The most important risk factor for the development of AAD is poorly controlled hypertension. Men are more often affected and the risk increases with age. Other important pathogenic factors are positive family history and genetic history (connective tissue disease, Ehlers-Danlos syndrome, Marfan syndrome), aortic disease and aortic valve (AV) diseases, history of cardiac surgery and previous trauma.3 ,4 Although dilatation of the aorta (aortic aneurysms) increases the risk through greater wall stress, AAD can as well occur in patients with …