Complications

The complications resulting from an aortic dissection can be catastrophic. Rupture into the mediastinum can occur anywhere along the dissected portion of the aorta. If the proximal ascending aorta ruptures, hemopericardium and potentially acute cardiac tamponade may result. Other serious complications can result from the expanding false lumen causing stenosis, occlusion, or continued propagation down branch vessels, compromising blood flow to the heart, brain, mesentery, liver, kidneys, spinal cord, or extremities. Finally, when the dissection involves the ascending aorta, the commissures of the aortic valve can be disrupted by the expanding false lumen, causing prolapse of the involved valve leaflet resulting in aortic insufficiency.

Aneurysms of the arch and descending thoracic aorta are frequently associated with atherosclerosis. In contrast, ascending aortic aneurysms are typically associated with bicuspid aortic valves, collagen-vascular defects, such as Marfan or Ehlers-Danlos syndrome, or less well-defined pathology, such as annuloaortic ectasia. Poststenotic aortic dilatation is an additional cause of ascending aneurysms thought to result from areas of the aortic wall exposed to flow derangements, usually as a result of aortic stenosis.

Microscopic findings in ascending aortic aneurysms commonly demonstrate fragmentation of elastin fibers within the media. As a result, the tensile strength of the aortic wall is reduced, leading to progressive dilatation. A dilated, thin ascending aorta is more prone to a disruption within the intima, which, in turn, can become the starting lesion for an aortic dissection. Other rare causes of thoracic aortic pathology include a variety of vasculitides (which more commonly cause occlusive disease), infections, trauma, and tertiary syphilis (which causes medial degeneration of the ascending aorta and aortic arch).

Classification

Aortic dissections were first classified by DeBakey according to the site of intimal tear and the extent of the false lumen within the aorta. A simpler and more clinically relevant classification was developed at Stanford and categorized dissections based on the region of the aorta involved (Table 51.1). Type A dissections include any dissections involving the ascending aorta. Such lesions may be isolated to the ascending aorta or may extend into the aortic arch and descending aorta. Type B dissections involve only the descending aorta (defined as aorta distal to the left subclavian artery). Type A dissections are frequently associated with chronic hypertension or some degree of annuloaortic ectasia or collagen-vascular defect, such as Marfan syndrome. Importantly, most type A dissections are not related to atherosclerotic disease. In contrast, patients with type B dissections typically have advanced atherosclerotic disease and labile hypertension. These patients are frequently older and often have serious comorbid conditions related to their profound systemic atherosclerosis.

Treatment

The Stanford group demonstrated better hospital survival in patients with type A dissections treated surgically, whereas medical therapy resulted in better survival rates for patients with type B dissections. As a result, emergent surgical repair is the therapy of choice for patients with type A dissections, whereas medical management is the preferred approach for patients with type B dissections, with surgery having only a limited role.

The goals of surgery in type A aortic dissections are related directly to the most frequent life-threatening complications associated with this disease. Specifically, by operating early, the intent is to avoid rupture of the ascending aorta (into the thorax or pericardium), prevent or correct malperfusion of the coronary arteries or the brachiocephalic vessels, and treat aortic insufficiency by repairing or replacing the aortic valve. Because it is not feasible to replace the entire segment of dissected aorta (frequently from the aortic valve proximally to the bifurcation of the iliac arteries distally), management of the residual dissected aorta is dictated by symptoms. For example, malperfusion syndromes are generally treated by extra-anatomic bypass.

Developments in thoracic endovascular repairs (TEVAR) have made stenting the descending aorta, particularly in regions of malperfusion, a viable option at some centers. To be a candidate for an endovascular procedure, the patient’s iliac vessels must be able to accommodate device entry, and there must be relatively normal aortic diameter on either side of the lesion for the stent to adhere to (the so-called landing zone). Complications that are specific to endovascular procedures involve angiographic evidence of persistent flow within the aneurysmal sac after stent placement. The location and severity of this ongoing leak dictate subsequent therapy (see Box 51.E1).

Surgical treatment in type B dissections is primarily indicated when there is ongoing malperfusion not amenable to TEVAR or, when present, to treat acute aortic rupture.