• Acute aortic dissection

Risk assessment and management of type B aortic dissection.

In acute aortic dissection, the aortic wall initially tears from the inside, resulting in separation of the wall layers. The result: an additional lumen is created. What to do?

In acute aortic dissection, there is initially a tear of the aortic wall from the inside and a resulting separation of the wall layers (intima-media of adventitia) through which an additional lumen (which we call the true lumen) is created in addition to the original vessel lumen (which we call the false lumen). The clinical correlate is acute, often migratory chest pain. The classic classification gives a dissection involving the ascending aorta, the definition type A dissection, a dissection involving the aortic arch without the ascending aorta; the definition type non-A-non-B dissection, and a dissection involving the descending aorta, the definition type B dissection [1].

The location of the primary tear (entry) determines the clinical course of acute aortic dissection. The essential principle of the underlying disease is that, after the primary entry has occurred, propagation in the aortic wall occurs with and against the blood flow, leading to widening of the dissection [2].

The location of the primary entry can often be assigned to an aortic segment. However, only its final extension along and against the blood flow determines the clinical course, our definition of the disease (type A, type non-A-non-B or type B) and the resulting immediate or delayed invasive therapeutic measure in addition to drug therapy which initially mostly consists of lowering the arterial blood pressure [3,4].

Propagation against the bloodstream

Acute dissection with a primary entry in the ascending aorta, regardless of propagation and extent, is always referred to as type A dissection, and acute surgical repair is the gold standard because retrograde propagation into the aortic root leads to acute high-grade aortic valve regurgitation due to commissural prolapse and transudation through the aortic wall leads to pericardial tamponade. In this case, aortic rupture is a metachronous process that may occur immediately, with a time delay, or in individual cases not at all [5].

A primary entry in the descending aorta is referred to as a type B dissection, but again, the location of the primary entry and the extent make all the difference for treatment, or whether an acute type B dissection has already caused complications, or complications are expected, or whether it is likely that the dissection will be uncomplicated. We refer to the occurrence of organ malperfusion due to dynamic or static obstruction by the dissecting membrane of lateral or terminal branches of the aorta (spinal cord, gastrointestinal, kidney, and extremities) as “complicated”; however, persistent pain symptoms (pain is a very good biomarker in the course of the first few days) and a difference in blood pressure between the upper and lower extremities (in the sense of pseudocoarctation caused by the dissecting membrane) are also considered “complicated” courses. Any form of bloody pleural effusion and, understandably, any form of covered and uncovered rupture are also considered “complicated.” If all the previously mentioned symptoms are absent, we speak of an “uncomplicated” type B dissection provided that the total diameter of the dissected aorta does not exceed 40 mm.

As “potentially complicated” we consider dissections that fulfill morphological criteria, which often precede the previously mentioned complications, the most important are localization of the primary entry at the inner side of the aortic arch (because in retrograde propagation no anatomical barrier can stop the progression of the process into the aortic arch and into the ascending aorta, which is often prevented at the outer side of the arch by the head and neck vessels) and a short distance between the primary entry and the left subclavian artery (distances less than 2 cm are considered short here) [2,6,7].

Propagation along the bloodstream

For many years, our main focus was almost exclusively on propagation along the blood flow, which is intuitively correct, since a primary entry located immediately at the level of the left subclavian artery shows its effect only in downstream aortic segments, mainly at the level of the visceral and renal vessels, by collapse of the true lumen with malperfusion of the affected end organs. [3,8].

Mechanisms for organ malperfusion

The main cause is static or dynamic compression of the true lumen. The presence or absence of malperfusion is highly dependent on the location of the primary entry and on the dynamics of the dissecting membrane over the cardiac cycle, with the location of the primary entry in angulated aortic segments (such as the aortic arch and proximal descending aorta) showing a stronger correlation with the occurrence of malperfusion [2–5].

Mechanisms for aneurysm formation

The main reason of aneurysm formation is blood pressure difference between true and false lumen and the angle at which blood flow hits the aortic wall. These factors are in turn determined by the localization of the primary entry and also by the number and size of communications between the lumina (formerly also referred to as multiple entries and reentries). Another essential factor is the size of the most distal communication between the lumens, or as the most distal tear (reentry), because – if the reentry is small or absent – the mean arterial blood pressure in the false lumen may be significantly higher than in the true lumen, resulting in an increase in peripheral resistance [9,10].

Active therapeutic strategy

The basic principle of any active therapeutic strategy is always the closure of the primary entry either by resection and vascular replacement in open surgery or by exclusion of the primary entry from the blood stream by insertion of a stent-graft either as “Thoracic endovascular aortic repair (TEVAR)” or in open surgery by the so-called Frozen Elephant Trunk (FET) technique. (Fig. 1). The resulting approximation of the intima-media cylinder and adventitia results in decompression of the true lumen with simultaneous restoration of regular transverse diameters of the downstream aortic segments and thus stabilization of the dissecting membrane In normal cases, this is sufficient for the acute situation, however, the number and size of interluminal communications also have an impact, so that it is always necessary to perform stent-graft lengthening, since large interluminal communications may continue to provoke persistent malperfusion syndromes despite successful closure of the primary entry. Therefore, in individual cases it is also necessary to place non-covered (open) stents over the outlets of the visceral and renal vessels.

Departure of the large lateral branches from the true and/or false lumen

In the course of the acute event, all branches initially continue to depart from the true lumen, and the intima/media cylinders of the large lateral branches initially extend like tubes through the newly formed false lumen to the respective end organ. Since these intima/media cylinders are very fragile, they often rupture sooner or later within the false lumen, which then morphologically results in the circumstance of departure from the false lumen. It is essential to be aware that this is a secondary effect and that the resulting communication between the lumina is always the size of the exit diameter of the side branch. For this reason, blood flow via this communication between true and false lumen is sufficient for end-organ perfusion in most cases, and occlusion of the primary entry with suppression of perfusion in the false lumen has no detrimental effect on blood flow to the respective end organs regardless of whether open surgery, TEVAR, or the FET technique has been used. [12].

Summary of pathophysiology

One should always be aware that the currently used definitions (type A, type non-A-non-B, type B dissection) are only approximations to describe the same pathophysiological process in which the beginning (primary entry) and the respective end (along and against the blood flow) of the dissection make the fundamental difference in the clinical course and the need for an active treatment strategy.

What is the best treatment strategy for uncomplicated type B dissection?

For many years, acute type B dissection was interpreted as the “harmless” aortic dissection in its clinical course (especially in comparison with type A dissection, which often progresses dramatically), because action was rarely required in the acute situation [13]. However, a closer look into the natural history of the disease has shown that a large number of patients develop complications at given time points and then require active treatment [14]. Causes and timing have been found to vary with organ malperfusion, retrograde propagation into the aortic arch and ascending aorta (retrograde type A dissection) being prominent in the acute phase of the disease and then aneurysm formation predominating in the subacute and chronic phases [15]. The answer to the question of which patients will follow which primary course and who will develop secondary complications has been demonstrated primarily in morphologic and functional parameters and has led to the definition of high-risk groups [16,17].

Timing of the disease

The acute phase is defined from the immediate onset of the primary pain event to day 14 thereafter, between day 15 and day 90 we refer to it as the subacute phase, and from day 91 we refer to it as the chronic phase [13].

INSTEAD trial

The INSTEAD trial (Investigation of STEnt Grafts in Aortic Dissection) and long-term follow-up (INSTEAD-XL trial) prospectively compared whether additional prophylactic stent-graft implantation (TEVAR) has a benefit compared with optimal drug therapy alone in patients with uncomplicated type B dissection between 2 and 52 weeks after the acute event. After 5 years, a significantly positive effect was shown in patients receiving additional prophylactic TEVAR in terms of aortic-related survival and on progression of the underlying disease [18,19].

ADSORB trial

The ADSORB Trial (Acute Dissection Stent Grafting or Best Medical Treatment) prospectively compared whether additional TEVAR has a benefit compared with optimal medical therapy alone in patients with acute uncomplicated type B dissection between 0 and 2 weeks after the acute event. The primary end point here was a combination of thrombosis status of the true lumen and, aortic dilatation or adverse aortic events (rupture) at one year. The conclusion drawn was that TEVAR could achieve both positive aortic remodeling and diameter reduction with consecutive (intentional) thrombosis of the false lumen, but long-term results had to be awaited, which are not available at this time [20].

These two studies represent the highest level of evidence available at this time. The INSTEAD XL Trial in particular has led to a modification of the latest ESC Aortic Guidelines and has prophylactically elevated TEVAR in uncomplicated type B dissection to a Class IIA, Level of Evidence B recommendation.

Natural history of uncomplicated type B dissection

After the acute phase, chronification occurs, with the dissecting membrane undergoing a transitional phase between the highly elastic and fragile acute state to a static state. The effect of complete reapposition of wall layers is best in the first few weeks after the acute event [21]. It is very rare for complications such as organ malperfusion or retrograde propagation into the ascending aorta (retrograde type A dissection) to still occur at this stage; however, there is always an increase in the maximum transverse diameter of the aorta. This circumstance of diameter increase can be anticipated by morphological criteria or traced by computed tomography angiography (CTA) controls and can then be stopped by TEVAR at an early stage and in the best case reversible [16].

Optimal treatment strategy for acute uncomplicated type B dissection.

Based on the currently available evidence, it is correct to recommend optimal drug therapy as the basis of treatment for any acute type B dissection. Accurate morphologic analysis allows identification of “high-risk” subgroups that benefit prognostically from early TEVAR. This is ultimately a very large number of patients, up to 80% in some collectives. The INSTEAD Trial and its 5-year follow-up (INSTEAD XL Trial) provide us with the best currently available evidence for the benefit of an endovascular strategy in patients with uncomplicated type B dissection. Prophylactic TEVAR should be considered if the anatomy is suitable [19]. In recent years, this expanded knowledge has already found its way into international guidelines and expert consensus documents [22,23].

 

Case study 1 – Acute complicated type B dissection

A 57-year-old man suffers sudden acute chest pain that begins between the shoulder blades and radiates migratory to the groin. After 5 minutes, he first develops sensory disturbances and then paraparesis and finally paraplegia of the right lower extremity. The emergency physician called to the scene clinically detects a pulse deficit in the right groin and suspects an acute aortic dissection in view of the wandering pain symptoms and the pulse deficit. In addition, the patient clinically develops an acute abdomen with pain and guarding. He is transferred to the nearest emergency department where a CTA of the entire aorta is performed based on the suspected diagnosis.

Results of CTA: CTA shows a type B dissection with the primary entry located at the inner aortic arch essentially without spacing from the left subclavian artery. There is collapse of the true lumen at the level of the visceral and renal vessels, and the right common iliac artery is also functionally occluded.

Clinical course: Serum lactate increases to 10 mmol/l and diuresis stops. Acute action is required to close the primary entry to decompress the true lumen and restore blood flow to the downstream aortic segments and right lower extremity.

Constellation favoring a primary TEVAR. As part of the diagnosis of CTA, the head and neck vessels were also examined; the left vertebral artery is small and does not contribute to the competence of the circle of Willisi. In this constellation, primary TEVAR with overstenting of the left subclavian artery outlet can be performed to resolve the acute situation, the likelihood of triggering acute upper extremity ischemia is low, but peripheral oxygen saturation measurement of the left arm should be performed and the further procedure should additionally depend on the clinical course (exertional claudication).

Constellation favoring TEVAR and simultaneous revascularization of the left subclavian artery: The left vertebral artery is a very large vessel and the circle of Willisi is interrupted, thus- in the case of hypoplastic right vertebral artery, the left is of fundamental importance. Therefore, carotid-subclavian bypass is performed before stent-graft implantation to preserve posterior cerebral circulation and to maintain inflow into the anterior spinal artery (avoiding hindmarch ischemia).

Constellation favoring primary FET implantation: The patient has an ascending aorta and an aortic arch aneurysm with a maximum transverse diameter of 5 cm, which does not provide an adequate proximal landing zone and prevents TEVAR from being performed.

 

“High-risk” subgroups with acute type B dissection- localization of primary entry.

The location of the primary entry at the inner side of the aortic arch has been found to be one of the most significant morphologic risk factors for the preexistence or for the occurrence of complications of acute type B dissection; this is especially true for the occurrence of organ malperfusion and for retrograde type A dissections within the first 14 days after the acute event [2,16,17].

Distance between the primary entry and the exit of the left subclavian artery

The distance between the primary entry and the exit of the left subclavian artery is also a significant predictor with the risk decreasing significantly with greater distance [16, 24-26].

Size of the primary entry

The size of the primary entry is also prognostically relevant, especially with regard to early increase in the maximum transverse diameter of the aorta; above 10 mm maximum transverse diameter, the risk increases significantly for early aortic expansion and rupture. The best method, but rarely used primarily for pragmatic reasons, is transesophageal echocardiography (TEE) [25]. The reason for this is also due to a blood pressure spike often associated with TEE, which one would generally want to avoid in aortic dissection.

Total diameter of the aorta and diameter of the false lumen

An overall diameter of 40 mm or greater initially measured at diagnosis of CTA and an initial diameter of the fibrous lumen equal to or greater than 22 mm have also been shown to be predictors of size increase over time and warrant endovascular stent-graft placement [17,27,28].

Number and size of communications between lumina

The number and size of communications between lumina throughout the thoracoabdominal aorta have also been shown to be major determinants of size increase over time. Even after TEVAR, large-caliber communications between lumens distal to the stent graft may functionally act like a new primary entry. A similar mechanism can be observed when, after TEVAR, the dissection membrane at the distal stent-graft end tears inward into the false lumen due to excessive shear forces (usually with oversized stent-graft), then this is referred to as distal Stent-graft Induced New Entry-(dSINE) [29,30].

Thrombosis of the false lumen to varying degrees

Partial thrombosis of the false lumen has also been shown to be a prognostic surrogate for adverse outcome. Partial thrombosis can often be characterized as a flow phenomenon with more modern imaging, but the hypothesis of increased mean arterial blood pressure in the false lumen due to delayed outflow (small distal interluminal communication) remains the same because peripheral resistance is increased in the false lumen [10].

TEVAR for every patient with uncomplicated type B dissection?

The purpose of prophylactic TEVAR remains to avoid later aneurysm formation and associated late complications, since malperfusion and spontaneous retrograde type A dissection occur only during the acute phase. However, retrograde type A dissection can also occur in the setting of TEVAR, and this circumstance, in combination with other very rare but occurring procedure-related complications such as stroke and symptomatic spinal cord ischemia, are the reasons why the indication must continue to be well justified. An ectatic ascending aorta, an ectatic aortic arch, and extensive transposition procedures to achieve an adequate proximal landing zone are additional risk factors [31,32].

Case study 2 – Acute uncomplicated type B dissection

A 64-year-old woman experiences acute chest pain that begins between the shoulder blades and continues to diaphragm level. She loses consciousness for 30 seconds, then the pain gets better. The emergency physician makes a suspected clinical diagnosis of acute coronary syndrome and refers the patient to the nearest emergency department with a catheter station for further diagnosis.

Further examinations: A blood draw is performed, cardiac enzymes are normal, but D-dimer is elevated. CTA is performed to rule out pulmonary embolism or aortic dissection. CTA shows a type B dissection with a primary entry at the aortic arch exterior without evidence of malperfusion.

constellation that favors a primarily conservative approach: The distance of the primary entry to the left subclavian artery is 3 cm, the maximum transverse diameter of the primary entry is 5 mm, the total diameter of the aorta is 37 mm, and the diameter of the false lumen is 16 mm. There are no imaging or clinical signs of malperfusion. Thus, a low-risk situation exists in this constellation and a primarily conservative approach with optimal drug therapy and control CTA are initiated.

Constellation favoring prophylactic TEVAR:

  • The primary entry is at the outside of the aortic arch, but the distance to the left subclavian artery is only 3 mm, and the total diameter of the aorta is 47 mm with a rapid progression between diagnostic and control CTA by 8 mm within a few days. The diameter of the false lumen is 38 mm and the true lumen at the level of the visceral and renal vessels is 5 mm.
  • The primary entry is located at the inner side of the aortic arch and the distance between the primary entry and the left subclavian artery is 7mm, the true lumen has a maximum transverse diameter of 10mm.

These two constellations may be considered “high-risk” despite formal “uncomplicated” type B dissection, and early TEVAR therapy to close the primary entry should be performed. Basically – if TEVAR is performed under planned circumstances, a CSF drain should be placed prior to the procedure for spinal cord protection (the CSF drain is the fasciotomy of the spinal cord).

Risk assessment of potential complications associated with therapy

The residual risk of stroke is in the low single-digit percentage range. In this case, an accurate statement can be made in advance by assessing the diagnostic CTA with regard to arteriosclerotic lesions near the outlets of the supraaortic branches and thus comprehending or ruling out a potential embolic risk by catheter manipulation.

A major issue remains symptomatic spinal cord ischemia of varying degrees, ranging from sensory disturbances to complete paraplegia. Here, a quantum leap in knowledge of the underlying mechanisms and their prevention has occurred in recent years. In this regard, it should be noted that the spinal cord, analogous to Riolan’s arcade of visceral arterial supply, has extra- and intraspinal back-up mechanisms that can compensate for acute and chronic inadequate perfusion to some extent. First, the “four-territory” concept will be discussed here [33]. This presupposes the anatomical existence of four arterial tributaries of the spinal cord, which are equal in value, namely the subclavian artery (with its continuation into the vertebral artery and thus into the anterior spinal artery, the thoracic segmental arteries (intercostal vessels), the lumbar segmental arteries (lumbar vessels) and the internal iliac artery, all of which form tributaries to the anterior radiculomedullary arteries and thus to the anterior spinal artery. If occlusion of one of these arterial tributaries occurs (as an example, covering multiple thoracic segmental arteries with a stent-graft), this does not significantly affect an increased risk of symptomatic spinal cord ischemia. However, if two tributaries are occluded at the same time (e.g., additional overstenting of the left subclavian artery), this significantly increases the risk of paraplegia because this extent of reduced blood flow can no longer be compensated. Even a single episode of marked hypotension may already increase the risk of paraplegia (e.g., acute TEVAR in rupture). Nature has the ability to compensate for acute inadequate blood supply to, for example, the thoracic section of the spinal cord via the autochthonous back muscles and to induce sprouting of capillary vessels in the inadequately supplied area [34]. Within the spinal cord there are even -preformed collateral vessels that can step in in such situations, but the capacity of this collateral network is just limited and any form of intra- or postoperative hypotension contributes to the risk [35].

An extremely helpful measure in the elective situation for the prevention of symptomatic spinal cord ischemia is the application of a cerebrospinal fluid drainage before surgery. Every tissue, including the spinal cord, reacts to acute ischemia with tissue swelling, but the spinal cord is very limited in its ability to swell in the narrow spinal canal due to the presence of its carrier fluid, i.e. the cerebrospinal fluid, and – analogous to limb ischemia without fasciotomy – the capillary bed is squeezed and a vicious circle ensues, which then ends with organ loss; in this respect, the cerebrospinal fluid drainage can be described as a fasciotomy of the spinal cord [36]. Even in cases of secondary symptomatic spinal cord ischemia, e.g., a few days after surgery, the application of a CSF drainage is often associated with impressive clinical success.

Another very useful monitoring measure in TEVAR is the measurement of motor and somatosensory evoked potentials (MEPs/ SSEPs) [37]. This makes it possible to detect ischemic areas functionally at an early stage and to counteract them accordingly, e.g. by increasing the mean arterial blood pressure or by raising the hematocrit; these measures can also be very helpful in the early phase of acute spinal cord ischemia.

In recent years, the FET technique has been established in the treatment of a variety of acute and chronic thoracic aortic pathologies but also in patients with complex type B dissection but without an adequate proximal landing zone for stent-graft anchorage. Although this indication is, rare, it should be considered if the assessed risk for retrograde type A dissection is high. The results of this procedure in this indication are very good in experienced centers [33]. Classical open surgery via left lateral thoracotomy, on the other hand, is no longer of any importance today.

Open fenestration surgery, in which the dissecting membrane is partially excised, is also obsolete today. Furthermore, the sole interventional treatment of a malperfused end organ has no value, because the cause of malperfusion would still exist due to the open primary entry and would remain unresolved.

 

 

Choosing the right time for treatment

Currently available evidence suggests that, assuming clinical stability, a longer interval between acute event and TEVAR (greater than 2 weeks) is favorable in terms of procedure-related complications [38,39].

The diagnosis of acute and subacute uncomplicated type B dissection requires a complex evaluation algorithm in which the surrogate parameters for early and late complications should be evaluated before the diagnosis of “uncomplicated” type B dissection is made. Figure 2 shows the diagnostic algorithm that is also recommended by the major professional societies to define these high-risk subgroups and then to follow the appropriate treatment path.

Take-Home Messages

  • The incidence of truly uncomplicated type B dissection is lower than previously thought.
  • A stepwise diagnosis of exclusion to confirm or rule out “high-risk” surrogates should be applied using CT angiography before establishing the diagnosis of “uncomplicated.”
  • The potential of the aorta for positive remodeling (diameter decrease, approximation of the wall layers) decreases with time, this should be taken into account when choosing the time of treatment (“window of opportunity of 90 days”).
  • Attention to maintaining spinal cord perfusion via the four major arterial tributaries to the greatest extent possible is a critical factor in reducing the residual risk of symptomatic spinal cord ischemia.
  • CSF drainage is a highly effective measure for the prevention and also the therapy of symptomatic spinal cord ischemia.
  • In patients who require treatment but are at high risk for retrograde type A dissection, the FET technique should be considered.

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CARDIOVASC 2022; 21(3): 6-12

Autoren
  • Prof. Dr. med. Martin Czerny; MD, MBA, FESC, FEBCTS, FEBVS
  • Prof. Dr. med. Christoph Nienaber
Publikation
  • CARDIOVASC
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