Anatomical considerations

The aortic media is composed of a series of concentric elastic lamellar plates, separated by smooth muscle and connective tissue. During development, in response to radial (compressive) and circumferential (tensile) stresses which are maximal at the intima and weakest at the adventitia, the inner lamellas thicken and smooth muscle cells develop more cell-cell contacts. Because of this structural modification, most of the stress-resistant properties are found in the inner two-thirds of the aortic media. There is a clear change at the junction between the middle and outer thirds of the media; this represents an area of weakness where tearing might be expected with exposure to high levels of stress and coincides with the observed plane of most aortic dissections.

The intimal tear is found most frequently approximately 4 cm above the aortic valve in the ascending aorta or just distal to the subclavian artery. The dissection usually propagates distally, but proximal extension from the ascending aorta may involve the aortic valve annulus, and tears distal to the subclavian artery may propagate in both directions to involve the aortic arch and ascending aorta as well as the descending aorta. The false channel usually extends 50 to 67 per cent around the aortic circumference, rarely involving the whole aortic wall. The outer wall of the false channel is thin and may rupture, particularly into the pericardium where the ascending aorta is unsupported, the pleural space (usually the left), or the abdomen. In the absence of frank rupture, blood may extravasate to form mediastinal or pericardial hematomas. In patients who survive the acute event, the false channel tends to become aneurysmal and may rupture subsequently. Occasionally, the channel may become thrombosed spontaneously. In a minority of patients there is a discrete re-entry tear so that the false channel produces a parallel aortic circulation, albeit not in communication with the aortic branch arteries.

Although an intimal tear is a universal finding in autopsy series, it may be difficult to identify clinically. The events leading to the intimal tear are poorly understood. It is uncertain whether the intimal tear is the primary event, or whether dissection is initiated by bleeding into the media from the asa vasorum and the intimal tear follows. The major predisposing factors to dissection appear to be the level of shear stress to which the aorta is subjected and, in a proportion of cases, medial degeneration and structural abnormalities of the aortic wall.

With advancing age, elastin fragmentation, fibrosis, and medial necrosis lead to degeneration of the aortic lamellas. These changes are most pronounced in the ascending aorta and become less prominent as the aorta descends into the abdomen. These changes occur as part of the normal aging process but are more prominent in hypertensive patients. Pre-existing dilation of the aorta (as occurs in Marfan's syndrome) may also be relevant. Laplace's law relates wall stress to pressure and diameter: as the aorta dilates, so wall stress increases. Medial degeneration may result from structural abnormalities (e.g. Marfan's and Ehlers-Danlos syndromes) in which dissection may occur without pre-existing hypertension or, possibly, from ischemic necrosis due to occlusion of the vasa vasorum.

A large proportion of dissections take place in aortas without evidence of excessive degeneration. This is true particularly in patients where dissection follows instrumentation of the aorta. It appears that, whereas abnormalities of the aortic wall may make dissection more likely, once the intima and underlying media are damaged, dissections propagate rapidly due to entry of the blood into the media under pressure.

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