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David Procedure—Reconstruction of the Native Insufficient Valve Chapter | 43 477
FAV = X1+ X2+ X3+ C4+ A5+ A6+ A7+ C8+ C9+ A10,
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probability of reimplantation success depends mainly on the morphologic constellation of all the three aortic cusps. The
AVSR formula could be modified in this case as follows:
where X
, three aortic cusps with possible pathology; C4, all commissures on the same level (height)—constant; A5,
1–3
sufficient effective height; A
, VAJ, aortic annulus; C
6–7
, aortic root, STJ; A10, virtual height of commissures/axis of the
8–9
valve; C, constant, prosthesis (choosing of optimal graft); A, adjustable (eH—caliper [6]) or basal purse string suture (VAJ
and aortic annulus), axis of the valve—placement of commissures.
REIMPLANTATION OF THE BICUSPID AORTIC VALVE
BAV is the congenital anomaly with the prevalence of 0.5%–2% in normal population [9]. Regurgitation of the BAV is usually accompanied with aortic root aneurysm (root phenotype); meanwhile, BAV stenosis is more associated with ascending
aortic aneurysm.
Successful reconstruction has to follow these basic recommendations. Long-term stability is attributed to the stability of
VAJ, aortic root, and STJ. According to this, David procedure for reimplantation of BAV seems to offer the best solution,
which meets all the abovementioned criteria for long-term stability. The reconstruction of an incompetent valve is controlled by the anatomic structure of the valve as described by Sievers [10]. Any other orientation as Sievers type 0 required
switch to 180-degree/180-degree orientation. Only this orientation ensures a maximal opening of the valve. The technique
of reimplantation should consider that the nonaxial opening of the AV could produce a rest gradient, although the opening
area is wide enough. The pliability of both leaflets has to be satisfactory. The geometric height of each leaflet must be at
least 19–20 mm. The aim of reconstruction is to achieve the same length of the free margins of both leaflets. The conjoint
leaflet has to be trimmed, the best way without raphe (raphe resection) or extension if needed.
After transverse aortotomy, careful examination of the valve configurations must be done. We should consider the
presence of fenestrations, calcifications, and/or raphe. To consider valve reconstruction, at least one cusp should be in
a good state, i.e., calcification should not be present and sufficient height should be present. In case of presence of such
factors, we could start with root and valve preparation. The aortic root is mobilized and both coronary ostia are freed.
Aortic wall is excised leaving 5–10 mm rim of tissue surrounding the valve and the commissures. The two main commissural sutures are placed, and the gentle traction and orientation of the valve must be changed to 180 degrees/180 degrees
and sufficient cusps material should be available (19–20 mm of geometric height). For a proper assessment of the cusps,
we follow these rules:
l Raphe should be excised when possible (as it reduces the free mobility of the leaflet).
l After raphe excision, enough cusp tissue must be found; otherwise, a substitute tissue material could be used (e.g.,
tissue-engineered scaffold CardioCel [11]).
l In case of cusp calcifications, we recommend a whole replacement of the cusp rather than the calcified part only.
l In case of whole cusp replacement, the same length of free margin of the concomitant cusp is used to minimize the
central plication sutures.
After creating a symmetric bicuspid valve, sizing of prosthesis is performed. Both commissural sutures are passed
through the sizing ring and the desired coaptation is created using a Duval clamp. The depth of the nadirs is checked by
scale on the inner side of the sizing ring. Then, the same principles followed for tricuspid AV are applied for choosing the
optimum size of the prosthesis.
Subannular Teflon-pledged sutures are placed underneath the annulus, allowing it to compress at the part of the conjoint
leaflet and facilitating symmetric 180-degree/180-degree orientation. Teflon-pledged stitches are placed vertically underneath the commissure to minimize the interference with the leaflets; other Teflon-pledged stitches are placed horizontally.
The height of both commissures (distance between the subcommissural Teflon-pledged stitch and the top of commissure) is measured. The Valsalva prosthesis is marked equally creating the new commissure opposite the mean commissure
(180 degrees/180 degrees) and the prosthesis is cut properly using prosthesis cautery. The tourniquet purse string suture is
placed on the basal part of the prosthesis allowing adjustment of the VAJ as a tricuspid AV.
The subannular stitches are passed through the basis of prosthesis (above the purse string suture), inversion of the
commissures in the outflow tract is performed, then the prosthesis is lowered down in position and the sutures are
tied. Both commissures are sutured to the neo-STJ. Then the valve is reimplanted in the prosthesis using 4/0 Prolene
stitch.
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Immediately after reimplantation the high-pressure angioscopy test is performed. The possible prolapse or asymmetry
could be corrected using central plication (using 6/0 Prolene) and angioscopy is repeated. Finally, reimplantation of both
coronary arteries and restoring the continuity of aorta is done.
FAQ
Q1: Does the reconstruction of a BAV considered successful if there is no rest regurgitation at the end of the procedure?
A: Not always. Especially in cases of BAV, a good reconstruction results should involve no rest regurgitation or stenosis.
Q2: Is it good to leave the native orientation of the bicuspid valve?
A: Actually, the switch to 180-degree/180-degree orientation provides a wider opening of the valve area and minimizes the
outflow obstruction, which might be caused by the nonaxial orientation of the valve.
Q3: Is it possible to leave the raphe in situ?
A: The raphe portion creates restriction in the mobility of the conjoint cusp. By changing orientation, the free margin
of the conjoint cusp should be shortened as well. Excision of the unwanted raphe will produce the desired shortening
of the cusp.
Q4: Could a triangular resection and replacement of the leaflet defect using autologous pericardium be a better option?
A: Not really, the two sutures in the center of the leaflet represent “locus minors” of reconstruction because of shrinking
and/or calcification, which was noted in follow-up. We believe that complete replacement of the defected cusp with tissue-
engineered pericardium (CardioCel) [11] could release a better long-term result.
ABBREVIATIONS
AR Aortic regurgitation
AV Aortic valve
AVSR Aortic valve–sparing repair
BAV Bicuspid aortic valve
eH Effective Height
FAV Functioning aortic valve “after valve–sparing procedure”
LCC Left-coronary cusp
LVOT Left-ventricular outflow tract
NCC Noncoronary cusp
RCC Right-coronary cusp
STJ Sinotubular junction
TAV Tricuspid aortic valve
TOE Transesophageal echocardiography
VAJ Ventriculoaortal junction
REFERENCES
[1] Sarsam MA, Yacoub M. Remodeling of the aortic valve anulus. J Thorac Cardiovasc Surg 1993;105(3):435–8.
[2] David TE, Feindel CM. An aortic valve-sparing operation for patients with aortic incompetence and aneurysm of the ascending aorta. J Thorac
Cardiovasc Surg 1992;103(4):617–21. Discussion 622.
[3] Boodhwani M, de Kerchove L, El Khoury G. Aortic root replacement using the reimplantation technique: tips and tricks. Interact Cardiovasc Thorac
Surg 2009;8(5):584–6.
[4] Jaroslav Benedik DW, Konstantinos T, El Khoury G, Jakob H. Novel sizing of Valsalva graft for David operation. 2015. [Video on CTSNet].
[5] De Paulis R, et al. One-year appraisal of a new aortic root conduit with sinuses of Valsalva. J Thorac Cardiovasc Surg 2002;123(1):33–9.
[6] Schafers HJ, Bierbach B, Aicher D. A new approach to the assessment of aortic cusp geometry. J Thorac Cardiovasc Surg 2006;132(2):436–8.
[7] de Kerchove L, et al. A new simple and objective method for graft sizing in valve-sparing root replacement using the reimplantation technique. Ann
Thorac Surg 2011;92(2):749–51.
[8] Tsagakis K, et al. Aortic valve repair: intraoperative evaluation of valve geometry by angioscopy. J Thorac Cardiovasc Surg 2015;149(6):1666–8.
[9] Prakash SK, et al. A roadmap to investigate the genetic basis of bicuspid aortic valve and its complications: insights from the International BAVCon
(Bicuspid Aortic Valve Consortium). J Am Coll Cardiol 2014;64(8):832–9.
[10] Sievers HH, Schmidtke C. A classification system for the bicuspid aortic valve from 304 surgical specimens. J Thorac Cardiovasc Surg
2007;133(5):1226–33.
[11] Neethling WM, et al. Evaluation of a tissue-engineered bovine pericardial patch in paediatric patients with congenital cardiac anomalies: initial
experience with the ADAPT-treated CardioCel(R) patch. Interact Cardiovasc Thorac Surg 2013;17(4):698–702.
Chapter 44
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Acute Aortic Syndrome: Current
Understandings
Simon C.Y. Chow, Randolph H.L. Wong, Malcolm J. Underwood
The Chinese University of Hong Kong, Shatin, Hong Kong SAR
Chapter Outline
Introduction 479
Epidemiology 479
Aortic Dissection 479
Pathophysiology and Hereditary Links 479
History and Clinical Presentation 480
Classifications Systems 480
Diagnostic Imaging 481
Management of Aortic Dissection 482
Type A Aortic Dissection 482
Type B Aortic Dissection 483
Intramural Hematoma 484
Penetrating Aortic Ulcers 486
Management of Penetrating Aortic Ulcer and Differentiation
from Ulcerlike Projections 487
Conclusion 487
References 488
Further Reading 489
INTRODUCTION
The acute aortic syndrome consists of a spectrum of pathologies characterized by disruption in the integrity of the aortic wall,
which may be associated with complications including ischemia, rupture, and death [1]. It comprises classical aortic dissection, intramural hematoma (IMH), penetrating aortic ulcer (PAU), acute aneurysm expansion, and traumatic aortic transection.
Among these entities, aortic dissection is the commonest and entails significant morbidity and mortality if not appropriately treated. The emergence of advanced diagnostics and imaging along with advances in surgical technique and the rapidly
expanding field of endovascular treatment mean we have a better understanding of the pathophysiology, natural history, and
management of acute aortic syndrome, resulting in improved clinical outcomes. In this chapter, we review the epidemiology,
pathophysiology, and clinical management of acute aortic syndrome, with particular emphasis on dissection, IMH, and PAU.
EPIDEMIOLOGY
The incidence of acute aortic syndrome as a whole is about 3–16 per 100,000 people per year. Various population studies esti-
mate an annual incidence between 2 and 3 per 100,000 people, but these estimates could have easily underestimated the true
incidence as data are derived from retrospective registries relying on coding and did not include deaths before admission. A
recent prospective analysis showed the incidence of acute aortic dissection at 6 per 100,000 people [2–4]. This higher incidence
might be accountable by deaths before admission and improved diagnostic imaging. Analysis from the IRAD (International
Registry of Acute Aortic Dissections) reported a mean age at presentation of 63 years and a male predominance of 65% [5,6].
This gender predominance changes in populations over 75 years old, with equal incidence between male and female gender.
Women are less frequently affected, but outcomes are worse because of delayed diagnosis and atypical symptoms.
Aortic Dissection
Pathophysiology and Hereditary Links
Aortic dissection occurs as a consequence of an intimal tear, allowing blood to be redirected from the true aortic lumen to
the false lumen in the medial layer of the aorta. The pathophysiology of acute dissection is affected by histopathology and
New Approaches to Aortic Diseases from Valve to Abdominal Bifurcation. http://dx.doi.org/10.1016/B978-0-12-809979-7.00044-4
Copyright © 2018 Elsevier Inc. All rights reserved.
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genetic components. Cystic medial necrosis is hypothesized to be a cause of dissection, but so far no definite causative
relationship has been established [7]. Aortic dissection can propagate in an antegrade or retrograde manner and can cause
multiple complications depending on the extent and location of the dissection. Complications such as cardiac tamponade,
aortic valve insufficiency, and malperfusion syndrome are a result of extension of dissection. Late complications include
expansion of false lumen, aneurysm formation, and frank rupture. Evidence also reveals a component of low-grade inflammation within the false lumen thrombus that may trigger further weakening of the smooth muscle cells and degeneration
of elastic tissue [8]. Indeed, an increased risk of aortic rupture is seen in patients with inflammatory disorders such as
Takayasu disease, Behçet disease, etc. Aortic dissection is recognized as a disease because of imbalance of the ability of
the aorta to withstand stress. Hypertension is present in up to 75% of aortic dissection, and the other risk factors include
connective tissue diseases, smoking, trauma, and drug abuse such as cocaine and amphetamine.
Hereditary traits linked to acute aortic syndrome usually affect younger patients. About 20% of aortic syndromes are associated with a genetic disorder, which affect connective tissue integrity and vascular smooth muscle function. Examples include
Marfan syndrome, Turner syndrome, Ehlers–Danlos syndrome, and Loeys–Dietz syndrome. In Marfan syndrome, mutations
are located in the fibrillin gene (FBN1). Mutations in the smooth muscle cell actin gene (ACTA 2) are also associated with aortic dissection [9–11]. Furthermore, annulo-aortic ectasia and bicuspid aortic valve are known to predispose to aortic dissection.
The association of genetic syndromes and mutations in genes relating to connective tissue integrity and smooth muscle cells
function suggest an important role of vascular smooth muscles in the response of aortic wall to stress. Recent studies on the
genetics of thoracic aortic dissection reflect that certain specific genetic abnormalities may have a different course of disease
compared with patients without mutations [12,13]. Recently, whole-exon sequencing was applied to detect genetic mutation
on susceptible individuals and showed promising early results; 25% of the patients had genetic mutations relevant to thoracic
aortic disease, and previously unreported variants on genes responsible for thoracic aortic disease have been discovered [14].
This potentially underlines a future therapeutic role of genetic screening for patients with thoracic aortic disease in terms of
providing personalized and tailored management for thoracic aortic diseases with different genotypes.
History and Clinical Presentation
Early detection is key in management of aortic dissection, and prompt appropriate management can prevent major complications and mortality. The most frequent presentation is sudden-onset severe chest or back pain. Affected patients often
complain that the pain is the worst ever experienced and reaches maximal intensity at the outset. The pain may migrate to
the lower back from the chest. Other signs and symptoms include pulse deficit (30%), focal neurologic symptoms (17%),
syncope, and limb weakness [15]. New-onset aortic regurgitation, pericardial effusion, and myocardial ischemia as evidenced by ECG changes or enzyme rise are indications of proximal dissection. In all, 69% of ECG in patients with dissection is abnormal with nonspecific changes, and 80% of chest X-rays (CXR) are abnormal with widening of mediastinum,
but a normal ECG or CXR does not exclude dissection. Overall, 16% of patients have pleural effusion either secondary to
hemorrhage or reactive in nature [16].
Classifications Systems
Aortic dissection is classified either temporally or in terms of anatomical location. Historically acute dissection is defined as
within 2 weeks of symptoms onset and chronic dissection as longer than 2 weeks. Anatomically, dissection can be classified
according to the site of tear or the part of the aorta that is affected irrespective of the location of the tear. Two anatomic classifications are in clinical use, the Debakey and Stanford systems. For the purposes of classification, the ascending aorta refers
to the part of aorta proximal to the innominate artery. The Stanford system is more commonly used in daily clinical setting
as it is simpler and categorizes dissections according to whether the ascending aorta is involved regardless of the origin of the
tear. Stanford type A dissections refer to dissections involving the ascending aorta and type B in which the ascending aorta is
spared. Dissections that involve the arch and not the ascending aorta are also categorized as type B. The Debakey classification system categorizes dissection according to the origin of intimal tear and the extent of dissection. Debakey category 1
refers to a tear in the ascending aorta with distal propagation to involve the arch or the descending aorta. Category II refers to
dissection tear only in the ascending aorta. Category III refers to dissection tear in the descending aorta propagating distally
(Fig. 44.1). These classifications have been in use for many years preceding the development of endovascular treatment and
improvements in diagnostics; although they are useful for guiding treatment, newer classification systems may be needed
to take into account functional characteristics, hemodynamics information, and tissue biomechanical parameters to better
guide treatment and predict prognosis.
The DISSECT system is a classification scheme designed to divide patients according to anatomy with relevance for
endovascular management [17]. The DISSECT system addresses additional information including clinical symptoms and
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FIGURE 44.1 Debakey and Stanford classification illustrating location of tears and extent of dissection.
false lumen status. The classification is based on six parameters: duration of dissection (D) less than 2 weeks, 2 weeks to
3 months, and 3 months or more; intimal tear location; size of the aorta; segment extent; clinical complications; and thrombosis of false lumen. The DISSECT system considers major prognostic elements and captures the plasticity of the aorta
within 90 days with its ability to remodel after treatment.
Diagnostic Imaging
Imaging studies have important roles in the management of aortic dissection, namely in confirmation and classification of
dissection, localization of tears, and assessment of complications. Imaging modalities widely used include the computed
tomography (CT) scan, transthoracic echocardiogram, transesophageal echocardiogram, magnetic resonance imaging (MRI),
digital angiography, and intravascular ultrasound. Of all the imaging modalities, CT scan remains the first choice of investigation because of its ease of access, wide availability, and noninvasiveness. It can allow immediate triage decisions and is usually
available 24 hours a day in most centers. Echocardiography is portable and like CT is widely available. Apart from anatomical
information of the aorta and function of the aortic valve, echocardiography is also able to provide parameters indicating flow
dynamics and flap movement, which may potentially bear prognostic implications. However, transthoracic echocardiography
is operator dependent and has limitations in that it has a narrow acoustic window with views obstructed by overlying lungs
resulting in poor image quality. Transesophageal echocardiogram offers a more complete imaging of the aorta and can be used
as intraprocedural monitoring, but expertise in use may not be readily available and insertion in the acute setting may worsen
pain in dissection patients, which can potentially exacerbate clinical condition. To date, there is no standout imaging that has
proven superior in terms of diagnostics than the other [18,19].
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FIGURE 44.2 Approach to patient with acute chest pain. Identification of risk factors in history and physical signs on examination is important for early
diagnosis and management.
Management of Aortic Dissection
Acute type A aortic dissection is indicated for urgent open surgical repair. In general, dissection limited to the descending
aorta is recommended to be treated medically with aggressive blood pressure control unless complicated by malperfusion,
impending rupture, intractable pain, resistant hypertension, or early false lumen expansion (Fig. 44.2). The differentiation
of complicated versus uncomplicated dissection is paramount for the management and prognosis of the patient. However,
with the emergence and further development of endovascular options, the role of endovascular treatment in uncomplicated
type B aortic dissection has raised general interest to achieve aortic remodeling and reduce aortic-related complications.
However, endovascular stenting is not a procedure without risks, surgeons should always balance the indications, risks, and
benefit before offering such procedures.
The highest mortality from aortic dissection occurs in the first 48 h after symptom onset, making immediate and timely
diagnosis critical for appropriate management. Initial management of all types of dissection aims to limit the further extension of the dissection flap by controlling the blood pressure [20]. Patients should be admitted to an intensive care unit or
cardiac care unit, with close blood pressure control by intravenous antihypertensives and monitored by an intravascular
arterial line. Beta blockade is the first-line treatment and can lower both the blood pressure and wall tension. Other choices
of intravenous antihypertensives include nitrates and sodium nitroprusside for patients who cannot tolerate beta-blockers.
Drugs should be adjusted to maintain a systolic blood pressure of 100–120 mmHg and a heart rate of 60–80 beats per min.
Often, multiple drugs are required to reach a satisfactory target blood pressure.
Type A Aortic Dissection
Patients with type A aortic dissection who do not receive treatment have a mortality rate of 1–2% per hour during the first
24 hours and up to 50% by the first week. Of type A aortic dissection, 50% patients die before hospitalization. IRAD found
mortality to be 0.22% per hour during the first 24 hours and 0.77% per hour in medically treated type A aortic dissection
[21]. Mortality is because of proximal or distal propagation of the dissection causing acute aortic valvular dysfunction,
pericardial tamponade, and malperfusion resulting in coronary, cerebral, or visceral ischemia or rupture. This contributes to
a mortality of 20% on day 1 and 30% in the first 48 hours.
The principle of surgery in type A aortic dissection is to reconstitute the patency of the true lumen, reestablish aortic valve competency, realign the normal position and patency of the coronary arteries, and excise the primary tear if
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appropriate. This is usually achieved by supracoronary replacement of the ascending aorta. Depending on the involvement
of the root, the presence or absence of valvular dysfunction and coronary involvement, additional procedures such as aortic
root replacement with reimplantation of coronary buttons, coronary artery bypass grafting, resuspension of aortic valve, or
aortic valve replacement have to be considered. Operative 30-day mortality for ascending aortic dissections is between 10%
and 35%. In another retrospective analysis, survival rates of patients with type A aortic dissection repair were 91% after
30 days, 74% after 1 year, and 63% after 5 years [21]. Endovascular options for type A aortic dissection have been reported,
but this approach is still under investigation and because of anatomical constraints cannot be considered a standard for
management of type A aortic dissections [22].
In a special subgroup of patients with Stanford type A aortic dissection, the primary entry tear is located in the arch
or descending aorta, which is called retrograde type A aortic dissection (RAAD). The prevalence of RAAD is reported
be around 7–25% of acute type A dissection. The management strategy for RAAD remains uncertain and controversial.
Although the principle of management of type A aortic dissection is still surgical repair, initial medical management has
been advocated in small-scale series and studies for patients with thrombosed false lumen in the ascending aorta (<55 mm)
who are clinically stable. Satisfactory outcomes with initial medical management followed by timely aortic repair have
been reported [23]. In general, surgical repair of RAAD is still widely practiced and various surgical strategies reported
in the literature include ascending/hemiarch replacement, total arch replacement with the use of elephant trunk implantation, and hybrid procedures involving endovascular thoracic stenting. The distal location of the primary tear demands a
more extensive aortic replacement, which increases the surgical risk of mortality and morbidity especially in the setting
of acute dissection. Risks such as bleeding, stroke, paraplegia, and mortality are considerable, and such approach should
not be advocated in less experienced centers. Hemiarch/ascending aortic replacement prevents ascending aortic complications and is more commonly performed; nonetheless, leaving behind the primary tear predisposes the patient to a higher
risk of aortic-related complications such as aneurysmal changes and rupture. The reported hospital mortality for surgery in
acute RAAD ranged from 15% to 19%, with trends showing higher incidence of aorta-related events postascending aortic
replacement than total arch replacement [24]. Endovascular stenting has emerged as a less invasive alternative to open surgery to exclude the primary tear and promote thrombosis of false lumen. Shu et al. performed thoracic endovascular aortic
repair (TEVAR) in 17 patients with RAAD, demonstrating that TEVAR for RAAD is a safe alternative in selected patients
with RAAD. The majority of the cases were performed during the subacute phase of dissection. All the patients survived
till follow-up (mean, 25.7 months), with imaging results showing thrombosis of false lumen, enlargement of true lumen,
and decrease in maximal aortic diameter [25].
To date, there is no conclusive evidence suggesting superiority of either approach to RAAD. The optimal management
strategy remains uncertain, and long-term effectiveness of each approach should be validated over time.
Type B Aortic Dissection
The mortality of type B aortic dissection is around 20–40% at 5 years on medical therapy alone [26]. Death is mainly caused
by rupture secondary to silent expansion of aortic diameter. Medical treatment cannot induce remodeling of the aorta and
can only delay the rate of chronic expansion.
Surgical or endovascular treatment is indicated for complicated type B aortic dissections. Complicated type B aortic dissections include patients with evidence of impending rupture, malperfusion, refractory hypertension, hypotension, shock,
hemorrhagic effusion, rapid enlarging aortic diameter, and persistent symptoms. Malperfusion syndrome is associated with
worse perioperative outcomes. Patients with malperfusion syndrome have a mortality rate of up to 40% if multiple organs
are involved and around 25% if a single organ is involved.
Since the advent and emergence of endovascular treatment, TEVAR has superseded open surgery as the primary option
of treatment for descending aortic dissections [27] (Fig. 44.3). Open surgical repair requires left heart bypass, single lung
ventilation, and hypothermia, and outcomes from surgery in patient with malperfusion are unpredictable. Risks of irreversible spinal cord injury and death ranged from 14% to 67%. In-hospital mortality rates are 17% for open surgery [28,29].
Data from IRAD, after propensity matching, showed that surgery is associated with increased rates of mortality compared
with TEVAR. Large-scale reviews also revealed that TEVAR has improved short-term mortality comparing with open surgery in complicated type B aortic dissections. A meta-analysis in 2006 found TEVAR to be safe and effective with procedural success rates up to >95% [29]. The 30-day mortality of 10.8% for endovascular treatment of complicated dissection
is comparable with the mortality in medically treated patients with uncomplicated dissection [30]. Another meta-analysis
of outcomes for TEVAR in type B aortic dissections reported an in-hospital mortality of 9% and low rates of complications; stroke 3.1%; paraplegia 1.9%, retrograde type A dissection 2%; intestinal infarction 0.9%, and limb amputation
0.2%; aortic rupture rate was 0.8% over 20 months. Other findings from large registries find an in-hospital mortality of
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FIGURE 44.3 Thoracic endovascular aortic repair (TEVAR) and examples of deployment of stents in different zones in the thoracic aorta. TEVAR is
emerging as the first-line treatment for complicated aortic dissection.
7% for endovascular treatment, 32% for patients treated with surgery, and 10% for those treated by best medical care alone.
About 60% of mortality beyond 5 years result from false lumen rupture, and a relationship between false lumen patency
and aortic dilatation has been observed [31–33]. Further evidence from observational studies suggests that depressurization of the false lumen by placing stent grafts to obliterate the entry tear can result in false lumen thrombosis and remodeling of aorta. Results show that TEVAR improves survival in complicated distal dissection but remodeling in patients with
connective tissue disease is less successful. Endovascular options for these patients remain controversial [34].
The role of TEVAR is less clear in patients with uncomplicated acute type B aortic dissection. Although medical therapy
is still the recommended treatment of choice, the role of preemptive TEVAR is increasingly studied. This in part is because
of observations of potential plasticity and remodeling capabilities of the aorta within 90 days and correlations between
early obliteration of false lumen and improvements in long-term aortic-related survival and complications. The randomized INSTEAD trial looked into the role of TEVAR in patients with uncomplicated type B aortic dissection and found that
there was no difference in all-cause mortality between patients treated with stent graft plus best medical therapy and best
medical therapy alone at 2 years [35]. However, in the INSTEAD-XL trial, at 5-year follow-up, aortic rupture, progression
of disease, and vascular mortality were reduced by preemptive TEVAR in the subacute phase of dissection. This finding
is supported by a meta-analysis and observations from registries, showing late advantages of TEVAR beyond 3 years of
follow-up [36]. Therefore, preemptive TEVAR may be considered in the subacute phase of type B aortic dissection to prevent future aortic complications provided the risks of procedure is low and should be weighed against the risks of TEVAR,
especially when head and neck vessels debranching is needed. This potentially heralds a paradigm shift in the management
of uncomplicated type B dissections from a complication-specific approach to preemptive approach.
The long-term outlook for patients surviving type A and type B aortic dissections are similar after discharge from hospital, whereas type A aortic dissection has a higher early in-hospital mortality. Thirty percent or more patients with medically
treated type B aortic dissection go on to require intervention in 5 years time. Patients with a false lumen diameter of >22 mm
in the upper descending thoracic aorta have a greater risk of aneurysm formation (42% vs. 5%) and increased mortality
(17% vs. 5%). Hypertension, older age, aortic size, and patency of false lumen (partial thrombosis of the false lumen) are
predictors of late complications. The 10-year survival of patients with aortic dissection ranges from 30% to 60% [37,38].
Therefore, stringent blood pressure control and regular assessments of the entire aorta is essential after discharge. Findings
such as progressive diameter increase, formation of aneurysms, and endoleaks require early attention.
Intramural Hematoma
IMH is defined as a hematoma within the aortic media without communication with the lumen of the aorta. Ever since its
first description by Krukenberg in 1920 during a postmortem examination, there has been considerable debate concerning the definition of IMH [36]. It is difficult to rule out with certainty the absence of intimal injury based on clinical and
imaging alone, and some suggest IMH should be considered a pathologic diagnosis rather than a clinical one. The most
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FIGURE 44.4 Computed tomography scan of descending aortic intramural hematoma showing crescent-shaped hematoma.
cited hypothesis of mechanism of IMH formation is rupture of vasa vasorum within the media, allowing blood or clots to
accumulate within the aortic wall. However, this concept has never been rigorously proven in clinical or experimental setting. Postmortem and surgical specimens demonstrate medial degeneration and elastin fragmentations in the aortic wall of
IMH patients. The major distinguishing feature of IMH is its exterior location within the media near the adventitia, whereas
dissection tends to extend into the media in closer proximity to the intima. Pathologic changes in the media have been
hypothesized to lead to structural failure of the aortic wall hence resulting in disproportionate high tension and strain over
the outer part of the media. With improving quality of imaging studies, increasingly, intimal defects have been identified in
cases of IMHs. In some series, mainly from Asian studies, around 70%–80% IMHs showed actual intimal tears identified
via CT and intraoperatively [39–41]. These studies suggest IMHs may actually result from micro or small intimal defects
rather than primarily a medial disease and that microtears may not be identifiable the with current imaging modalities.
Thus, IMH is considered as an AD with a closed and thrombosed lumen by some.
IMH accounts for between 5% and 20% of patients admitted for acute aortic syndrome. Clinically, IMH is indistinguishable from acute dissection. Chest and back pain can be very severe in IMH but malperfusion is rare in IMH. Imaging is the
cornerstone of diagnosis, and by far, CT scan is commonly used for diagnosis for IMH because of its wide availability and
relative ease in interpretation. On CT scans, IMHs are characterized by the findings of a crescent-shaped area of hyperattenuation (60–70 HU), associated with aortic wall thickening (Fig. 44.4). There is no increase in enhancement upon contrast
filling. Intimal displacement of calcium may also be present to help distinguish IMH from intramural clot. MRI has almost
100% sensitivity for IMH and can provide details concerning the acuity of hematoma on T2-weighted images. Patients with
IMH tend to be older, and IMH is uncommonly seen in patients with connective tissue disease.
IMH is more often observed in the descending aorta, and the behavior and prognosis of IMH are dependent on its location [42]. IMH is generally classified according to the Stanford classification. Acute mortality rate of IMH in the ascending
aorta is 42% versus 8% in the arch and descending aorta based on data from IRAD, supporting upfront surgery for type A
IMH [43]. Patients with type A disease are more likely to have pericardial effusion and cardiac tamponade compared with
aortic dissection. The natural history of IMH can vary from complete resolution to aneurysmal formation and frank rupture.
Progression to frank dissection has been reported in as high as 16% of patients under observation. Traditionally, medically
managed type A IMH have poor outcomes with 27–96% of patients eventually experience adverse aortic events and require
aortic surgery on follow-up [44,45].
However, recent conflicting evidence especially from Asian studies has suggested initial expectant nonoperative
approach for type A IMH, citing superior outcomes of type A IMH versus dissection. Song et al. published results in support of medical management of type A IMH with favorable in-hospital mortality of type A IMH than that of dissection
(7.9% vs. 17.2%) and equivalent mortality rates of those who were surgically managed [46]. Other Asian centers have
published similar medical management strategies with reasonable in-hospital outcomes [47]. But critics of the medical
management approach point out that observing patients with IMH generally requires additional intensive care resources,
prolonged hospital stay, and repeated CT scans for a disease process that has a high conversion to surgery in the short and
long term. In light of discrepant findings, it will be unfair to completely disregard medical therapy and timed intervention
approach. As it stays, the general consensus at the moment is still inclined to offer emergent surgery for patients with type
A IMH. The incidence of early rupture in type A IMH is reported to be 26% versus 8% of type A aortic dissection and can
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also evolve into frank aortic dissection [48]. Overall, data from retrospective studies and registries suggest that in-hospital
mortality rates of IMH are equivalent to aortic dissection.
Overall, type B IMH has a more favorable outcome in comparison with type A IMH. Mortality rates are low in type B ranging from 0 to 4%, mainly attributable to the infrequent development of malperfusion and cardiac complications [49]. Long-
term survival is favorable with 5-year survival as high as 85%. There is broad acceptance for medical management for medical
therapy in type B IMH. Indications for surgery in type B IMH include recurring and refractory chest pain and increasing size
and extent of diameter of IMH and pending rupture. Of the patients, 50%–80% achieve complete resolution of type B IMH
on medical therapy alone, and multiple studies suggest an indolent course for most type B IMHs [50]. Predictors of resolution
include young age, aortic diameter at 40 mm, thickness of IMH < 1 cm and postoperative beta-blocker use. However, type B
IMH is not a benign condition and some patients do progress to frank dissection and close follow-up is recommended. Aortic
diameter and thickness remain consistent predictors of progression to rupture, dissection, and dilatation. Seuyoshi reported a
diameter of >40 mm and aortic wall thickness >10 mm as significant predictors of progression of type B IMH [51].
Endovascular stenting (TEVAR) for IMH remains controversial and its application is unclear. Theoretically, in IMH
there is no tear to exclude and neither is there a false lumen to thrombose by radial pressure of the graft. Hence, an IMH
aorta may not tolerate a stent graft in dissection or PAU. The liberal use of stent grafting, in the face of low complication
rates from medical treatment, is not recommended in IMH.
Penetrating Aortic Ulcers
The true incidence of PAUs is unclear and is quoted to be around 7%–8% from retrospective studies. The description of this
entity was by Stanson and colleagues in 1986. The histopathology was described as “an atherosclerotic lesion with ulceration that penetrates the internal elastic lamina and allows hematoma formation within the medial layer of the aortic wall.”
[52] PAUs appear as an ulcer in the media and can occur without IMH or pseudoaneurysms (Fig. 44.5). PAU commonly
leads to IMH and is frequently observed in the descending aorta. Extensive atherosclerosis is often associated with PAU,
and calcifications can be noted throughout the aorta [53].
PAUs need not be symptomatic and indications for management of PAU remain controversial. In a Mayo Clinic
series, around 20% of PAUs were asymptomatic. Conflicting evidence exists concerning the aggressiveness of management for PAU. A report from the Mayo Clinic suggested an expectant approach was appropriate. In the Mayo Clinic
series of 107 patients, 72% of the patients were managed nonoperatively. Late survival was comparable between those
operated and those treated medically [54]. Rupture at presentation and maximum aortic diameter were predictive of
failure of medical therapy defined as death from aortic cause [49]. Despite the disparity in management, investigators
agree that IMH or PAU should be followed up closely by aortic specialists to monitor for aneurysmal changes and
complications.
FIGURE 44.5 Computed tomography scan showing penetrating aortic ulcer of the arch with ulceration into the media.
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