Nonoperative Medical Management of Acute Aortic Dissection



Nonoperative Medical Management of Acute Aortic Dissection



Christoph A. Nienaber, Ibrahim Akin, Stephan Kische and Tim C. Rehders


Acute aortic dissection should be considered a constituent of acute aortic syndrome (AAS) together with intramural hematoma (IMH), penetrating atherosclerotic ulcer (PAU), and aortic rupture. The common denominator of AAS is disruption of the media layer of the aorta, with bleeding within the media layers or separation of the layers of the aorta (dissection). In 90% of cases, an intimal disruption is present that results in tracking of the blood in a dissection plane within the media, potentially rupturing through the adventitia or back through the intima into the aortic lumen (Figure 1). The most common aortic syndrome is aortic dissection, featuring a tear in the aortic intima commonly preceded by medial wall degeneration or cystic media necrosis. Blood passes through the tear, separating the intima from media or adventitia and creating a false lumen. Propagation of dissection can proceed in anterograde or retrograde fashion involving side branches and causing complications such as tamponade, aortic valve insufficiency, or proximal or distal malperfusion syndromes.




Epidemiology


Historically, acute aortic syndrome was attributed to syphilis; today, contributing factors are diverse (Box 1). The most common risk condition for aortic dissection or IMH is hypertension (75% of patients have a history of hypertension). Other risk factors include smoking, direct blunt trauma, and use of illicit drugs (such as cocaine or amphetamines). Population-based studies suggest that the incidence of acute dissection ranges from 2 to 3.5 cases per 100,000 person-years, which correlates with 6000 to 10,000 cases annually in the United States. There is weak evidence that aortic dissection is more common in the winter compared to warmer summer months.



A review of 464 patients from the International Registry of Acute Aortic Dissection (IRAD) reported a mean age at presentation of 63 years, with significant male predominance (65%). The incidence of dissection appears to be increasing, independent of the aging population, to 16/100,000 men per year. Interestingly, women may be affected less often, but they have worse outcomes as a result of atypical symptoms and a delayed diagnosis. It may in fact be that two to three times as many patients die from aortic dissection than from ruptured abdominal aortic aneurysm, particularly women and younger patients (Marfan’s syndrome, Loeys–Dietz syndrome, Turner’s syndrome, or Ehlers–Danlos syndrome, especially type IV).


The most common mutations appear to lie in either the fibrillin gene (FBN-1) or the transforming growth factor (TGF)-β receptor II gene (TGFBR2) in Marfan and Loeys–Dietz syndromes, respectively. There appears to be little difference in the clinical presentations of these two syndromes; more than half of each group present with aortic symptoms. The commonest nonsyndromic mutation associated with thoracic aneurysms and dissections is in the smooth muscle cell (SMC) actin gene, ACTA2, found in about one sixth of these patients. The association of mutations in genes encoding the SMC contractile apparatus in both aortic dissections and thoracic aneurysms indicates that SMC tonus and function may be an important phenotype influencing the response of the aorta to wall stress. Two other conditions that affect the proximal aorta and that predispose to acute aortic syndromes are annuloaortic ectasia and bicuspid aortic valve, and both of these might have a genetic basis.



Clinical Signs and Symptoms


Patients with acute aortic syndromes often come to the hospital with similar symptoms, regardless of the underlying condition. Pain is the most common presenting symptom of acute aortic dissection independent of age, sex, or other associated clinical complaint. Pooled data from more than 1000 patients showed that acute dissection is perceived as abrupt pain in 84% (95% confidence interval [CI], 80%–89%), with initially severe intensity in 90% (95% CI, 88%–92%). Although the pain is classically described as tearing or ripping, patients are more likely to describe the pain of acute dissection as sharp or stabbing, and fluctuating. Pain of aortic origin is often confused with acute coronary syndromes.


Cardiac enzymes, troponin, and electrocardiogram (ECG) changes may be instrumental in the diagnostic workup, but only the absence of both D-dimer elevation and ECG changes is considered specific to rule out acute aortic syndromes. D-dimers elevated above 500 μg/L appear to correlate with extent and severity of acute aortic dissection, but they fail to distinguish AAS from pulmonary embolism. Critically elevated D-dimer should, however, prompt undelayed computed tomography or transesophageal echocardiography for confirmation of either life-threatening entity.


Acute aortic dissections can be classified according to either the origin of the intimal tear or whether the dissection involves the ascending aorta, regardless of the site of origin. Accurate classification is important because it drives decisions regarding surgical versus nonsurgical management. The two most commonly used classification schemes are the DeBakey and the Stanford systems (Table 1). For purposes of classification, the ascending aorta refers to the aorta proximal to the brachiocephalic artery, and the descending aorta refers to the aorta distal to the left subclavian artery. The DeBakey classification system categorizes dissections based on the origin of the intimal tear and the extent of the dissection. The Stanford classification system divides dissections into two categories, those that involve the ascending aorta and those that do not.



TABLE 1


Classification of Aortic Dissection

































Type Description
Stanford Classification
A All dissections involving the ascending aorta regardless of the site of origin (surgery is usually recommended)
B All dissections that do not involve the ascending aorta (nonsurgical treatment is usually recommended)
Note that involvement of the aortic arch without involvement of the ascending aorta in the Stanford classification is labeled type B
DeBakey Classification
I Dissection originates in the ascending aorta and propagates distally to include at least the aortic arch and typically the descending aorta (surgery is usually recommended)
II Dissection originates in and is confined to the ascending aorta (surgery is usually recommended)
III Dissection originates in the descending aorta and propagates most often distally (nonsurgical treatment is usually recommended)
 IIIa Dissection is limited to the descending thoracic aorta
 IIIb Dissection extends below the diaphragm

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Aug 25, 2016 | Posted by in CARDIOLOGY | Comments Off on Nonoperative Medical Management of Acute Aortic Dissection

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