Aortic Dissection and Stroke

Introduction

Aortic dissection occurs in about 3–4 per 100,000 persons per year. A common clinical error is to equate aortic dissection with aneurysm. This misconception unfortunately has been propagated since the earliest descriptions of these diseases, describing a “Dissecting Aneurysm of the Aorta” . While some aneurysms can be complicated by, and predispose to, dissection, and dissections can become aneurysmal over time, the disease processes are relatively distinct.

Aortic aneurysm is an abnormal dilation of the diameter of the aorta usually caused by longstanding atherosclerotic disease, hypertension, and/or a history of smoking. Aortic dissection, in contrast, is the result of an intimal tear of the aorta. This tear is often rapidly propagated within the three layers of the aortic wall to various extent due to the forces exerted by the systemic blood pressure, which quite commonly is elevated. Thus blood rushes directly into the separated wall of the aorta creating a false passageway for blood to travel. This “false lumen” of blood flow may thrombose, rupture, or obstruct blood flow to branch vessels, including coronary and carotid arteries, visceral organs, or the extremities. Dissection may also extend to the aortic valve sinuses and cause acute aortic insufficiency. Risk factors for aortic dissection include hypertension, male gender, bicuspid aortic valve, connective tissue disorders such as Marfans and Ehlers–Danlos syndrome, and age greater than 60.

Several classifications exist for aortic dissection, but the most common and functionally useful is the Stanford classification . Dissections that occur proximal to the left subclavian artery are termed Type A. Aortic dissection occurring distal to the left subclavian artery are described as Type B. This distinction of location of the dissection dictates natural history, management, and surgical approach, if necessary. Type A dissections represent surgical emergencies. Left untreated, Type A dissections carry a mortality rate of 50% within 48 h, and 90% at 2 weeks. Death is usually due to tamponade or aortic rupture. In contrast, Type B aortic dissections are usually managed medically, and have an overall lower short-term mortality, but with a progressive long-term mortality. Surgery for Type B dissection, when necessary, is usually to address complications of malperfusion or later development of aneurysm.

Since brain perfusion arises normally from the aortic arch (carotid arteries) and its branches (vertebral arteries by way of the subclavian arteries), dissection involving this region can lead to acute neurological injury in the form of branch obstruction or embolism. Thus all organs are potentially at risk of ischemia from dissection, typically categorized as either involvement of the visceral, extremity, or neurological (cerebral or spinal) vessels. Most reports find that the innominate (brachiocephalic) artery is the most commonly involved with dissection, followed by the left carotid, and then left subclavian arteries. The vertebral arteries normally take their origin from the subclavian arteries, and can be secondarily affected by subclavian artery dissection.

Epidemiological studies report an incidence of aortic dissection of 5–30 cases/million people. About 17–40% of acute dissections present with evidence for neurological injury .

Neurological injury, when manifest, can present as focal neurological deficit due to brain injury, encephalopathy, or paralysis due to either spinal cord ischemia or acute limb ischemia. It is generally believed that aortic dissection presenting with neurological injury has a higher morbidity and mortality, but there is some conflicting data.