169 16.4.4 Aortic Dissection Evolution

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Contents

16.1 Introduction . . . . 165

16.2 Dissection Mechanism . . . . 165

16.3 Pathogenesis . . . . 166

16.3.1 Aortic Parietal Stress . . . . 166

16.3.2 Tunica Media Degeneration . . . . 166

16.4 Pathophysiology . . . . 167

16.4.1 Mechanical Factors . . . . 167

16.4.2 Morphologic Aspects . . . . 167

16.4.3 Mechanism of Vascular Complications . . 169

16.4.4 Aortic Dissection Evolution . . . . 170

16.4.5 Aortic Dilatation and Complications in Chronic Phase . . . . 170

16.1 Introduction

Aortic dissection is defined as the separation of the aortic media with presence of extraluminal blood within the layers of the aortic wall. In most patients one tear or one or more entries are present in the aortic intima, resulting in an abnormal communication between the true aortic lumen and the split aortic media. With primary intimal dissection the media is exposed to pulsatile aortic flow, likely to create a false aortic lumen and propagate a dissection, typically antegrade but some- times retrograde from the site of the intimal tear. The vast majority of aortic dissections originate in one of the two sites where the greatest hydraulic stress is located in the ascending aorta, within several centimetres above the sinuses of Valsalva, and in the descending aorta, just distal to the origin of the subclavian artery at the site of the ligamentum arteriosum. Sixty-five per- cent of intimal tears occur in the ascending aorta, 20%

in the descending aorta, 10% in the aortic arch and 5%

in the abdominal aorta [17]. Most dissections have a reentry site and some communication sites throughout the descending aorta. The reentry tear is usually located in the abdominal aorta, iliac arteries or other aortic branches. These small communications, less than 2 mm in diameter, are not reentry tears but the ostia of the

intercostal or lumbar arteries that have been severed by the dissecting haematoma. Reentry of the dissection is a predisposition for chronic false lumen perfusion with no tendency to thrombus formation.

16.2 Dissection Mechanism

The two mechanisms regarding the initial event in aortic dissection are primary intimal tear and initial dela- mination of the tunica media produced by the formation of an intramural haemorrhage. There are different lesions which can generate a primary entry tear of dissection, such as atherosclerotic lesions of the aortic intima, penetrating aortic ulcers, or iatrogenic intimal lesions [7, 21]. The second mechanism arises from bleed- ing of the vasa vasorumof the media (Fig. 16.1). All mechanisms weakening the aorta's media layers via mi- croapoplexy of the vessel wall lead to higher wall stress, which can induce aortic dilatation, eventually resulting in intramural haemorrhage, aortic dissection or rupture [16]. The evolution of symptomatic intramural haematoma is to reabsorption, aneurysm formation or dissection [5]. Only 12% of intramural haematomas evolve to

Pathophysiology of Aortic Dissection

Artur Evangelista, Teresa Gonzlez-Alujas

16

Fig. 16.1.Intimal flap (arrow) from an intramural haematoma which led to a classic dissection. TL true lumen, FL false lumen

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classic dissection and 24% present only a localised dissection which eventually progresses to pseudoaneurysm formation [5].

Deterioration and loss of collagen and elastin in the media layer appear to be the major predisposing factors in cases of aortic dissection. Therefore, any disease process undermining the integrity of elastic and muscular components of the media predisposes to aortic dissection [9, 24].

Different processes may produce rupture of the intima:

1. Weakness of the aorta wall due to connective tissue disease such as Marfan syndrome, Edler±Danlos disease and bicuspid aorta [12, 22].

2. Mechanical stress induced froman aortic lesion secondary to jet impact as in aortic valve disease or aortic valve prosthesis [12, 22].

3. Atherosclerotic disease of the aorta wall [21].

4. Aortic intramural haematoma evolution [5, 18, 26].

5. Iatrogenic lesion by catheters or surgery. Trauma [10, 16].

6. Aortic inflammatory diseases [16].

Among the predisposing factors, untreated systemic hypertension is encountered in almost 80% of cases of aortic dissection [8]. Hypertension may not only directly weaken the aortic media, but may also initiate atherosclerosis of the vasa vasorumand thus intramural haemorrhage due to rupture of nutrient intramural vessels [26]. The causative role of systemic hypertension is further supported by the finding that coarctation of the aorta predisposes to aortic dissection [9, 26].

16.3 Pathogenesis

16.3.1 Aortic Parietal Stress

Aortic wall integrity depends mainly on two factors:

contention resistance of its internal and external layers, determined by their biochemical and anatomical struc- ture, and aortic parietal stress, which is in relation to arterial tension, luminal diameter and parietal thickness. All this can be expressed by a modified equation similar to the law of Laplace, where circumferential stress is directly related to blood pressure and aortic diameter, and inversely to parietal thickness.

As mentioned previously, aortic diameter is the main determinant of parietal stress. The aorta usually dilates before dissecting and the geometry of the dilated segment changes from cylindrical to spherical, passing through ellipsoidal. This change in aortic morphology causes a slow, progressive increase in circumferential stress and a rapid increase in longitudinal stress and accounts for the fact that the majority of intimomedial

tears may be transverse. A further consideration to bear in mind regarding parietal stress is that its distribution in aorta wall thickness is not uniform. Since the pressure falls upon the internal arterial surface, parietal stress is greater on the internal than the external part.

This is, in part, why the internal layers usually tear and the external layers do not [20, 23].

Arterial hypertension is considered to be a leading factor in the production of an arterial tear. However, the frequency of dissection in hypertensive patients is low and, furthermore, unpredictable. In fact, arterial pressure is only one of the components of parietal stress and, in some cases, is not even the most important. An aorta with the same pressure may dissect or not, depending on the anatomical characteristics (thickness and composition) of its walls and degree of dilatation. Therefore, the factors that may lead to dissection are as follows: (1) decrease in contention resistance of the internal layer; (2) increase in arterial pressure; (3) increase in aortic diameter; and (4) decrease in parietal thickness.

In the hypertensive type, the internal layer is normal, but there is an increase in parietal stress as a consequence of the increase in arterial pressure. This im- balance will produce a gradual increase in aortic diameter and, with time, a dissection [23].

16.3.2 Tunica Media Degeneration

Degenerative changes produced in the tunica media of patients who evolve to dissection may affect the elastic architecture, collagen and muscular component. Loss or fragmentation of any of these elements diminishes resistance of the aorta wall to haemodynamic stress. This may lead to aneurysmal dilatation of the aorta wall and subsequent dissection. In Marfan syndrome, as in other connective disorders, the dissection is due to medial degeneration. There is enhanced expression of metallopro- teinases in vascular smooth muscle cells which may promote both fragmentation of medial elastic layers and elastolysis, and may lead to significant medial degeneration. In these circumstances, despite normal aortic pressure, the aorta dilates. When the aortic diameter increases, parietal stress increases and eventually a dissection ensues. In the hypertensive type, circumferential stress increases linearly with the increase in arterial pressure. In these cases, an increase of some degree of dilatation aggravates the circumferential stress even more. By contrast, in Marfan syndrome, the circumferential stress does not increase linearly, but exponen- tially. In these patients, a slight rise in arterial pressure accentuates the circumferential stress even more [23].

In some patients with dissection, rupture or loss of structural elements of the capa media is evident on op- tical microscopy; however, in other cases changes are

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difficult to perceive or are even absent. These structural defects do not in themselves explain why some aortas dilate or rupture, others dissect and many remain free of any complications despite the presence of capa media degeneration. It is wrongly assumed that degeneration of the media is a lesion that diffusely affects the dissected aorta. However, as Prokop et al. [20] pointed out, once the dissection has begun, it may extend distally, affecting histologically normal segments, since propagation of the dissection depends basically on the pulse pressure wave.

According to Hirst and Gore [9], the capa media lesion in the majority of patients with dissection can be classified in two groups, depending on whether it pre- dominantly affects the muscle or the elastic architecture. Separation and fragmentation of elastic fibres is more frequent in young patients (under 40 years) and particularly in individuals with Marfan syndrome or other hereditary defects.

Weakening of the aorta wall does not only occur as a consequence of elastic fibre fragmentation but also be- cause of collagen and mucoid material accumulation.

These changes are more prominent in ascending aorta, with the segment subjected to greater pulsatile expansion and, therefore, greater stress. As a result of the loss of elastic tissue, media cohesion is altered, muscle cells change their usual parallel orientation and cell deterioration is accelerated. Loss of muscle cells is usually fo- cal and more frequent in hypertensive patients and those over the age of 40. Smooth muscle cells require oxygen and other nutrients to survive and consequently depend on adequate blood flow. Thickening of the intima, particularly that due to atherosclerosis, may inter- fere with its diffusion and permeability and affects the internal part of the capa media, whereas the external part may be threatened by atherosclerosis of the vasa vasorum.

Schlatmann and Becker [24] studied aortas of 100 patients with no known aortic disease and observed that the degree of elastic fragmentation was greater in older patients, the changes were more pronounced in the ascending aorta and the arch than in descending aorta, and the internal layer of the media was the most affected.

Larson and Edwards [12] studied 161 necropsies of patients with dissection. All patients with type A dissection had severe histologic changes. Patients with type B dissection with and without Marfan syndrome had few cystic changes in the descending aorta and many atherosclerotic lesions.

The typical histologic findings of tunica media degeneration detected in patients with dissection can also be observed in elderly patients and hypertensive patients without dissection. In this respect, many authors consider the changes in the media to result from the mixture of damage and repair lesions produced by haemodynamic aggressions repeated throughout the pa-

tients' lives [24]. The histologic difference between aortas with and without dissection may be more quantita- tive than qualitative and aorta wall anomalies in young patients with Marfan syndrome represented the accel- eration in those that appear with ageing.

16.4 Pathophysiology

16.4.1 Mechanical Factors

Several types of mechanical forces that act on the aorta wall have been described: (1) those related to the vessel curve in certain sites; (2) those produced by the radial impact of the pulse pressure wave; and (3) the shearing longitudinal effect of blood flow.

The heart, ascending aorta and arch forma relatively mobile complex that hangs from the supraaortic trunks.

In contrast, the descending aorta is more fixed on the left side of the spinal column. Flexion forces are maximum in the root and aortic isthmus. It is in these sites where the dissection entry tear is most frequently located. Tears are believed to occur in these areas since torsion movement of the aortic annulus provokes an ad- ditional downward traction of the aortic root and provokes an increase in the longitudinal stress in this segment; and in the isthmus area where the tension is due to the union of the aortic arch, which is relatively mobile, with the descending thoracic aorta, which is quite fixed [20]. Several studies have proved that the reduc- tion in pulse pressure wave inhibits dissection progression [27]. The pulsatile nature of aortic flow is one of the principal causes of dissection progression. The aorta is quite resistant to increases in static pressure. Ex- perimental studies show that the aorta only dissects when flow is pulsatile [20]. The longitudinal shearing forces that act on the direction of blood flow are directly related to the pressure gradient between the two aortic lumina, which is small and due to decreased pressure in the true lumen by the Bernoulli effect at high velocity. In the false lumen, there is not the same decrease in pressure during propagation of the dissection since it does not carry a net flow.

16.4.2 Morphologic Aspects

All dissections are characterised by a separation of the media layer of variable circumferential and longitudinal extension. Furthermore, a tear of the intima and media (entry tear) is observed in classic aortic dissection (Fig. 16.2). In the classic series, an entry tear could not be identified in less than 5% of necropsies. This intimomedial tear is, in general, perpendicular to the long axis of the aorta. Blood enters through this orifice, separat-

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ing the media into two layers over a distance that varies in each case. The most internal two thirds of the media layer form, together with the intima, the internal wall of the false lumen. This flap is formed not only by the intima but also by the internal layer of the capa media and, consequently, should be termed intimomedial flap.

The internal wall of the false lumen is thicker than the external wall which comprises the external part of the media and the adventitia.

Once the intimomedial tear has been produced, blood enters under pressure and a longitudinal dissection of the whole aorta may occur in a few seconds [21]. The dissecting haematoma can evolve to external false lumen rupture, reentry tear formation or end in a cul-de-sac. Thinness of the external wall of the false lumen is the anatomical finding related to aortic rupture.

The thinner it is, the greater the probability of aortic rupture will be. It may also be assumed that the thicker it is, the thinner the intimomedial flap will be and, consequently, the greater the probability of a reentry being produced [21]. Rupture of the false lumen is the most frequent cause of death. The rupture site is usually near the entry tear and, therefore, the segment which breaks most frequently is the right anterolateral wall of the ascending aorta. Blood extravasation usually accumulates in the pericardial sac (haemopericardium), and death fromcardiac tamponade is therefore frequent. If the arch ruptures, a haemomediastinum is usually produced; if it is the descending aorta, a left hemithorax;

and if it is the abdominal aorta, a haemoperitoneum.

On occasions, a wide intimomedial tear may serve as an entry tear and reentry of the false canal. In this case, flow in the false canal is usually anterograde and retrograde [21]. When the dissecting canal ends in a cul-de- sac with no exterior rupture of a reentry tear, anterograde and retrograde flow may be observed (Fig. 16.3);

however, in some cases, particularly if the entry tear is

small, an acute total thrombosis of the false lumen might be produced. Diagnostic techniques have difficul- ties in distinguishing the latter froman intramural haematoma. Throughout the aorta, the portion of dissected aortic circumference is quite predictable since, albeit variable, the longitudinal course of the dissection has a determined trend. When the dissection begins in ascending aorta, the dissecting haematoma involves the larger curve of this arch and affects the right lateral region of the ascending aorta. Fromthe isthmus, the dissection usually adopts a spiral route. The infradiaphrag- matic and infrarenal aortas tend to dissect their left posterior region, leaving the right anterior vessels in- tact. Further down, the dissection usually affects the two iliac arteries, though more often the left one. The common femoral artery rarely dissects. For this reason, although any of the aorta branches can be affected by dissection, the right coronary artery, the supraaortic vessels, the left intercostal arteries, the left renal artery and the left common iliac artery are more frequently affected. On the other hand, the left coronary artery, the coeliac trunk, the superior mesenteric artery and the right renal artery are usually connected to the true lumen. Ambos et al. [1] qualified chronic dissection with reentry as a ªhealed dissectionº. Nevertheless, the false lumen is usually larger than the true lumen; with time, the former dilates and becomes tortuous. Aneurysmal dilatation of the false lumen is the most frequent late complication of dissection. The larger the aneurysm, the more likely rupture of its wall will be (Fig. 16.4).

Some publications suggest that a reentry tear in pa- Fig. 16.2.Transoesophageal echocardiography shows a large en-

try tear (greater than 10 mm) localised distally to the subclavian artery in type B dissection

Fig. 16.3. Computed tomography study showing a type A dissection with an entry tear in the ascending aorta (black arrow) and a false lumen ending in a cul-de-sac due to a total thrombosis of the abdominal false lumen (white arrow). TL true lumen, FL false lumen

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tients with chronic dissection does not protect against rupture of the false lumen.

16.4.3 Mechanism of Vascular Complications

The mechanism by which dissection can affect any of the branch arteries fromthe aorta is twofold:

1. Dynamic obstruction. In this case, the obstruction of the compromised vessel is dynamic, the true lumen is in the form of a ªCº and the intimomedial flap has a concave arrangement towards the false lumen. This mechanism has been described from aor- tographic and computed tomography (CT) findings and, characteristically, at surgery or during necropsy, there are no data on the previous existence of arterial obstruction. Usually the true lumen is compressed by the false lumen and this generates an obstruction of the arterial ostia (Fig. 16.5).

2. Static obstruction. Here, two situations should be distinguished ± arterial dissection and location of the origin of the arterial branch in the false lumen.

In the first case, the intraarterial dissecting haematoma may obstruct the vessel lumen or intraarterial rupture of the haematoma may be produced, with formation of the dissection reentry tear. In some cases, the circumferential laceration of the arterial ostiummay be accompanied by a circumferential dissection of the proximal segment of the artery and, thus, the intimomedial flap of the arterial branch

may be distally impacted, affecting arterial flow. In many cases, obstruction of arterial branches is twofold: static and dynamic.

Ischaemia of the lower limbs as a complication of dissection has been described in up to 26% of patients with dissection and may occasionally be isolated [19], with no other clinical data of suspected dissection. Ce- rebral vascular accident is associated with increased early mortality in patients with dissection. The most frequently involved arteries of the supraaortic trunks are the innominate artery and the left common carotid artery. The left subclavian artery is less frequently affected than the right subclavian artery. The characteris- tic pattern of dissection propagation consists of involve- ment of the left side of the descending aorta which occurs preferably in the branches which originate on this side of the aorta. The left kidney is the organ at greatest risk of ischaemia. Kidney failure and mesenteric infarct have been identified by different groups as risk factors of early death in patients with dissection [6]. If the dissecting haematoma only affects the intercostal arteries on one side (generally the left), the arteries on the other side perfuse the spinal cord; however, if the haematoma affects the arteries on both sides, a medul- lary infarct will be produced.

The inexistence of a reentry tear in the distal aorta or its branches may jeopardise perfusion through the true lumen to such an extent that it collapses from the pressure or thrombosis of the false canal.

Fig. 16.4.Type B dissection by MRI. Large false lumen presenting high risk of aortic rupture due to high wall stress of the dilated false lumen (arrows)

Fig. 16.5.Compression of the ostium of the superior mesenteric artery (SMA) by the intimal flap secondary to severe compression of the true lumen by the false lumen (arrow)

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16.4.4 Aortic Dissection Evolution

Despite the significant advances in imaging techniques and therapeutic procedures in the last decade, dissection mortality in the first month of evolution continues to be very high: 25±30% for patients with type A dissections and 10±14% for patients with type B dissections [8]. Acute aortic dissection has a high risk of complications, clearly higher when the ascending aorta is affected than when it occurs distally to the innominate trunk. Risk factors for complications and mortality for patients with type A dissection are shock, hypotension and tamponade [14]. In contrast, in patients with type B dissection, mortality is related to shock and vis- ceral ischaemia [16].

Once the acute phase has been overcome, the prognosis of dissection is clearly better, but at 10 years the survival rate averages 44% for patients with type A aortic dissection and 32% for patients with nonoperated type B dissection [16]. Mid-to-long-termmortality does not depend on aortic disease alone but also on different factors such as age, associated diseases and comorbidity.

One of the factors better related to aortic rupture evolution is aortic dilatation. Juvonen et al. [11] fol- lowed 50 type B dissections. At a mean of 3 years, 18%

presented aortic rupture and 20% required elective surgery for rapid expansion of the aneurysm. Variables associated with aortic rupture were age, chronic obstruc- tive pulmonary disease and elevated mean blood pressure. The last median descending aorta diameter before rupture in the rupture group was 54 mm. This study suggested that the continued patency of the false lumen was not an important predictor of rupture. On the other hand, two further studies showed aortic dilatation predictors to be an aorta diameter over 40 mm during the acute phase and an entry tear in the thoracic aorta or the presence of flow in the false lumen [13]. Neverthe- less, the absence of flow in the false lumen in 55% of cases is surprising, and raises the suspicion that many of these cases were, in fact, intramural haematomas.

Sueyoshi et al. [25] recently reported the follow-up by CT of 62 type B dissections, 75% of segments increased in size during a mean follow-up of 4 years. The presence of blood in the false lumen was the only significant risk factor, showing an increase of 3.3 mm/year, while in the group without flow in the false lumen the increase was 1.4 mm/year. In this study, total false lumen thrombosis was present in 51 of 176 cases. An- other interesting finding was that the growth rate of aortic dissections in the thoracic aorta was higher than that of the abdominal aorta: 4.1 and 1.2 mm/year, re- spectively.

Previous studies revealed that aortic diameter was a strong predictor of enlargement and rupture. The maximum aortic diameter was considered to be between 40

and 60 mm [13]. These results can be explained by the law of Laplace, which states that the perpendicular stress on a cylinder is directly proportional to the pressure exerted by the fluid content and its radius and is inversely proportional to wall thickness. This means that the larger the diameter, the faster the growth rate will be if the pressure is constant.

Some results have shown that age is a significant risk factor for an increase in diameter in univariate analysis [11]. Anatomically, elasticity and distensibility of the aorta decline with age. Such changes occur even in normal healthy adults and, for some reasons, these changes appear earlier and are more progressive in men than in women.

Erbel et al. [3] proposed a classification based on dissection extension and the presence and location of an entry tear. Patients with aortic dissection types with absence of communication or with localised retrograde flow in the descending aorta alone had better survival.

Thrombosis formation in the false lumen was a predic- tive factor of good prognosis. Although the results of this European multicentre study contribute very interesting data, they are limited by the single use of mono- plane transoesophageal echocardiography (TEE), which limits visualisation of entry tears located in the distal ascending aorta and the proximal arch.

Some studies have shown that survival at 6 years is worse for patients with type B dissections than for patients with operated type A dissections [4]. Ergin et al.

[4] reported the survival rate of patients with operated type A dissections without false lumen flow to be 85%

versus 62% in the group with false lumen flow. Notably, in this series, false lumen flow was absent in 53% of cases [15]. In other studies, total obliteration of the false lumen in the descending aorta was achieved in only 10±20% of operated type A dissections [4, 15]. The better prognosis of operated type A dissections could be due to a smaller entry tear than for type B dissections.

16.4.5 Aortic Dilatation and Complications in Chronic Phase

The pathophysiology of aortic dissection in the chronic phase is essential to foresee possible complications and to select patients who are candidates for more aggres- sive treatment. Most complications occur in the acute phase and mortality continues to be relatively high, owing essentially to comorbidity due to associated diseases, aortic rupture due to progressive dilatation, or extension of the dissection.

Dilatation of the aorta in the long-termevolution of aortic dissection has been studied by our group.

Although aortic diameters were determined by CT or MRI, haemokinetic variables of the aorta were defined

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by TEE performed prior to discharge. Forty-seven patients had type B dissections and 40 had operated type A dissections. The maximum aortic diameter presented dilatation between 0.2 and 6 mm/year. Dilatation of the descending aorta was greater in medically treated type B dissections than in operated type A dissections.

Variables related to greater aortic dilatation were entry

tear size, maximum descending aorta diameter in the subacute phase and the high-pressure pattern in the false lumen. An entry tear size over 10 mm implies higher risk of false lumen enlargement. Maximum aortic diameter in the subacute phase was a significant predictor of progressive dilatation since, according to the law of Laplace, maximum aortic diameter is the factor Fig. 16.6.High-pressure pattern in the false lumen owing to a large entry tear and a small distal reentry tear. Transoesophageal echocardiography shows how contrast in the false lumen has a low rate of progression compared with that in the true lumen. TL true lumen, FL false lumen

Fig. 16.7.Low-pressure pattern in the false lumen owing to similar-sized entry and reentry tears. By transoesophageal echocardiography contrast moves with similar velocity in the true lumen and the false lumen. TL true lumen, FL false lumen

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influencing increased wall stress. Finally, increased false lumen pressure was another important factor implying false lumen enlargement. The high false lumen pressure was due, in the majority of cases, to a large entry tear without distal emptying flow or a reentry site of similar size. It is often impossible to identify the reentry tears;

thus, they were considered to be indirect signs of high false lumen pressure by TEE when the velocity of the echocardiographic contrast in the false lumen was slow and the contrast moved up and down for several cycles (Figs. 16.6, 16.7). MRI also permitted assessment of time and false lumen flow at different levels of the aorta, which helps to define whether the sizes of the entry and reentry tears are similar.

A suspicious, though not very specific, finding of high pressures in the false lumen is when the true lumen is compressed by the false lumen and the ratio is under 1:5. The lesser dilatation of the false lumen in operated type A dissection patients is due to the small entry tear size and the tear is often located in the distal part of the ascending aorta prosthesis. These patho- physiologic data of aortic dissection evolution may be of great interest for selecting asymptomatic patients who would benefit more from endovascular treatment in the subacute phase of aortic dissection.

On the other hand, evolution of dissection at some level of the aorta occurs in approximately 25% of haematomas [5]. The majority of dissections are localised and only are 20% classic. Extension, echolucency and thickness of the haematoma are variables related to aortic dissection evolution, most of which are asymptomatic and evident in the first 3±6 months after onset of the intramural haematoma. Small intimal tears can be iden-

tified on TEE and in a small proportion of cases trigger a dissection. Localised dissections (Fig. 16.8) evolve to pseudoaneurysm, disappearance of the intimal flap and produce an ulcerlike image. Some authors have suggested poor prognosis for haematomas presenting this evolution. In our series, two of the 17 images had dis- appeared at 6 months and only one case presented progressive dilatation and was treated with endovascular therapy.

Knowledge of the pathophysiology of aortic dissection is essential to understand the short- and long-term evolution, complications and most appropriate therapeutic management. Genetical or acquired structural al- terations, secondary to the atherosclerotic process, are the causal substrate of most dissections. Nevertheless, the most therapeutically controllable variables are those secondary to the decrease in wall stress, both by hypertensive therapy and by surgical or endovascular treatment.

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