“On the 25th of October he [King George II] rose as usual at six, and drank his chocolate; for all his actions were invariably methodic. A quarter after seven he went into a little closet. His German valet de chambre in waiting heard a noise, and running in, found the King dead on the floor.”1 Nichols was directed to open and embalm the royal body. What he found (and meticulously described2) was the first clear account of the condition we now know (after Laennec) as aortic dissection (AD): “...the pericardium was found distended with a quantity of coagulated blood, nearly a pint...; the whole heart was so compressed as to prevent any blood contained in the veins from being forced into the auricles; therefore the ventricles were found absolutely void of blood...; and in the trunk of the aorta we found a transverse fissure on its inner side, about an inch and a half long, through which some blood had recently passed under its external coat and formed an elevated ecchymosis.” The King (Fig. 1) passed away at Kensington Palace while straining on the toilet. His death was caused by cardiac tamponade from an acute dissection of the ascending aorta that ruptured into the pericardial sac. He had reigned for 33 years. Such was the well-documented ‘beginning’ of the storied chronicle of AD, the most lethal and most frequent of all aortic catastrophes. It is an affliction that has been enveloped in awe and mystery for several centuries. From the King’s death, to the many celebrities that have exsanguinated and succumbed to a ruptured aorta, to Dr Michael DeBakey himself being stricken by the very disease he famously classified3 — and surviving (at age 97!) the operation he pioneered in the 1950s, AD inspires fear still and provides a reality-check of the continuing uncertainties surrounding a condition that has been known for more than 2 centuries. Many aspects related to its nature and pathogenesis remain only partially understood. Consider these: • The intimal tear: is it truly the initial event that leads to the dissection per se as blood is allowed to penetrate the intima and medial layers and flow through the aortic wall? Or, is it all the way around? The recognition of intramural hematoma (IMH) as a distinct but closely related entity lends some credence to the latter theory as IMH is now widely accepted to constitute a form of AD or, at a minimum, to carry the potential to become a full-blown case of dissection in some cases; • Arterial hypertension is of course a near-constant companion for most patients, but can it cause AD without any other predisposing condition? In other words, can dissection occur without an intrinsically abnormal (weak) aortic wall? Certain connective tissue diseases — Marfan’s syndrome most notably — are well known to have a much increased predisposition for the occurrence of AD. About 2/3 of cases are type A (“proximal”) and the rest are type B (“distal”). The mortality rate is staggering: up to 1%/hr or more during the first 2–3 days! Much of this relates to type A with its well-known propensity to expand rapidly and rupture into the pericardial sac causing fatal cardiac tamponade. When left untreated, about 33% of patients die within the first 24 hours, and 50% are dead by the end of the second day. The 2-week mortality approaches 75% in patients with undiagnosed ascending aortic dissection. Surgical treatment remains the mainstay in treatment of these patients and, while surgical mortality and morbidity rates continue to be a source of concern, there is currently no other reasonable treatment option. Management of type B acute AD patients is another story: medical treatment has long been the preferred choice for the majority — because it works, and because surgical treatment has produced (truly) dismal results. The article by Manning and Ivancev appearing in this issue of VDM constitutes a succinct and thoughtful report on the present status of our knowledge, mainly from the perspective of emerging endovascular technologies. The latter represent an entirely new opportunity that is likely to change the AD landscape in a profound and lasting manner. In fact, this writer would go as far as to predict that stent-graft intervention is likely to replace open surgery — essentially — for treatment of patients who present with acute dissection and a clinical imperative for intervention. But, once again, we are faced with a number of important questions we cannot yet answer with confidence. Here are some of the most salient: are there patients with uncomplicated acute type B who might benefit from early stent-graft repair? What’s the optimal extent of endograft coverage of the dissected thoracic aorta: short-segment to cover entry site only, 15–20 cm, or perhaps the whole of the above-diaphragm thoracic aorta? What if anything should be done with the below-diaphragm dissected aorta in patients with extensive type B (type IIIb) AD? Looking forward, I have no doubt we will have the ability to make these and other important decisions based on evidence, but it is not going to happen soon or easily. And new endovascular solutions will likely emerge for treatment of acute type A dissection — at least for some cases. That said, I feel confident in making this pronouncement here and today: “the winds of change have already hit the shores of AD” as the endovascular revolution marches on, promising to provide a truly exciting new capability for the management of a centuries-old condition that still ranks high amongst the worst human calamities.