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TABLE 27.1 The Extent of Hypothermia During Hypothermic Circulatory Arrest, as Established by the International
Aortic Arch Surgery Study Group [2]
Nasopharyngeal Temperature
Profound hypothermia ≤14°C
Deep hypothermia 14.1–20°C
Moderate hypothermia 20.1–28°C
Mild hypothermia 28.1–34°C
FIGURE 27.1 Comparison of estimated safe hypothermic circulatory arrest duration against cerebral metabolic rate. HCA, hypothermic circulatory
arrest. Adapted from McCullough JN, Zhang N, Reich DL, Juvonen TS, Klein JJ, Spielvogel D, et al. Cerebral metabolic suppression during hypothermic
circulatory arrest in humans. Ann Thorac Surg 1999;67(6):1895–9.
lowering parenchyma temperatures, intracellular enzymatic activity is reduced, thus prolonging the duration of “safe”
circulatory arrest time.
Several in vivo metrics have been evaluated to guide safe circulatory arrest temperatures. In a landmark study,
McCullough and colleagues measured cerebral oxygenation via the jugular venous bulb and determined that the body
needs to be cooled to 15°C to have up to 30 min of safe HCA time (Fig. 27.1) [4]. In contrast, electrocerebral inactivity, as measured by electroencephalography, has been offered by others as a gauge of metabolic standstill. A contemporary analysis of 396 patients by the Duke group found that even at 15°C, nearly 60% of patients still did not reach
electrocerebral inactivity [4]. It was only by cooling to 12.7°C that electrocerebral inactivity was achieved in >95% of
patients.
Clinically, the duration of DHCA has been associated with the incidence of TND. It is recommended that DHCA be
limited to less than 30–40 min, with prolonged durations resulting in poorer short- and long-term outcomes [5,6]. Within
these limits, the adequacy of DHCA has been demonstrated even in high-cognitive patients [7]. Additionally, proponents
of DHCA contend that the technique does not require introduction of additional catheter (thereby reducing opportunities
for embolism-related complications), does not risk hyperperfusion and associated cerebral edema, and is simple and can
be employed quickly [6]. Although not as popular in Europe, this practice still maintains popularity with some centers in
China and the United States [6,8].
Antegrade Cerebral Perfusion
If the anticipated circulatory arrest duration is greater than 30 min, ACP is typically used as an adjunct. By directly supplying the brain with metabolic sustenance via the axillary or supraaortic vessels, a closer approximation to the normal

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physiologic state is maintained. This approach is preferred by most European and Japanese centers, representing up to 90%
of surveyed institutions and cases [9,10].
Although simplistic in theory, ACP has numerous complexities, much of which remain poorly understood, in particular,
the application of unilateral ACP (typically via the axillary artery) or bilateral ACP (with addition of left common carotid
or left subclavian artery). It is argued that unilateral ACP, although faster to establish and can avoid manipulation of supraaortic arteries, risks cerebral hyperperfusion of the supplied hemisphere and hypoperfusion of the contralateral hemisphere.
Anatomically, this nonphysiologic perfusion pattern relies on the competency of the circle of Willis and secondary extracranial collateral networks. Numerous angiographic and cadaver studies have so far demonstrated that up to 15% of patients
have incompletely closed circle of Willis, with up to 40% patients having variants of normal circles [11,12]. During surgery,
there is also evidence that oxygenation is reduced in the contralateral hemisphere; in a study of 13 patients undergoing aortic arch surgery with moderate HCA and unilateral ACP by Harrer and colleagues, 12 patients had a reduction in oxygenation in the contralateral hemisphere as measured by near-infrared spectroscopy (NIRS) that necessitated commencement
of bilateral cerebral perfusion [13]. Despite scientific evidence favoring bilateral ACP, clinical evidence thus far has not
demonstrated a clear superiority. Numerous propensity-matched studies and metaanalyses have demonstrated comparable
results between unilateral and bilateral ACP [14,15], although a possible trend for increased stroke rate in bilateral ACP has
been documented [15]. It is generally recommended that should circulatory time extend beyond 30 min, bilateral ACP be
considered [16].
Contemporarily, ACP is typically used as an adjunct with moderate hypothermic circulatory arrest (MHCA). As the
brain is actively supplied with metabolites, the need to severely reduce metabolic activity by extra cooling is greatly lessened. The increase in circulatory arrest temperature to above 20°C reduces cooling and bypass time and reduces the risks
associated with bleeding. At these temperatures, however, the visceral organs and the spinal cord become more susceptible
to ischemic damage.
Although it is generally accepted that MHCA + ACP is the preferred approach by most centers if longer periods of circulatory arrest are required, the consensus approach for simpler cases is less clear. Given the relative complexities of ACP,
some have argued that DHCA is sufficient if circulatory arrest is anticipated to be less than 30 min, whereas other centers
prefer MHCA + ACP for all cases [6]. To date, there is no clear evidence conclusively favoring either approach in such situations, and surgical judgment and institutional experience should be taken into account.
Retrograde Cerebral Perfusion
First described by Ueda and colleagues in 1990 [17], RCP relies on supplying cerebral blood flow through the superior
vena cava (SVC) and the associated venous system. RCP’s theoretical foundations rest on three factors: provision of metabolic substrates (and elimination of catabolites), maintenance of cerebral hypothermia, and flushing out of embolic debris.
However, numerous animal and in vivo models have challenged the role of RCP, particularly the ability for RCP to adequately perfuse the brain. As such, its practice has waned significantly in recent decades and is only used in select centers.
Notably, numerous animal and human studies have contested the benefits of RCP. In porcine models, it has been
shown that perfusion via the SVC largely bypasses the cerebral parenchyma. Indeed, by using radiolabeled microspheres,
Ehrlich and colleagues demonstrated that only 0.01% of the SVC inflow traversed cerebral parenchyma, with 90% diverted
through veno-venous shunts to the inferior vena cava [18]. Such findings have also been validated in primates as well [19].
In humans, using either radiolabeled perfusate or cerebral oxygenation as an indirect measure of perfusion, RCP similarly
offers limited perfusion, with as low as 10% of antegrade flow [20–22].
Despite less-than-impressive scientific studies, clinically, RCP has provided acceptable, even positive, outcomes.
Although no conclusive Level 1 evidence exists regarding the benefits of RCP, several case series have demonstrated
superior short-term outcomes, notably reductions in mortality and incidence of stroke, and long-term survival compared
with straight HCA [23–25]. Furthermore, compared with ACP, RCP has been shown to offer similar cerebral protection.
Analysis of 1141 propensity-matched pairs of ACP versus RCP patients in the Japan Adult Cardiovascular Database in
2015 showed nonsignificant differences in the incidence of death, stroke, TND, prolonged ventilation, spinal complications, reoperation, and composite outcomes [10]. Similarly, a metaanalysis of more than 5000 patients in 2014 calculated
comparable mortality between the two groups (5.2% in both) [26]. Interestingly, RCP had a significantly reduced risk of
postoperative stroke (risk ratio 0.538, P = .001), although this was perhaps colored by the presence of publication bias.
Although there exist a large body of scientific studies on RCP, there still remains little clinical evidence to demonstrate
conclusively RCP’s superior metabolic benefits or clinical outcomes. It seems that the utility of RCP rests on its ability to
provide localized topical cooling of parenchymal tissue and potential for embolic washout.

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Brain Monitoring
Various technologies have been used to monitor brain activity and gauge ischemia. NIRS is a continuous, real-time, and
simple noninvasive bedside monitor of frontal cerebral oxygen saturation and should routinely be applied in all cases.
Fluctuations in sensor levels can alert surgeons to potential risks and aid in rapid institution of correction measures.
However, it is important to understand that NIRS does not measure cerebral blood flow nor does it measure brain ischemia;
indeed, saturation levels may be normal even when positioned over regions lacking cerebral perfusion and the underlying
tissue is dead [27]. Other monitoring methods include electroencephalography, transcranial Doppler, and jugular venous
oxygen saturations.
SURGICAL CONSIDERATIONS
In addition to improvements in neuroprotection strategies, there have been considerable refinements in surgical practice.
From variations in cannulation strategies to changing paradigms of focusing on long-term outcomes and to availabilities of
new technologies, the cardiothoracic surgeon now has greater flexibility and many options to tailor management specifically to patient presentations.
Cannulation Site
Much has been discussed regarding the optimal site for arterial inflow. In early series, the femoral artery was used as a
cannulation site by Griepp and colleagues [28]. In the decades since, the risks of retrograde embolization, particularly in
a diseased descending aorta, have diminished the popularity of femoral cannulation. In aortic dissections, the incidence of
malperfusion can also be increased because of the unpredictable shifting of the intimal flap [29].
To overcome these limitations, cannulation of the axillary artery has become the preferred option in many centers
because it reduces the likelihood of embolic strokes, minimizes the disruption of atheroma or calcified plaques, decreases
the risk of malperfusion in dissection cases, and has the ability to provide supplementary ACP if required [30]. Indeed, both
animal study and computational flow dynamics (CFD) simulations have demonstrated the capacity for this retrograde flow
to divert emboli into the descending aorta [31,32]. This has been seen in clinical trials, with a metaanalysis of nine clinical
studies in 2015 highlighting that the incidence of short-term neurologic dysfunction was nearly halved when compared
with femoral cannulation (odds ratio 0.46, P = .0007) [33]. However, some surgeons prefer the rapidity with which femoral
cannulation can be established, and it remains a preferred option for many [9].
Developments in Management of Type A Aortic Dissections
The aggressiveness of surgical repair for type A aortic dissections (in particular, DeBakey I dissections) has been under considerable debate in the past decade. Given the hemodynamic instability of a dissected patient, the primary objective in aortic
dissections is to save the life of the patient by excising the primary entry tear and restore dominant true lumen flow in the
downstream aorta. The traditional model adopts a conservative approach, with resection of the intimal tear done by replacing the ascending aorta or hemiarch. However, it has been recognized that a residual patent false lumen in the descending
thoracic aorta is present in up to 60% of patients [34]. Because of residual wall stresses caused by residual intimal tears,
leakage from the distal anastomotic sites, and reentry in the distal aorta, these lumens will become more susceptible to further dilation, with up to 30% of patients requiring reoperations [35]. In light of the long-term complications and availability
of endovascular stent-graft devices, numerous centers have started to advocate for a more extensive initial repair, typically
involving the frozen elephant trunk (FET).
The deployment of a stent graft, known as a FET, into the descending aorta during open arch replacement has radically
changed the management of aortic pathologies (Fig. 27.2). By exerting radial pressure to promote false lumen thrombosis, this procedure obviates the need for second-stage operations to repair the downstream aorta. Several open stentedgraft exist, including the E-vita Open Plus (Jotec GmBH, Hechingen, Germany), Thoraflex Hybrid (Vascutek, Inchinnan,
Scotland, UK), Cronus (MicroPort, Shanghai, China), Chavan-Haverich (Curative GmbH, Dresden, Germany), and the J
Graft (Japan Lifeline, Tokyo, Japan) [36]. To date, none of these devices have received commercial approval in the United
States, hence restricting their broad use to Europe and Asia.
Clinically, FETs have shown satisfactory results, with acceptable mortality and morbidity, and high rates of false lumen
occlusion at 10-year follow-up, albeit with concerns of spinal cord ischemia related to the length of the prosthesis [37,38].
Compared with the conventional hemiarch replacement, total arch replacement with FET is technically more demanding
and is associated with prolonged circulatory arrest times. It is recommended to be used by experienced surgeons in younger

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FIGURE 27.2 Deployment of a stent graft in the descending thoracic aorta during open total arch replacement. During a period of hypothermic circulatory arrest, the aorta is visualized and the stent graft prosthesis is guided into the descending aorta via a guidewire. A balloon catheter is deployed,
which will radially expand the stent-graft into its final position. Reproduced with permission from Ma W-G, Zhu J-M, Zheng J, Liu Y-M, Ziganshin BA,
Elefteriades JA, et al. Sun’s procedure for complex aortic arch repair: total arch replacement using a tetrafurcate graft with stented elephant trunk
implantation. Ann Cardiothorac Surg 2013;2(5):642–8.
populations (e.g., <70 years old, for whom there are substantial long-term prognostic benefits), those with enlarged proximal descending aorta, and those with entry tears in the proximal descending aorta. More extensive and longer durations of
follow-up are required to determine the long-term benefits of the FET.
Finally, in addition to covered stent-grafts, several bare-metal stents have been developed and approved for use in
type A dissections. Similar in concept to coronary stents, these stents purport to conform to the shape of the aorta to compress the false lumen while maintaining patency of the adjoining arteries. However, these devices, such as the Djumbodis
Dissection System (Siant Come-Chirurgie, Marseille, France) and E-XL aortic stent (Jotec GmBH) have not yet reached
clinical maturity, with their indications and roles yet to be clearly defined. Early results have been disappointing, with
between 44% and 65% false lumen thrombosis with the Djumbodis system (compared with up to over 90% with FETs),
with incidents of stent deformity and fracture reported [39,40]. Further research is required to clarify the utility of these
bare-metal stents.
FUTURE DIRECTIONS
Open aortic arch surgery has developed significantly in the past few decades. With the introduction of newer technologies
and greater collaborations in research, surgical practice will continue to be refined in the coming decades. In particular,
several avenues of research stand out.
The development of CFD modeling has shown great promise. CFD is able to capture the specific anatomy of a patient’s
aorta, through either computed tomography or magnetic resonance imaging, and recreate a mathematical model of the
hemodynamic stresses on the aortic wall in a computer simulation. Current work is ongoing to correlate these hemodynamic models with clinical outcomes, to ideally be able to generate a tool that can predict the development of dissections
and outcomes after vascular interventions.
In the past decade, there has also been a growing trend toward collaborative research. Several databases and research
groups, including the International Registry for Acute Dissections Interventional Cohort Registry, the International Aortic
Arch Surgery Study Groups Multi-institutional Database and upcoming ARCH Prospective Registry, and the newly formed

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Aortic Research Consortium in the United States, will amalgamate and enrich clinical data to overcome the research limitations that have previously stymied advances in surgical practice.
Finally, surgical boundaries will continue to be surpassed. With increasing practice of minimally invasive cardiac surgery and the continued development of endovascular devices, open aortic arch surgery will continue to evolve and develop.
ABBREVIATIONS
ACP Antegrade cerebral perfusion
CFD Computational flow dynamics
DHCA Deep hypothermic circulatory arrest
EEG Electroencephalography
HCA Hypothermic circulatory arrest
IAASSG International Aortic Arch Surgery Study Group
IRAD International Registry for Aortic Dissection
MHCA Moderate hypothermic circulatory arrest
NIRS Near-infrared spectroscopy
RCP Retrograde cerebral perfusion
SVC Superior vena cava
TND Temporary neurologic deficit
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Thorac Surg 2014;97(1):e17–20.

Chapter 28
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Dissection of the Ascending Aorta and
Aortic Arch
Horatiu Moldovan
1
“Titu Maiorescu” University of Bucharest, Bucharest, Romania; 2Romanian Academy of Medical Sciences, Bucharest, Romania; 3SANADOR
Hospital, Bucharest, Romania; 4C. C. Iliescu Institute of Cardiovascular Disease, Bucharest, Romania
1,2,3
, Celia Georgiana Ciobanu
4
Chapter Outline
Introduction 315
Open Surgery in ATAAD—Supportive Techniques 317
Cannulation and Establishment of CPB 317
HCA and Cerebral Protection Strategy 318
Replacement of the Proximal Aorta—Aortic Root and
Ascending Aorta 318
The Elephant Trunk Procedure 326
Hybrid Procedures 327
Total Thoracic Endovascular Aortic Repair for Acute
Thoracic and Ascending Aorta Dissection 329
References 330
Further Reading 337
INTRODUCTION
Aortic dissection, defined as a cleavage between the intima-media layers of the aortic wall, is created by tears in the intima,
the so-called primary entry or primary tear [1], where the blood first enters the aortic wall. So the blood is redirected from
the aorta [true lumen (TL)] into the media [false lumen (FL)] [2–6], resulting in the existence of two flow channels communicating with one another, thus evolving in propagation of the dissection (proximally or distally) [3,7–10] (Fig. 28.1).
Anatomically, aortic dissection has been classified by two principal schemes. The DeBakey et al. classification distinguishes the following three types of patients based on the location and extent of aortic dissection: type I, dissection
beginning in the ascending aorta and involving the entire or most of the descending aorta; type II, only the ascending aorta
is involved; and type III, sparing the ascending aorta and the arch [11–13]. The Stanford classification proposed by Daily
et al., which, in fact, is more like a functional classification system, consists of the following two types: type A, involving
the ascending aorta regardless of the entry site location and type B, involving the aorta distal to the origin of the left subclavian artery [14] (Fig. 28.2). Antegrade dissection is defined as the dissection associated with an entry tear in the ascending
aorta, and retrograde dissection originates beyond the origin of the great vessels. A more appealing, simple, and practical
classification of this entity for the triage is proposed by Dake et al., which highlights the anatomic and clinical features
necessary to make treatment decisions using the mnemonic “DISSECT”: Duration, Intimal tear (location), Size (maximum
diameter), Segmental Extent (ascending, descending, etc.), Complications, and Thrombosis of the FL [15,16].
Acute aortic dissection is a challenging clinical emergency that was first described more than 250 years ago, but who
was the first to describe it is not certain yet; there are more than seven authors who are given the credit of doing so: Vesalius
in The Boerhaave—first edition (1543), Theophile Bonet in Sepulchretum: sive anatomia practica ex cadaveribus morbo
denatis (1679) [17], Fernelius in De morbis universalibus et particularibus (1645), Sennertus in Opera omnia (1650),
Nicholls in 1761 presented the autopsy report of King George II of Great Britain, the same year Morgagni presented a
clearer picture of this disease in his biggest work De sedibus et causis morborum per anatomen indagatis—The Seats and
Causes of Diseases, Investigated by Anatomy [1], Maunoir in 1802, and later in 1819 Laennec enhances the aneurysmatic
property of chronic aortic dissection [18]. Two hundred years later, in 1958, Hirst et al. [19] reviewed 505 patients with this
condition, highlighting the high mortality rate and the infrequency of antemortem diagnosis.
New Approaches to Aortic Diseases from Valve to Abdominal Bifurcation. http://dx.doi.org/10.1016/B978-0-12-809979-7.00028-6
Copyright © 2018 Elsevier Inc. All rights reserved.
315

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(B)
FIGURE 28.1 (A) Chronic type A aortic dissection. (B) Acute type A aortic dissection.
FIGURE 28.2 Stanford classification of aortic dissection.
Aortic dissection was exclusively a postmortem diagnosis until the first part of the 20th century, when Gurin, in
1935, attempted surgical intervention to decompress a nonreentering FL causing acute leg ischemia with the first iliac
fenestration procedure [20,21], followed later on, by Shaw in 1955, with the first aortic fenestration [22]. In 1949, Abbott
and Paulin advanced the surgical management by preventing aortic rupture, at least theoretically, by wrapping the aorta
with cellophane [23]. Other attempts of surgical treatment over the years met with limited clinical success, though certain concepts regarding surgical management are still in use today. With the advent of cardiopulmonary bypass (CPB),
DeBakey and Cooley, in 1955, forever altered the natural history of aortic dissection by successfully performing the first
surgical repair using techniques that have steadily advanced, but steel remains the basis and outlines the principles for
the contemporary procedures [24,25].

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It is imperative to highlight that once diagnosed, emergent surgery is the prime choice of treatment for patients with
acute type A aortic dissection—acute thoracic and ascending aorta dissection (ATAAD) [26,27]. Surgery has emerged as a
classic treatment algorithm because ATAAD is an inherently lethal condition if not detected and treated promptly [28–34]
and it is of paramount importance to provide better outcomes, whereas optimal medical therapy is appropriate in patients
with type B dissection, in the absence of complications [35].
The high rates of morbidity and mortality could be the result of either aortic rupture or extension of dissection into the pericardium, aortic valve, or branches (coronary arteries, supraaortic trunks, visceral arteries, lower limbs, or lumbar arteries) [36–38].
Appropriate management is crucial to achieve satisfactory outcomes, but the optimal surgical approach remains a challenging and controversial decision, although no matter what the technique, the primary goal is to restore the blood flow
into the dominant TL in the downstream aorta [39]. Present surgical techniques target primarily the ascending aortic tear by
replacing or repairing the ascending and aortic root and the aortic valve apparatus (if necessary); meanwhile, the remaining
FL and potential remodeling of the dissected descending aorta currently play a secondary role [13].
The armamentarium of surgeons includes nowadays a wide spectrum of methods, ranging from conventional open procedures to minimally invasive endovascular and hybrid procedures [40].
OPEN SURGERY IN ATAAD—SUPPORTIVE TECHNIQUES
Cannulation and Establishment of CPB
Some of the operations on the proximal thoracic aorta require conventional modes of extracorporeal circulation, such as
dissections limited to the ascending aorta (DeBakey type II) with the downstream vessel of normal caliber, where cannulation does not differ from that of routine cardiac surgery, made into the proximal aortic arch and cavoatrial drainage,
whereas some procedures are performed using more sophisticated techniques that include alternative arterial cannulation
sites, hypothermic circulatory arrest (HCA), and/or selective cerebral perfusion [41]. This means that the choice of an ideal
site for arterial cannulation should be made after careful assessment of the preoperative imaging.
To date, in the majority of cases, CPB could be instituted by femoral arterial inflow. Femoral cannulation could be made
via a direct cutdown or by Seldinger technique [42,43]; however, this approach carries the risk of possible complications
such as atheroembolism because of retrograde aortic perfusion or it is undesirable because it is seldom involved in severe
atherosclerotic disease, which could lead to organ malperfusion [44–49].
Corrective measures can be instituted including changing or adding extra arterial inflow sources.
Alternative arterial cannulation sites include the following: (1) the axillary artery, (2) the common carotid artery, as
described by Urbanski et al. [50], (3) the innominate artery used by Preventza et al. [51,52], (4) direct TL cannulation of the
ascending aorta under ultrasound guidance using a Seldinger technique, and (5) transapical cannulation [42].
Currently, cannulation of the axillary artery or right subclavian artery has shown to be superior compared with femoral
artery cannulation [53,54]. A significant advantage of this approach is that it allows both antegrade distal perfusion and
antegrade brain perfusion during circulatory arrest, which reduces cerebral ischemic events. Although it is not flawless, it
requires a more precise technique and more time. It also may result in insufficient flow rate in cases of small axillary arteries, but this could be managed by using a conduit or if they are deeply located or damaged. Important complications such
as retrograde carotid dissection and cerebral malperfusion might be advocated by an intimal tear present in the brachiocephalic artery or its branches [55–60] or embolization with fatal or nonfatal neurologic events from some washout of mobile
atheromatous debris from the ascending aorta [61].
In contrast, transapical aortic cannulation has the advantage of avoiding these problems, such as antegrade blood stream,
and involves a simpler and quicker cannulation technique [62]. The advantages of transapical aortic cannulation are thought
to be as follows: simple and quick cannulation technique, sufficient antegrade aortic flow, and secured TL perfusion with
decreased risk of embolization and malperfusion; the disadvantages include the following: not practical for use in patients
with severe aortic stenosis because the cannula might completely occlude the aortic orifice, or after cardiovascular surgery
with median sternotomy and cardiac adhesion because of the difficult and longer time to establish transapical cannulation.
Bleeding at the access site of the apex could be a serious problem [63–65].
Another option for obtaining an arterial inflow is by cannulating the ascending aorta itself, at a nondissected or less
dissected segment, as determined by means of palpation, to perfuse the TL, when other cannulation options are not suitable. Usually, the left lateral portion of the ascending aorta adjacent to the pulmonary artery is performed by the Seldinger
technique (a guide-wire technique) under ultrasonographic guidance, and the first successful report of this technique was
published in 1998 by Lijoi et al., but this option will have not abolished the use of the femoral or axillary artery, and one
should be aware that this simple method could be applied safely in many cases of ATAAD [66,67].
In conclusion, there is no arterial inflow site that is always safe or reliable in the presence of acute aortic dissection [52].

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HCA and Cerebral Protection Strategy
Whenever the operation of ATAAD requires open distal anastomosis and replacement of part or all of the aortic arch, pre-
cautions are required to avoid brain damage.
The enduring gainsaying over the last decade regards which of the three cerebral protection techniques—straight DHCA,
antegrade cerebral perfusion (ACP), and retrograde cerebral perfusion (RCP)—is superior [68,69].
Hypothermia has been known for its organ preservation properties since the Hippocratic era. In the mid-20th century, it
was introduced into surgical practice for operations on the brain and heart; furthermore, Griepp et al. advanced and popularized this method, which is providing both safety in stopping circulation and an appealing bloodless operative field [70,71]
for meticulous inspection of the aorta. But optimal temperature during HCA arrest steel remains a debate because the
advantages of deep hypothermic technique (e.g., brain protection as it slows injury-inducing pathways by limiting cerebral
metabolism and providing distal organ protection alone) may be outweighed by the complications (prolonged extracorporeal circulation time by cooling and rewarming, coagulation disorders, and increased systemic inflammatory response
syndrome) [72], thus necessitating the adjunctive use of ACP or RCP [73]. Circulatory arrest is typically undertaken at
18–20°C, and a range of safe periods for DHCA have been reported at this temperature. Most patients tolerate 30 min
of DHCA without significant neurologic dysfunction, but when this is extended to longer than 40 min, there is a marked
increase in the incidence of brain injury. Above 60 min, the majority of patients will suffer irreversible brain injury [74].
The duration of safe DHCA is extended by the use of RCP [as cold oxygenated blood is directed into the snared superior vena cava (SVC) via an arteriovenous CPB shunt with flow rates of 200–500 mL/min at a pressure of no greater than
25 mmHg, although emerging evidence suggests that perfusion pressures of up to 40 mmHg are both safe and more effective]
or selective ACP—the right or both carotid arteries are perfused using balloon-tipped arterial cannulae placed directly into the
proximal common carotid arteries, via the brachiocephalic artery or via the side branch of an arch graft, with the left subclavian
artery clamped, and perfusion commences at 10–20 mL/kg/min to maintain a right radial artery pressure of 50–70 mmHg [74].
Several publications show safety and efficacy and the broad implementation of milder HCA arrest temperatures up to 22–25°C
without compromising safety. Although both techniques increase the complexity of surgery, they do permit a lesser degree of
systemic hypothermia and it is an increasingly used strategy to optimize brain and end-organ protection [75–77]. Consequently,
the 2014 European Society of Cardiology guidelines on the diagnosis and treatment of aortic diseases recommend antegrade
selective cerebral perfusion during HCA arrest to reduce the stroke risk during aortic arch surgery (Class IIa, Level B) [78].
Replacement of the Proximal Aorta—Aortic Root and Ascending Aorta
The surgical management of dissected ascending and aortic root has two primary objectives: the prevention of dilatation
and rupture and in many cases the repair or replacement of the aortic root with a synthetic presealed woven polyester vascular graft, and the best technique has yet to be determined. But in many centers, there has been a transition in mindset and
surgical approach away from a purely central aortic operation focusing on the ascending aorta and a “live to fight another
day” philosophy. The current more global perspective recognizes the importance of aortic valve function, malperfusion, FL
patency, and the potential for future complex aneurysm development.
Furthermore, when deciding on the most appropriate procedure to be performed on acutely dissected proximal aorta,
there are at least two questions that must be answered: (1) what is the diameter of the aortic root and ascending vessel at the
time of dissection and (2) can the aortic valve be preserved? [79].
The selection of a particular surgical technique is to be determined by each surgeon in the light of his own experience.
So, in case of nondilated Valsalva sinuses and normal low location of the coronary ostias, we can distinguish three options:
1. If aortic root is not involved by dissection, interposition of a tubular graft is made which is anastomosed at the sinotubular
ridge, proximally and distally to uninvolved aorta, most frequently just near the origin of the innominate artery. The dis-
sected aorta is completely resected, and the cuffs are prepared using biological glue (gelatin–resorcine–formaldehyde) to
obliterate the FL—the layers are conjoined by sandwiching them between strips of Teflon-felt—inside and outside and
included in a through-and-through mattress, to reinforce the wall, and afterward sutured to the vascular graft into over-and-
over suture (Fig. 28.3). The glue aortoplasty is an important contribution to modern-day aortic dissection surgery. Tissue
adhesives are used to conjoin the dissected aortic wall layers and to aid the performance of blood-tight anastomosis on
the aorta, reducing significantly the number of aortic valve replacements, the amount of intraoperative and postoperative
bleeding, the volume of intraoperative blood transfusions, and the frequency and severity of postoperative complications
[80–84]. Another technique for friable aortic wall reinforcement is described by Floten and coworkers and consists in inver-
sion of the redundant adventitia into the true aortic lumen and conjoining them by using pledgeted interrupted transmural
mattress sutures, but most often, it is used for the distal aortic anastomosis [85–88]. The resection margin is sandwiched this
way between two layers of adventitia and the residual FL is thus excluded from the antegrade blood flow [89].
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