Abstract
Background : Type A aortic dissection (TAAD) involves a tear in
the intimal layer of the thoracic aorta proximal to the left subclavian
artery, and hence, carries a high risk of mortality and morbidity and
requires urgent intervention. This dissection can extend into the main
coronary arteries. Coronary artery involvement in TAAD can either be due
to retrograde extension of the dissection flap into the coronaries or
compression and/or blockage of these vessels by the dissection flap,
possibly causing myocardial ischaemia. Due to the emergent nature of
TAAD, coronary involvement is often missed during diagnosis, thereby
delaying the required intervention.
Aims : The main scope of this review is to summarise the
literature on the incidence, mechanism, diagnosis, and treatment of
coronary artery involvement in TAAD.
Methods : A comprehensive literature search was performed using
multiple electronic databases, including PubMed, Ovid, Scopus and
Embase, to identify and extract relevant studies.
Results : Incidence of coronary artery involvement in TAAD was
seldom reported in the literature, however, some studies have described
patients diagnosed either preoperatively, intraoperatively following
aortic clamping, or even during autopsy. Among the few studies that
reported on this matter, the treatment choice for coronary involvement
in TAAD was varied, with the majority revascularizing the coronary
arteries using coronary artery bypass grafting or direct local repair of
the vessels. It is well-established that coronary artery involvement in
TAAD adds to the already high mortality and morbidity associated with
this disease. Lastly, the right main coronary artery was often more
implicated than the left.
Conclusion : This review reiterates the significance of an
accurate diagnosis and timely and effective interventions to improve
prognosis. Finally, further large cohort studies and longer trials are
needed to reach a definitive consensus on the best approach for coronary
involvement in TAAD.
Keywords: Aortic Dissection, Type A Aortic Dissection (TAAD), Aortic
Surgery, Coronary Artery, CAD, CABG.
Introduction
Aortic dissection (AD) is a life-threatening medical condition that
annually affects 3-4 people per 100,000 [1][2]. The underlying
pathology is defined by a tear in the aortic intima producing medial
layer separation, creating a space known as the false lumen (FL) into
which bloods flows. If this entry tear originates proximal to the left
subclavian artery (LSA) (Zone 0-2), the event is classified as Type A AD
(TAAD); otherwise, the dissection is Type B (TBAD) with the originating
entry tear located distal to the LSA and without arch involvement
[1][3]. AD can be further classified based on timeframe into
acute (<15 days since symptom onset), subacute (15-90 days
since symptom onset), and chronic (>90 days since symptom
onset) [1][3]. Acute TAAD has the highest mortality, which can
reach 50% within the first 48 hours without prompt intervention
[4].
Treatment for acute TAAD involves open surgical repair/replacement of
the affected segment, with or without total arch replacement (TAR) using
frozen elephant trunk (FET), if the aortic arch is involved [5]. The
extent of dissection flap in TAAD can sometimes involve the main
coronaries, either by causing coronary artery dissection or by blocking
the coronary ostia, causing myocardial ischaemia. Given the acute
setting of TAAD, coronary involvement is often missed [6].
This review will highlight the mechanisms behind TAAD with concomitant
coronary involvement as well as the diagnostic methods and corrective
approaches. A comprehensive literature search was conducted using
multiple electronic databases including PubMed, Ovid, Scopus and Embase
to identify and extract all the evidence in the literature on coronary
artery involvement in TAAD.
Diagnosing Type A Aortic Dissection with Concomitant Coronary
Malperfusion
Despite great advances in the field of aortovascular surgery, TAAD with
concomitant coronary artery involvement still poses a significant
diagnostic challenge. With its rare incidence, and variable clinical
presentation, coronary involvement is often difficult to diagnose and
may go undetected for a significant amount of time [6]. Due to the
paucity of literature on this topic, acute coronary involvement has been
loosely associated with coronary dissection, malperfusion, or occlusion
and resulting ischaemia. Unfortunately, many research papers have not
differentiated between these specific anatomic scenarios.
It is important to note that coronary involvement in TAAD does not
strictly lead to myocardial ischaemia and infarction. This is evidenced
in a study by Chen et al. [7] where 6 out of 20 patients (30%)
presented with aortic dissection and acute coronary involvement without
evidence of myocardial ischaemia. This has also been supported by other
studies in the literature, where patients who presented with the
dissection extending retrogradely to the coronary ostia were assessed
for myocardial ischaemia, and remarkably between 21.4% and 25% showed
no such evidence [6-8]. The most common mechanism of myocardial
ischaemia as a result of acute aortic dissection is the retrograde
extension of the dissection into the coronary arteries [8]. In
addition to this, coronary malperfusion can result from compression of
the coronary arteries by the dissection flap or a haematoma [6].
The Neri classification was repeatedly cited throughout the literature
to highlight the different mechanisms behind coronary malperfusion
[9]. As illustrated in Figure 1 , Neri et al. [9]
described 3 main types of coronary lesions that result from aortic
dissection. Type A is considered coronary ostium dissection and is
limited to the ostium, while type B features a coronary false channel.
On the other hand, type C coronary artery dissection involves detachment
of the coronary circumference and associated intussusception. As
described by the authors, ostial dissection may not always result in
coronary malperfusion, unless a local flap occludes blood flow,
essentially working as a ‘trapdoor’. When a dehiscence in the coronary
wall forms, a coronary false channel can be created, allowing for a
retrograde extension of the dissection into the coronary artery. The
distal extent of this coronary artery dissection can vary amongst
patients. When the coronary artery is separated from the aortic root, as
seen in type C, occlusion of the blood flow can subsequently result in
coronary ischaemia and myocardial damage [9].
Table 1 summarises the patient demographics and comorbidities
of those that were diagnosed with TAAD and concomitant coronary
involvement which we identified upon searching the literature.
Additionally, it depicts the mode of diagnosis, which coronary arteries
were involved, and the cause of coronary malperfusion, if reported.
Reported incidence of coronary malperfusion in association with acute
aortic dissection has been variable, ranging from 6.1% to 14.1% in the
literature [6,7]. As shown in the table, there was a mixed gender
dominance in this group of patients. However, paradoxically, patients
who developed coronary malperfusion were younger (p=0.001) and were also
at a lower risk of intramural haematomas (p=0.001), as demonstrated by
Chen et al. [7]. As expected, a large number of patients had a
history of coronary artery disease, hypertension, chronic obstructive
pulmonary disease, diabetes and were known smokers. Some patients also
had Marfan’s syndrome, and this was found to be significantly associated
with coronary involvement (p=0.008), in addition to hypertension
(p=0.003). Moreover, patients who developed coronary involvement were
associated with an increased aortic regurgitation rate (p=0.001), which
often warranted valve replacement [7].
The mode of diagnosis of concomitant coronary malperfusion varied
greatly, as evident in Table 1 . Patients were diagnosed either
preoperatively, or following aortic clamping amidst surgery, or even
during autopsy. Prior to surgery, some patients had presented with new
ST-segment elevation on ECG, in addition to abnormalities in the motion
of the left ventricle (echocardiogram) and very high levels of serum
creatine kinase. A recent systematic review and meta-analysis suggested
that ECG changes indicating ischaemia were not helpful in diagnosing
patients with aortic dissection [10]. Although ECG changes tend to
be more consistent with coronary involvement, overall, less than around
50% of aortic dissections are discernible on ECG [11]. Some studies
have also evaluated the benefit of using coronary angiography to
diagnose coronary involvement prior to surgery, however, such an
approach showed no effect on coronary artery bypass grafting (CABG)
rates and did not improve the prognosis for these patients.
Additionally, and interestingly, it was even noted that performing this
investigation can cause critical delays in treatment [12].
As also seen in Table 1 , the right coronary artery was more
commonly involved in aortic dissection, hence, myocardial ischaemia is
expected to impact the inferior, rather than the anteroseptal walls,
more commonly [13]. These findings are concurrent with a study
involving 236 aortic dissection patients, whom the right coronary artery
was more commonly affected [14]. Although higher rates of myocardial
ischaemia have been reported related to the right coronary artery, a
significant link has been established between left coronary involvement
and pre-operative cardiopulmonary arrest (p=0.004) [15].
Furthermore, the mechanisms of coronary malperfusion described earlier
in this paper are all identified in the Table, with the main cause being
coronary dissection due to retrograde extension of the aortic
dissection, as expected.
It is also important to note that various patients presented with
haemodynamic instability, often requiring cardiopulmonary resuscitation
(CPR) and other interventions such as percutaneous cardiopulmonary
support (PCPS) preoperatively [6]. The role of such interventions in
producing a successful outcome in cases of coronary involvement must be
evaluated in future studies. Moreover, many patients also presented with
hemopericardium, cardiac tamponade, intramural hematoma, pleural
effusion, limb ischaemia, and other complications that may have had an
impact on treatment options and prognosis [7].
The Surgical Approach
When a patient presents acutely with aortic dissection symptoms, the
appropriate investigations and medical management are initiated. Once
the diagnosis is confirmed with imaging (echocardiogram, CT, MRI), more
invasive surgical treatment is usually undertaken [16,17]. This
section will describe the surgical approach for managing TAAD with
concomitant coronary involvement, in addition to other treatment
modalities reported in the literature.
In TAAD, surgical aortic repair is the definitive management of choice
in most circumstances. The aim of this procedure is to resect the
intimal tear and, depending on the location and extent of the tear,
replace the aortic root, ascending aorta and/or the arch (which can be
partial or total) [16]. Other factors that dictate the type of
surgical intervention are branch vessel impairment, coronary artery
involvement, and aortic valve involvement [17].
TAAD Repair
The majority of studies reported performing an open aortic repair
through a median sternotomy, with cardiopulmonary bypass, as illustrated
in Table 2. If the tear is in the ascending aorta, this portion is
resected and replaced with a synthetic graft. The distal anastomosis is
often done open, under deep hypothermic circulatory arrest. Then,
perfusion is resumed, followed by establishment of the proximal
anastomosis [6]., Eren and others described using the Bentall
technique for these tears in selected cases with root enlargement or
dissection [8]. If the tear is in the aortic arch, partial or
complete replacement of that segment can be done [6].
Surgical management of coronary malperfusion is dependent on when
coronary involvement is identified. In the study by Kawahito et al.
[6], myocardial protective measures were established early during
the surgery. Systemic cooling was done instantly after CPB was started.
When ventricular fibrillation was identified, the ascending aorta was
clamped and incised. If the coronary ostia were involved or if
annuloaortic ectasia was present, the aortic root was replaced using the
composite valve-graft conduit technique. For myocardial protection,
cardioplegia can be delivered through the coronary sinus in a retrograde
manner or antegradely through a non-dissected ostium. During systemic
cooling and rewarming, myocardial protection was administered
frequently, every 20 minutes. If coronary involvement is identified
earlier, the cardioplegic solution may be passed through constructed
CABG grafts and the coronary ostium, before aortic repair is started
[6]. However, some studies, like the one by Eren et al. [8],
used continuous retrograde cold blood cardioplegia uninterruptedly
through the coronary sinus. [8]. If coronary involvement was evident
only after aortic declamping (through impaired myocardial performance),
saphenous vein grafting can be performed during the rewarming phase.
The surgical approach is a theme of controversy in the literature and
current practice, even the timing of intervention has also been
challenged. A delay in surgical management is thought to allow time for
inflammation to abate and is thought to yield benefit in peripheral
malperfusion. Despite this, in patients presenting with TAAD with
coronary involvement, delaying surgical management can result in
permanent myocardial ischaemia and necrosis [7].
Coronary Revascularisation
Figures 2, 3 and 4 illustrate the reconstruction technique for
Type A, B and C coronary dissections as well as the underlying pathology
behind each, respectively.
Regarding the choice of coronary management, Kawahito et al., and others
described their preference of CABG over local coronary repair for
revascularisation out of fear of operating on friable arteries and the
delicacy and complexity associated with local coronary ostial repair
[6]. Neri et al. [9], on the other hand, explained the various
benefits of local repair for coronary revascularisation and their
encouraging results with this technique. They noted the reduced risk of
competitive flow from CABG grafts and discouragement of re-dissection of
the coronary arteries because antegrade flow has been established.
Additionally, as described in type A coronary dissection, where the
coronary ostium is involved, reconstruction can be done without
revascularising (by CABG) vessels that have unknown measure of
impairment [9]. Despite this, it is important to keep in mind that
local repair cannot take place without utilising the damaged and fragile
dissected coronary arteries, and this may not be feasible in all cases
[13]. A 2014 study by Xiao et al. [18] also described total arch
replacement for TAAD in 33 patients, with concomitant CABG to treat 2
RCA involvements.
What is the optimal approach?
Neri et al. [9] proposed their classification system in order to
facilitate the understanding of the extent of the coronary artery
dissection and its most appropriate management. For type A coronary
dissections, a continuous suture to affix the interrupted arterial
layers is sufficient, allowing for the ostium to be continuous with the
aortic wall. If this is not possible, the authors describe excising the
ostial button and reattaching this using gelatin– resorcin-formalin
glue and a running suture line to connect the ostial button to the
graft. Meanwhile, in type B coronary dissections, a cardiac patch, in
the form of a saphenous vein or autologous pericardium, is used with a
running suture to repair the dissected layers. Type C coronary
dissection management involves the vessel being transected and an
end-to-end, bevelled saphenous vein reconstruction being performed
[9,13].
Lajevardi et al. [19] described a case of full intimo-intimal
intussusception producing left coronary occlusion in a 73-year-old
patient with concomitant TAAD. The circumferential tear found at
aortotomy was located 3 cm from the sinotubular junction in the
ascending aorta, causing left coronary artery occlusion and aortic
regurgitation. This case was successfully treated with replacement of
the affected ascending aorta with aortic valve resuspension [19].
Despite the Neri classification being quoted repeatedly in the
literature, a 2013 study suggested a more novel denomination of coronary
malperfusion for surgical management guidance [7]. Changes suggested
by Chen et al. [7] include adding a fourth category, Type D, which
highlights dissection into the sinuses of Valsalva or through the aortic
annulus into the left ventricular outflow tract, resulting in
commissural detachment and aortic regurgitation.
It can be suggested that surgical management decisions should be based
on three factors. Firstly, one must consider the presence of
annuloaortic ectasia, often present in patients with connective tissue
disorders like Marfan’s and those with a bicuspid aortic valve. In this
case, a modified Bentall or valve-sparing procedure is recommended.
Secondly, the presence or absence of a damaged coronary ostium, which
often must be resected. And finally, the absence of an ostial tear as
other recommendations based on specific coronary dissection anatomy were
described by Chen et al. [7]. Nevertheless, CABG is required to
revascularize the coronary arteries.
Despite guidelines by Neri and Chen, specific management of coronary
involvement in TAAD remains controversial, with studies recommending
using CABG under all circumstances and others suggesting using solely
local repair in type A coronary dissection [13]. Pêgo-Fernandes et
al. [20] reported repairing 11 dissections with Dacron grafts.
However, for coronary involvement repair, the authors used saphenous
vein bypass grafts in 63.6% (7/11) of patients. The remaining patients
had right coronary dissection, which was re-implanted using saphenous
vein grafts or an ImpraTM vascular graft
(Becton-Dickinson, NJ, USA). For some of these cases, a Cabrol-like
technique was used, employing a smaller Dacron graft to connect the
aortic graft to the coronary ostia. This provides ‘tension-free’ method
for attachment. [20].
The Percutaneous Approach
Lentini et al. [13] documented managing the dissected coronary
arteries by preliminary stent implantation and passive perfusion balloon
catheters. The authors emphasized that these interventions, although
yielding some benefit, do not treat the underlying aortic dissection and
will act only as a temporary solution to restore coronary blood flow
until definitive surgical repair can take place [13]. In 2013, Imoto
et al. [15] reported 75 Type A dissection patients, out of whom 7
were treated with pre-operative coronary stents, and 23 with bypass
grafting. If the dissection occurred in the left main trunk, a stent was
inserted during catheterisation followed by open surgical repair of the
aorta. However, when the right coronary artery was involved, a stent was
only placed prior to surgical repair if the dissection was diagnosed
during catheterization. Balloon inflation was done early when the stents
were inserted to reduce the ischaemic damage. Fourteen patients were
found to have entry to ruptures sites to the root of the aorta and
underwent aortic root replacement as a result. Twelve of these patients
also had a direct anastomosis performed to the damaged coronary artery
involved, using a synthetic graft. In addition,
gelatin-resorcin-formaldehyde or fibrin glue were used to repair any
local damage to the arteries, or if the ostia was also involved. Out of
all techniques used to repair the coronary arteries, including stenting,
biological glue, aortic root reconstruction, and even CABG, there was no
significance found in the incidence of operative mortality (p=0.192).
However, incidence of low cardiac output syndrome was significantly
lower where coronary stents were utilised (p=0.042) [15]. These
findings by Imoto and colleagues [15] are summarised inTable 3 .
Studies that evaluate various surgical strategies for coronary
involvement and associated outcomes are very limited in the literature.
Further appraisal of our current coronary repair techniques is vital. In
a systematic review of 31 studies, only 1 reported the concomitant use
of percutaneous coronary intervention (PCI) in addition to TAAD repair
[21]. Despite this, PCI can yield significant benefit to patients
who are deemed unsuitable for surgical repair, such as those with
advanced age, significant comorbidities, and those with neurological
deficits.
Zimpfer et al. [22] successfully treated a TAAD patient with
endovascular stent-graft placement. A graft was passed through the right
coronary artery and extended from the sinotubular junction to the
brachiocephalic trunk. A temporary pacemaker was also used to reduce
cardiac output to ensure safe and controlled placement of the
stent-graft. The authors reported complete success with full exclusion
of the dissection and no evidence of malperfusion in the coronary or
supraaortic vessels. In addition, no associated complications were
reported during the early follow-up period (30 days) [22].
Outcomes
It is well-established in the literature that the presence of coronary
involvement in aortic dissection increases mortality (8.2% vs. 3.3%,
p<0.019) [7]. This review found that the main cause of
mortality intraoperatively was the inability to wean patients off CPB,
for instance due to critical left or right ventricular malperfusion and
consequent mechanical failure. Imoto et al. attributed this to pressure
differences that may occur after repair between the true and false lumen
at the aortic root. Pooling of blood into the false lumen may prevent a
drop in the lumen pressure during diastole, which may subsequently
compress the true lumen [15].
The higher mortality rate in patients with coronary involvement may also
be attributed to delays in diagnosis and often even refusal of surgical
treatment in the scenario of association coronary dissection treatment.
Hesitation to operate may be critical, given that mortality increases by
1% with each hourly delay [23]. Table 4 summarises the
complications associated with coronary involvement concomitant with
TAAD.
Conclusion
Coronary involvement in TAAD increases morbidity and mortality if
undetected or untreated; thus, it is important to identify this
condition early in the diagnosis of TAAD and to manage it accordingly.
However, further large cohort studies and longer trials are needed to
reach a definitive consensus on the best approach for coronary
involvement in TAAD.