Surgical Management of Acute Type A Aortic Dissection: An Overview

Abstract

Acute type A aortic dissection is a catastrophic disease that develops from a tear within the intima of the aortic wall, thereby creating a false lumen in the ascending aorta. Early suspicion, diagnosis, and prompt surgery play a key role in the survival of patients. It is a surgical emergency and requires replacement of the ascending aorta/aortic root with or without aortic arch replacement. Over the past decade the surgical outcomes have improved in specialized tertiary centers.

Full text

Review Article
Surgical Management of Acute Type A
Aortic Dissection: An Overview
Sreedhar Reddy Nagaradona,1 Krishna Machiraju,2 Srinivasulu Reddy Kurapati,3
Srinivas Boggula,4 Sridhar Anumala Setty,5 and Sadiq Azam6
Abstract
Acute type A aortic dissection is a catastrophic disease that develops from a tear within the intima of the aortic wall, thereby
creating a false lumen in the ascending aorta. Early suspicion, diagnosis, and prompt surgery play a key role in the survival of
patients. It is a surgical emergency and requires replacement of the ascending aorta/aortic root with or without aortic arch
replacement. Over the past decade the surgical outcomes have improved in specialized tertiary centers.
Keywords
Type A, aortic dissection, management, surgery, review
Indian Journal of Clinical Cardiology
2(1) 23–31, 2021
© 2021 Telangana Chapter of Cardiological
Society of India
Reprints and permissions:
in.sagepub.com/journals-permissions-india
DOI: 10.1177/2632463620978047
journals.sagepub.com/home/occ
1 Indian Association of Cardiovascular and Thoracic surgeons, Krishna
Institute of Medical Sciences, Secunderabad, Telangana, India
2 Indian Association of Cardiovascular Thoracic Anaesthesiologists, Krishna
Institute of Medical Sciences, Secunderabad, Telangana, India
3 Indian Society of Extracorporeal Technology, Krishna Institute of Medical
Sciences, Secunderabad, Telangana, India
4 Krishna Institute of Medical Sciences, Secunderabad Hospital,
Secunderabad, Telangana, India
5 Indian Society of Anesthesiologists, Krishna Institute of Medical Sciences,
Secunderabad, Telangana, India
6 Cardiology Society of India, Krishna Institute of Medical Sciences,
Secunderabad, Telangana, India
Corresponding author:
Sreedhar Reddy Nagaradona, Krishna Institute of Medical Sciences, Minister
Road, Secunderabad, Telangana 500003, India.
E-mail: reddy_ns@yahoo.com
Introduction
Acute type A aortic dissection is a lethal disease with a
reported incidence of 2.5 to 6 per 100 000 patient years.1 The
first reported aortic dissection and the concept of true and
false lumen is attributed to Shekelton in the early 1800. If
left untreated, a patient with acute type A aortic dissection
has a 50% to 70% risk of dying within 48 h of the event.2 For
this reason, it is essential to operate immediately. Untreated
patients usually die of rupture of false lumen, acute cardiac
tamponade, acute high-grade aortic valve insufficiency,
and malperfusion syndromes. Despite surgery, the overall
30-day mortality remains around 20% to 25% as reported by
international registry of aortic dissection.3 The international
registry of acute aortic dissection (IRAD) is a multinational
registry that initiated enrolling of patients in 1996. This
project has provided contemporary insight into the short-
term and long-term outcomes of acute aortic dissection and
proposed therapeutic options.
The ideal surgery for acute type A aortic dissection should
replace the diseased aortic segment as long as possible and
obliterate the false lumen in the remaining aorta with minimal
operative risks and reduction in the need for reintervention.
Over the last decade, improved understanding of the dynamics
of aortic dissection has led to lower mortality and morbidity
in selected centers.
Pathogenesis and Classification
Acute type A aortic dissection develops from a tear within the
intima of the aortic wall. Blood flows across the entry point
into the weakened media, splitting the medial layer along the
direction of blood flow, creating a new false lumen within
the aortic media. Subsequently the false lumen can extend in
both directions and could affect most of the branches of aorta
including coronary, carotid, mesenteric, and limb arteries.
Acute type A aortic dissection can also happen secondary
to trauma, most often iatrogenic—during percutaneous
Creative Commons Non Commercial CC BY-NC: This article is distributed under the terms of the Creative Commons Attribution-
NonCommercial 4.0 License (http://www.creativecommons.org/licenses/by-nc/4.0/) which permits non-Commercial use, reproduction
and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages
(https://us.sagepub.com/en-us/nam/open-access-at-sage).

24 Indian Journal of Clinical Cardiology 2(1)
interventions, aortic cannulation for cardiopulmonary
bypass (CPB), cross-clamping of aorta in open heart surgery,
endovascular interventions like transcatheter aortic valve
implantation (TAVI), endovascular aneurysm repair (EVAR),
or insertion of intra-aortic balloon pump (IABP). Intramural
hematoma involving ascending aorta also falls into the
category of type A aortic dissection.
Risk Factors
Hypertension is present in nearly 75% of individuals with
aortic dissection. Other risk factors include pre-existing
ascending aortic aneurysms,4 smoking, Marfan’s syndrome,
hereditary TAA/D, Ehlers-Danlos syndrome, Turner’s
syndrome, penetrating atherosclerotic ulcer, giant cell
arteritis, Takayasu arteritis, Bechet’s disease, aortitis, cocaine
use, and pregnancy. Genetically triggered disorders are
important and often unrecognized causes of aortic dissection.
The first classification scheme of aortic dissection was
designed by DeBakey, who separated dissections into the
following types:
Type I: The dissection involves the ascending aorta, aortic
arch, descending aorta, and often abdominal aorta.
Type II: The dissection involves ascending aorta but stops
at the level of aortic arch and does not involve the aorta
beyond the left subclavian artery take off.
Type III: The dissection starts distal to the left subclavian
artery and extends to the entire descending thoracic aorta
(IIIa) or the descending thoracic and abdominal aorta (IIIb).
The following Stanford classification has become popular,
primarily because of its therapeutic implications.
Type A aortic dissection: Dissection involves ascending
aorta and will most often extend into the arch, descending
thoracic as well as abdominal aorta.
Figure 1. Pictorial Depiction of Aortic Dissection.
Figure 2. Classification of Aortic Dissection.
Type B aortic dissection: Dissection starts beyond aortic
arch usually at the subclavian artery, progresses distally thus
not involving ascending aorta or the arch.
Dissection based on timing of presentation5:
Acute aortic dissection: Patient presenting within 2 weeks
from the onset of pain.
Subacute aortic dissection: Patient presenting between 2
and 6 weeks of onset of pain.
Chronic aortic dissection: Patient presenting after 6 weeks
from the onset of pain.
Epidemiology
Acute type A aortic dissection constitute about 60% of all
aortic dissections. About 49% of these patients die before
they reach the hospital. The incidence of acute type A aortic
dissection has been reported to be 2.5 to 6 cases per 100 000
patient years. The increasing life expectancy of population
is probably contributing to the higher incidence. Men are
affected about 4 times more commonly than women.
Clinical Presentation
The aortic media has high density of nerve endings,6 so when
medial disruption takes place the acute onset of sharp pain
is a uniform presenting symptom. The pain is classically
described as acute ripping, tearing, or knife-like chest pain,
which then migrates to the upper back and often progresses
down to the lower back depending on the dynamics of growth
of false lumen. Once the false lumen is fully established
and has stabilized, the acute pain may change into a more
persistent and dull pain, which is often not so easy to localize
and may involve chest and back in variable patterns with
additional elements of nausea, abdominal pain, diaphoresis,
and shortness of breath.

Nagaradona et al. 25
Cardiac symptoms are usually secondary to acute aortic
regurgitation, myocardial ischemia, or cardiac tamponade.
About 50% to 80% of patients with acute type A aortic
dissection develop moderate to severe aortic regurgitation,
due to prolapse of the intimal layer at the level of one or
more commissures. In about 10% to 15% of the patients the
false lumen can compromise coronary ostium (usually RCA),
causing myocardial ischemia or infarct. These patients can
present with heart failure or cardiogenic shock.
Nearly 10% to 40% of the patients with acute type A
aortic dissection can have neurological symptoms, due
to malperfusion of arch vessels/thromboembolism or
hypotension. Neurological symptoms can be transient in
about 50% of these patients.
Mesenteric ischemia secondary to gut vessel malperfusion
can occur in about 5% of the patients and the reported
mortality in these patients is as high as 70% to 80%. Flank
pain can also be present, especially in patients who are
suffering from an acute malperfusion of one of the kidneys.
Additional presenting symptom can be sudden onset of a cold
and pulseless extremity.
Medical Management
During the initial assessment, it is imperative to control pain
and blood pressure in these patients to prevent aortic rupture.
To achieve this, morphine and intravenous B-blockers
(Labetalol, Esmolol) are administered. The target systolic
blood pressure should be less than 120 mmHg and heart rate
less than 60 beats/min. Intravenous B-blockers are favorable
to reduce the force of left ventricular ejection (dP/dt), which
will otherwise continue to weaken the aortic wall. Combined
use of intravenous B-blockers and sodium nitroprusside
might be required in some patients with severe hypertension.
Patient with significant hemodynamic instability might need
intubation and ventilation.
Diagnosis
A high degree of clinical suspicion leads to timely diagnosis
of acute type A aortic dissection, which in turn leads to
successful treatment. Screening test should include ECG and
chest X-ray. ECG is often nondiagnostic and occasionally
may show inferior wall changes suggestive of right coronary
artery compromise by dissection. Chest X-ray may show a
dilated mediastinum or a large cardiac silhouette possibly due
to acute pericardial effusion. The next screening test should
be a transthoracic echocardiogram. It might show a variable
degree of aortic valve insufficiency with a dilated root or
presence of intimal flap along with pericardial effusion if any.
Computed tomography (CT) aortogram, transesophageal
echocardiogram (TEE), and magnetic resonance imaging
(MRI) are highly accurate in the diagnosis of aortic dissection.
The selection of specific imaging modality is influenced by
individual patient characteristics, variabilities, institutional
capabilities, and expertise.
The best diagnostic modality for confirmation of an
aortic dissection is CT aortogram. It has high sensitivity and
specificity.7 It will reveal the extent of dissection, true and
false lumen, and the involvement of branch or arch vessels.
Usually the false lumen is greater than the true lumen. CT
aortogram also aids in decision making regarding the arterial
cannulation site and surgical planning.
Figure 3. CT Aortogram Showing Type A Aortic Dissection.
Figure 4. CT Aortogram Showing Intramural Hematoma.

26 Indian Journal of Clinical Cardiology 2(1)
TEE has an advantage of being portable and can be
performed at the bedside in an unstable patient. TEE is
helpful in evaluation of aortic valve leaflets, pericardial
effusion, and detection of intimal flap in the aortic root. TEE
is usually performed as an intraoperative test after intubation
for obtaining accurate and detailed information.
Because MRI imaging takes longer for image acquisition
and leaves the patient relatively unmonitored, it is usually not
the procedure of choice.
A question usually arises over the value of coronary
artery evaluation after making the diagnosis of type A
aortic dissection. Retrospective reviews suggest that the
incidence of coronary artery disease in this population is
sufficiently low. More patients are placed at risk by the delay
and technical risks of cardiac catheterization. CT coronary
angiogram or intraoperative coronary angiogram is an option
in these patients.
It is important to understand malperfusion, before we
proceed into further discussion about aortic dissection.
Malperfusion
Malperfusion means compromised blood flow to the organs
resulting in organ ischemia. It is secondary to increased
pressure in the false lumen which compresses and jeopardizes
flow in the true lumen and its branch vessels. Branch vessel
compromise can often be seen on CT aortogram, but it is the
presence or absence of end organ ischemia that decides the
prognosis.
Malperfusion occurs in the following scenarios:
Presurgery malperfusion: Malperfusion phenomenon
might already be existing prior to surgery in the form of pulse
deficit (carotid or peripheral) or organ ischemia.
Malperfusion on institution of cardiopulmonary bypass:
Peripheral arterial cannulation at any site like common
femoral artery or axillary artery can precipitate or worsen
malperfusion on initiation of CPB. The retrograde arterial
flow towards the heart, even when cannula lies within the true
lumen, may lead to differential false lumen dominance via
primary or secondary tear and cause cerebral, cardiac or other
organ malperfusion.
Malperfusion during aortic cross-clamping: Malperfusion
can also occur during cross-clamping of aorta. The existing
communication between true and false lumen can be
obstructed by the cross-clamp, resulting in increased pressure
in the false lumen and can cause cerebral malperfusion or
rupture of aorta.
Surgical Technique
There are 5 primary causes of death in acute type A aortic
dissection. They are (1) aortic rupture, (2) congestive heart
failure due to acute aortic valve insufficiency, (3) acute
myocardial infarction secondary to malperfusion of coronary
arteries, (4) stroke resulting from malperfusion of aortic arch
vessels, and (5) mesenteric or other organ ischemia.
A successful operation for acute type A aortic dissection
will leave the patient with a reconstructed or replaced aortic
root, a well-functioning aortic valve, a completely replaced
ascending aorta, a partially or completely replaced aortic arch
with true lumen patency in the arch vessels and a distal type
B aortic dissection in the residual aorta.
Once the patient has confirmed diagnosis of acute type
A aortic dissection, an expeditious surgical repair may be
done after arranging for blood and blood products. Patient
is anesthetized under endotracheal general anesthesia.
Blood pressure monitoring consists of bilateral radial
artery catheterization or right radial artery and a femoral
artery catheterization. The most common vessel to suffer
malperfusion is the innominate artery. Therefore, the right
radial artery would provide early warning of the most likely
malperfusion syndrome affecting the brain. Left radial
artery or femoral artery catheter monitoring will give further
information about the presence of downstream and less
common arch malperfusions. A wide bore peripheral cannula
and a central line are inserted. Some centers would prefer to
insert PA catheter as a routine in these patients.
Patient’s chest, abdomen, and both lower extremities are
prepped and draped. It is advisable to perform peripheral
arterial cannulation for CPB before performing the sternotomy.
Because of the size and ease of access, common femoral
artery is often used for arterial cannulation to establish
cardiopulmonary bypass. But, retrograde perfusion through
femoral artery can cause pressurization of false lumen and can
compromise the true lumen flow resulting in malperfusion.
Over the last decade, right axillary artery is being used
more often. It is an excellent alternative site for peripheral
arterial cannulation.8 Usually an 8 mm Dacron graft is sown
to the right axillary artery, which in turn is connected to the
arterial circuit of CPB. It facilitates anterograde flow and has
a decreased probability of creating cerebral malperfusion.
Other alternative arterial cannulation sites include carotid
artery, innominate artery, direct aortic cannulation (with
the help of epiaortic scanning and Seldinger technique) and
trans LV apical-aortic cannulation. However, cannulation at
any of the aforementioned sites can still create malperfusion
on establishment of CPB. Thus, it is very important to be
extra vigilant during the institution of CPB. Detection of
malperfusion at this time should prompt the surgeon to
change the arterial cannulation site immediately to ensure
true luminal flow.
Intraoperatively blood gas analysis, lactate measurement,
and mixed venous saturation monitoring from CPB circuit
will give an indication of a global organ perfusion. Evidence
of ongoing profound lactic acidosis will alert the possibility
of malperfusion phenomenon either related to limb or
visceral ischemia.
Once the sternotomy is performed, the pericardium is
opened. It is common to find a variable amount of blood tinged

Nagaradona et al. 27
pericardial fluid or even moderate amount of blood under
tension. Often the ascending aorta will be moderately dilated
because aneurysm is a major risk factor leading to ascending
aortic dissection.4 We find the most common area of intimal
tear is at mid ascending aortic level. Most often the blood
enters the loose areolar tissue between the main pulmonary
artery and the ascending aorta, sometimes dissecting down
onto right ventricular outflow tract (as shown in the picture).
It is important early in the process not to disturb this
dissected tissue because it is easy to convert dissection process
into free rupture. With arterial access obtained peripherally,
right atrium is cannulated in routine manner. Patient is
placed on full CPB. During institution of bypass, very close
monitoring of arterial wave form, from both radial arteries, is
used to detect any malperfusion syndrome. In several patients,
significant aortic valve insufficiency will be present hence the
left atrium and left ventricle are vented through right superior
pulmonary vein. Patient is subjected for cooling with a goal
of achieving nasopharyngeal temperature of 16°C.
Temperature monitoring: Organ protection constitutes an
important aspect while performing surgery for acute type A
aortic dissection. Core cooling of the patient up to 16°C is
necessary to reduce the metabolic activity of all the organs
including brain during total circulatory arrest. Patients
temperature can be monitored from various sites such as
nasopharyngeal, jugular bulb, esophageal, rectal, arterial
inflow, urinary bladder, skin, and tympanic membrane. Most
of these sites do not reflect true brain temperature. Out of
all these sites, jugular bulb temperature correlates best with
cerebral temperature, but it is very invasive and not routinely
used. In a study published by Kaukuntla et al,9 the authors
concluded that nasopharyngeal temperature monitoring as an
easy and safe method for measuring brain temperature.
Cerebral blood flow and metabolism: The incidence of
neurological compromise happening during the surgical
procedure is quoted between 5% and 20% and is associated
with poor early and midterm outcomes.
To avoid cerebral hypoxia during surgery, it is essential
to monitor cerebral metabolism and blood flow. A number
of gadgets are available for this purpose. These include
transcranial doppler, EEG, near-infrared spectroscopy
(NIRS), jugular venous oxygen saturation. We routinely use
NIRS as a cerebral monitoring device in all these patients.
NIRS is a simple and noninvasive way to monitor rCSo2—
regional cerebral tissue oxygen saturation. The mean cerebral
tissue oxygen saturation is around 60% to 70%. Any drop in
the rCSo2 of more than 20% from the baseline during surgery
can be associated with ischemic neurological injury.10
Figure 7. Near-Infrared Spectroscopy With Adhesive Patches
(NIRS).
Figure 5. Type A Aortic Dissection—Appearance of Ascending
Aorta.
Figure 6. Type A Aortic Dissection Showing Clot Around RVOT.

28 Indian Journal of Clinical Cardiology 2(1)
Figure 8. Transected Ascending Aorta Showing True and False
Lumen.
Figure 9. Ascending Aorta Showing Intramural Hematoma.
As the core cooling progresses, patient’s heart will
fibrillate. Aorta is then cross-clamped at mid-ascending aortic
level. Although in the past there has been reluctance to cross-
clamp dissected ascending aorta, over the past decade no
aortic disruption has resulted from cross-clamping, even in
patients with connective tissue disorders. Clearly the cross-
clamp should be placed well below the innominate artery
take off. After the ascending aorta is cross-clamped without
malperfusion, it is divided at the level of right pulmonary
artery and cold blood cardioplegia is given via direct coronary
osteal cannulation.
The generally accepted repair of Acute type A Aortic
dissection involves:
1. Ascending aortic replacement with aortic valve
resuspension (for correction of aortic valve
regurgitation) or
2. Aortic root replacement (where in the ascending
aorta and aortic valve are excised and replaced with a
valve conduit along with reimplantation of coronary
buttons).
3. With or without arch replacement depending upon
the presence or absence of intimal tears in the arch
of aorta.
The distal anastomosis is usually performed in an open
manner after the cross-clamp is removed under hypothermic
circulatory arrest (HCA). However, HCA allows only limited
time for distal aortic anastomosis. In order to extend the
potential safety duration of circulatory arrest, adjunctive
techniques have been developed. For a long time, retrograde
cerebral perfusion (RCP) through superior vena cava was used
as an adjunctive technique during HCA for improved cerebral
protection. The advantages of RCP are cerebral perfusion,
cooling of brain and washing out of metabolites and embolic
debris. Disadvantages in this technique includes increased
risk of cerebral edema and inadequate neuroprotection.
The adjunctive technique most often used now a days is
selective antegrade cerebral perfusion. In this method, we
selectively cannulate and perfuse one or both carotid arteries
antegradely.11
Once the cardioplegia is given, the aortic root is evaluated
to see if it is repairable. The prerequisites for aortic root
repair are (1) there should not be any intimal tear in the aortic
root, (2) aortic leaflets should be normal, and (3) aortic root
should not be dilated. Mild dilatation of sinotubular junction
up to 30 mm in maximum diameter can be tolerated with an
adequate repair. If the above requirements are met with, the
aortic leaflets are resuspended with commissural sutures and
the entire ascending aorta is replaced with a Dacron graft.
If the aortic root is severely aneurysmal or if there are
intimal tears in the root or if the aortic leaflets are damaged,
then usually aortic root replacement is performed. A
mechanical valved Dacron conduit is a good option in most
of the patients who are less than 60 years old. A biological
valved conduit should be considered in patients more than 60
years old. Although valve sparing root operation is an option,
it should be reserved for patients less than 50 years old and
with normal leaflets.12

Nagaradona et al. 29
Figure 10. Performing Aortic Root Replacement.
Figure 11. Completed Aortic Root Replacement and Distal Aortic
Anastomosis.
Usually adequate cooling will be reached before
completion of root replacement. Attention is directed toward
distal aorta. Total circulatory arrest is instituted and antegrade
cerebral perfusion is commenced at a rate of 10 to 15 mL/kg/
min. Then the rest of ascending aorta is debrided. Majority of
the undersurface of the aortic arch is excised. A thin teflon felt
strip is placed within the false lumen area in the arch. Again,
the primary goal here is to prevent arch malperfusion with
a secondary goal to create a layer that would hold sutures
well for aortic arch reconstruction. A Dacron graft is then
appropriately beveled and sewn to the reinforced arch tissue.
Occasionally the aortic arch disruption is so severe that a
total arch replacement is necessary (elephant trunk or frozen
elephant trunk (FET) can be used if there is involvement of
descending thoracic aorta).
Figure 12. Pictorial Representation of Different Surgical
Options Used During Treatment of Type A Aortic Dissection. (A,
B, C) Resuspension of Aortic Valve, Aortic Root Reinforcement
With Teflon Felt. (C, D) Hemiarch Replacement. (E, F) Total Arch
Replacement Along With Frozen Elephant Trunk.
Arch replacement along with antegrade stent graft
placement into the descending aorta is known as FET
technique. It is a hybrid surgical approach used in cases of
complex type A aortic dissection. Indications are as follows:
(1) When the primary tear is located in the transverse arch
or proximal descending thoracic aorta. (2) Dilated arch and
descending thoracic aorta (size >50mm). (3) Severe dissection
involving the arch vessels or when there is extensive intimal
intussusception. FET obliterates the false lumen at the
proximal descending thoracic aorta and also covers secondary
entry tears located in proximal descending thoracic aorta.
After the hemiarch or total arch repair, the Dacron graft is
directly cannulated, and CPB is reestablished. The proximal
reconstruction is then sewn into the arch graft. Cardiac
deairing maneuvers are performed and the heart is allowed to
reperfuse. After complete rewarming, the patient is weaned
off CPB. Early postpump is important to assess aortic valve
insufficiency and ventricular function with TEE.
Postoperative Complications
According to the NORCAAD registry,13 the common
complications following surgery for acute type A aortic

30 Indian Journal of Clinical Cardiology 2(1)
dissection include major bleeding (39%), stroke (20%), acute
kidney injury requiring renal replacement therapy (12%),
malperfusion (16%) (resulting in myocardial infarction,
mesenteric ischemia, limb ischemia), prolonged ventilatory
support(33%), and infections(2%-10%) of the patients.
Postoperative bleeding in these patients is due to
pre-existing coagulopathy (secondary to tissue factor exposure
in the false lumen), coupled with surgery, hypothermia, and
poor-quality tissues. There is a progressive reduction in
clotting factors, platelet function, and fibrinogen resulting in
coagulation derangement similar to disseminated intravascular
coagulation. The optimal approach to the management of
coagulopathy consists of (1) use of thromboelastography to
identify blood component deficiency, (2) aggressive goal
directed replacement of fibrinogen, platelet, and factor
deficiencies, and (3) use of fibrinolytic agents.
Prolonged duration of CPB and HCA contribute to being
important risk factors for perioperative stroke. NORCAD
registry shows that preoperative cerebral malperfusion is
associated with a 3-fold increase in stroke rate.
Patients’ age, BMI >30 kg/m2, hypertension, prolonged
CPB time,14 multiple transfusions are independent risk factors
for acute kidney injury and is associated with poorer 30-day
survival.
Major predictors of 30-day mortality include cardiac or
visceral malperfusion, postoperative stroke, acute kidney
injury and massive bleeding. Short- and long-term survival
following repair of acute type A aortic dissection has ranged
between 52% and 95% at 1 year and 45% and 88% at 5 years.
One recent study reported a 10-year survival of 55% and a
20-year survival of 30% after surgery.15
Single Surgeon Experience
Between 2008 and 2020 a total of 60 cases underwent surgery
for acute type A aortic dissection (performed by a single
surgeon). Mean age of the patients was 48 +/- 21 years. In
total, 80% were male and 11 patients had Marfan’s syndrome.
Moderate to severe aortic regurgitation was present in 88%
of the patients on presentation. Features of significant
pericardial effusion/tamponade were present in 9 patients.
The duration between the diagnosis and operation was less
than 2 h in all the patients. Axillary artery cannulation was
performed in 60% of patients and the remaining patients had
femoral artery cannulation. Distal open anastomosis was done
in all the patients. Cerebral protection was ensured by HCA
along with antegrade cerebral perfusion, which was used in
55% and RCP was used in 45% of the patients. Concomitant
procedures performed include mitral valve repair in 3 patients,
mitral valve replacement in 1 patient, coronary artery bypass
grafting in 3 patients, full arch replacement was performed
in 2 patients. Postoperatively, significant neurological
dysfunction was present in 2 patients, out of which 1 patient
recovered completely within 6 weeks. Total arch replacement
in aortic dissection patients was a significant predictor of
poor neurological outcome. In hospital 30-day mortality was
3.38% (2 patients). The presence of low ejection fraction,
post-operative renal failure, and the need for aortic arch
replacement are significant predictors of mortality. Long-
term survival in these patients was 96%, 72%, and 55% at 1,
5, and 10 years, respectively.
Follow-up
It is important to understand that long-term follow-up is
essential in these patients after initial successful treatment.
Aortic dissection is a chronic disease and patients can
develop aneurysm, progression of dissection or aortic rupture
in the distal residual aorta. So, it is mandatory to monitor all
these patients with yearly CT aortogram. The predictors of
progression of this disease include uncontrolled hypertension,
dilated distal aorta and perfused false lumen. Effective
B-blockade and control of hypertension is important to
reduce these vascular complications. By and large about 30%
of patients who underwent successful surgery for acute type
A aortic dissection will have disease progression and will
need further intervention in about 5 years.
Acknowledgment
Vikram, Vishnu, Srikanth, Vamshi, Haseena, Rajamma, Soundarya,
Honey, Soniya, Aruna, Mounika, and Ridhima have contributed
equally to this work.
Declaration of Conicting Interests
e authors declared no potential conicts of interest with respect to
the research, authorship, and/or publication of this article.
Funding
e authors received no nancial support for the research, author-
ship, and/or publication of this article.
References
1. Howard DP, Banerjee A, Fairhead JF, et al. Population based
study of incidence and outcome of acute aortic dissection and
premorbid risk factor control: 10 year results from the oxford
vascular study. Circulation. 2013;127(20):2031-2037.
2. Melvinsdottir H, Lund SH, Agnarsson BA, et al. The
incidence and mortality of acute thoracic aortic dissection:
results from a whole nation study. Eur J Cardiothorac Surg.
2016;50(6):1111-1117.
3. Hagan PG, Nienaber CA, Isselbacher EM, et al. The
international registry of acute aortic dissection (IRAD): new
insights into an old disease. JAMA. 2000;283:897-903.
4. Davies RR, Gallo A, Coady MA, et al. Novel measurement of
relative aortic size predicts rupture of thoracic aortic aneurysms.
Ann Thorac Surg. 2006;81,169-177.

Nagaradona et al. 31
5. Nienaber CA, Powell JT. Management of acute aortic
syndrome. Eur Heart J. 2012;33:26-35.
6. Berthond HR, Neuhuber WL. Functional and chemical
anatomy of the afferent vagal system. Auton Neurosci.
2000;85(1-3):1-17.
7. Rogers IS, Banerji D, Siegel EL, et al. Usefulness of
comprehensive cardiothoracic computed tomography in
the evaluation of acute undifferentiated chest discomfort
in the emergency department (CAPTURE). Am J Cardiol.
2011;107(5):643-650.
8. Sabik JF, Nemeh H, Lytle, BW, et al. Cannulation of the
axillary artery with a side graft reduces morbidity. Ann Thorac
Surg. 2004;77(4):1315-1320.
9. Kaukuntla H, Harrington D, Bilkoo I, et al. Temperature
monitoring during cardiopulmonary bypass—do we
undercool or overheat the brain. Eur J Cardiothorac Surg.
2004;26(3):580-585.
10. Levy WJ, Levin S, Chance B. Near infra-red measurement of
cerebral oxygenation: correlation with electroencephalographic
ischemia during ventricular fibrillation. Anesthesiology.
1995;83(4):738-746.
11. Kruger T, Weigang E, Aebert H, et al. Cerebral protection during
surgery for acute aortic dissection type A—results of German
registry for Acute Aortic Dissection Type A (GERAADA).
Circulation. 2011;124:434-443.
12. Goldfinger JZ, Halperin JL, Marin ML, et al. Thoracic
aortic aneurysm and dissection. J Am Coll Cardiol.
2014;64:1725-1739.
13. Zindovic I, Gudbjartsson T, Ahlsson A, et al. Malperfusion
in acute type A aortic dissection. An update from the Nordic
Consortium for Acute Type A Aortic dissection. J Thorac
Cardiovasc Surg. 2019;157(4):1324-1333.
14. Xu S, Liu J, Li L, et al. Cardiopulmonary bypass is an
independent risk factor for acute kidney injury in emergent
thoracic aortic surgery: a retrospective cohort study. J
Cardiothorac Surg. 2019;14(1):90.
15. Stevens L-M, Madsen JC, Isselbacher EM, et al. Surgical
management and long term outcomes for acute ascending aortic
dissection. J Thorac Cardiovasc Surg. 2009;138(6):1349-1357.