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Acute and Chronic Aortic Dissection: Medical Management, Surgical Management, Endovascular Management, and Results
Introduction
Aortic dissection was first described in the autopsy of King George II of England in 1761, and later the term “dissecting aneurysm” was coined by Morgagni and Laennec in 1819: “aneurysme dissequant.” It is a life-threatening condition that is challenging to diagnose and one of the most complex clinical conditions encountered by vascular surgeons.
An aortic dissection is a tear in the intima of the aortic wall. Once an intimal tear occurs, propagation of the dissection is a dynamic process that can result in both antegrade and less commonly retrograde blood flow between the inner and outer layers of the media along the length of the aorta. This produces a false lumen separated from the true lumen by a septum composed of the aortic intimal and medial layers and creates a double-barreled aorta ( Fig. 40.1 ). Fenestrations between the two channels connect the true and false lumen and usually occur at the origin of branch vessels. The most common location of the false lumen in descending thoracic aortic dissections is in the posterolateral aorta. Although significant variation occurs, the celiac trunk, the superior mesenteric artery, and the right renal artery most commonly arise from the true lumen, and the left renal artery often arises from the false lumen. Because the blood in the false lumen is contained by the thin outer third of the media and loose adventitial connective tissue, rupture of the aorta into the pericardial space, pleural space, or mediastinum is not uncommon.
Classification
Several classification systems have been used to describe aortic dissections. These are based on either the duration of symptoms or the anatomy of the aortic dissection. Treatment varies based on the age of the dissection and the anatomic location of the entry tear; therefore appropriate classification is crucial for initiation of proper therapy.
Temporal Classification
An aortic dissection has been classically classified as acute if the diagnosis is made within 2 weeks of the initial onset of symptoms, subacute if within 6 weeks of the initial dissection, and chronic if the diagnosis is beyond this time period. More recently, the International Registry of Aortic Dissection (IRAD) investigators proposed a more contemporary classification of: hyperacute (symptom onset up to 24 hours), acute (2 to 7 days), subacute (8 to 30 days), and chronic (>30 days).
Anatomic Classification
Two distinct classification systems are currently used to classify aortic dissection based on the location of the intimal tear and the degree of distal extension ( Fig. 40.2 ). Neither scheme addresses dissections originating in or limited to the aortic arch.
DeBakey Classification
The DeBakey classification , first developed in 1965, classifies aortic dissection into four types :
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Type I: The entry tear originates in the ascending aorta and extends from the aortic arch into the descending or abdominal aorta for varying distances.
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Type II: The dissection originates and is confined to the ascending aorta.
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Type IIIa: The entry tear is just distal to the left subclavian artery, and the extent is limited to the descending thoracic aorta.
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Type IIIb: The dissection originates just distal to the left subclavian artery and extends for a variable distance of the abdominal aorta.
Stanford Classification
The Stanford classification categorizes the dissection primarily based on the location of the intimal tear :
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Stanford type A dissection : originates in the ascending aorta and encompasses DeBakey types I and II.
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Stanford type B dissection : originates in the descending aorta and includes DeBakey types IIIa and IIIb.
The Stanford classification is the most widely adopted system for classification and management of the aortic dissection. The majority of patients with Stanford type A dissections require urgent surgical repair, because this disease entity is associated with high rates of mortality if left untreated. Conversely, patients with Stanford type B dissections do not usually require urgent surgical treatment and are treated with medical therapy. Certain indications for surgical treatment exist for these patients and will be discussed later in this chapter.
Incidence and Survival Rates of Aortic Dissection
The annual age- and sex-adjusted incidence of acute aortic dissection has been estimated at 2.9 to 3.5 per 100,000 persons. It is the thirteenth leading cause of death for individuals between the ages of 55 and 64 years. In the United States, it is estimated to affect 5 to 10 people per million per year with 43,000 to 47,000 deaths from involvement of the aorta and its branches. Approximately 48.6% of patients with aortic dissection die before hospital admission.
Aortic dissection is more common in males than females with a 4 : 1 ratio. The entry tear originates in the ascending aorta in 65% of the cases, the arch in 10% of the cases, the descending aorta in 20% of cases, and the abdominal aorta in 5% of the cases. In a report by the IRAD, a total of 67% ( n = 2,952) of all patients enrolled in IRAD presented with type A aortic dissection, whereas the remaining 33% ( n = 1476) presented with type B aortic dissection.
The age at dissection ranges between 40 and 70 years, with dissections seen on the lower end of the spectrum in patients with heritable thoracic aortic disease (e.g., Marfan syndrome, Loeys-Dietz syndrome). In a report by the IRAD, the mean age of patients with type A aortic dissection was 62 ± 14.6 years, while the mean age of those with type B AAD was older, at 64 ± 14.1 years.
Mortality of aortic dissection varies according to the entry tear location. The mortality associated with acute type A aortic dissection is estimated at 30% in the first 24 hours, 50% by 48 hours, and 90% at 1 year in a classic study by Hirst and colleagues in 1958. Surgical mortality for acute type A dissections is 25.1% in IRAD. The long-term survival rates for surgically treated type A aortic dissection patients who survive until hospital discharge range from 52% to 96% and 37% to 91% at 1 and 5 years, respectively.
In contrast, early mortality for patients with acute uncomplicated type B aortic dissection ranges from 10% to 12%, while operative mortality in patients with acute, complicated type B dissection approaches 25% to 50%. The long-term survival of surgically treated patients with type B aortic dissections after discharge ranges from 56% to 96% and 48% to 83% at 1 and 5 years, respectively.
Pathophysiology of Aortic Dissection
Cystic Medial Degeneration
The pathogenesis of aortic dissection is complex. Our true understanding of aortic dissection pathology began with the dissertation by Shennan in 1934 describing cystic medial necrosis (degeneration) in autopsy results of patients with aortic dissections. Cystic medial degeneration is a process that leads to loss of aortic wall smooth muscle cells, fragmentation of the elastic fibers, and accumulation of proteoglycans, effectively weakening the aortic wall.
Aortic Wall Stress
Aortic dissection is believed to occur when intraluminal wall stress exceeds aortic wall strength. Nathan and colleagues demonstrated, in a study using electrocardiogram-gated computed tomography angiography in 47 individuals with normal thoracic aortas, that peaks of aortic wall stress exist in the sinotubular junction and distal to the left subclavian artery ostium. These two locations are typically the entry point for aortic dissection: Ascending thoracic aorta dissections typically result from intimal tears above the sinotubular junction while descending thoracic aorta dissection originate distal to the left subclavian artery ostium. These authors also found that the wall stress proximal to the sinotubular junction exceeded that of the area distal to the left subclavian artery, thus supporting the increased prevalence of ascending thoracic aortic dissections compared with descending thoracic aortic dissections ( Fig. 40.3 ). In contrast, significant atherosclerosis is relatively infrequent in patients with acute aortic dissection, and it has been hypothesized that the presence of atheromatous plaque may serve to terminate or limit the extent of the dissection. One potential theory is enhanced fusion of the aortic wall layers secondary to inflammatory aortic wall plaques.
Hypertension
Hypertension is a well-known risk factor for aortic dissection. More than 75% of patients with aortic dissection are hypertensive, although patients with type B aortic dissection are more likely to present with hypertension than those with type A aortic dissection. Conditions associated with hypertension have also been associated with aortic dissection such as advanced age, pregnancy, especially with accompanying preeclampsia (rare), cocaine, and methamphetamine abuse.
Other Risk Factors
An increase in aortic diameter has been implicated as a risk factor for type A dissection but not for type B dissection. Structural abnormalities of the aortic wall, including bicuspid aortic valve, aortic coarctation, and chromosomal abnormalities (Turner syndrome and Noonan syndrome), have also been implicated. Seasonal variation has been observed in the development of aortic dissection, with more patients being seen in the winter months. As with acute myocardial infarction or myocardial ischemia, physical and mental activities can also be triggers for acute aortic dissection.
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